What are the symptoms of herpetic stomatitis. How is herpetic stomatitis diagnosed. What treatments are available for HSV-1 mouth ulcers. Can herpetic stomatitis be prevented. How long does a herpetic stomatitis outbreak typically last. What triggers HSV-1 mouth ulcer outbreaks. Are there any home remedies for managing herpetic stomatitis symptoms.

What is Herpetic Stomatitis?

Herpetic stomatitis is an infection of the mouth caused by the herpes simplex virus (HSV), typically HSV-1. This condition primarily affects young children, but can occur in individuals of any age. It results in painful sores and ulcers in the mouth, often accompanied by fever and general discomfort.

The herpes simplex virus is highly contagious and can spread through direct contact with infected saliva or skin. Once contracted, the virus remains dormant in the body and can reactivate periodically, causing recurrent outbreaks.

Key Facts About Herpetic Stomatitis:

• Most commonly caused by HSV-1
• Primarily affects children under 5 years old
• Characterized by painful mouth sores and ulcers
• Can be accompanied by fever and difficulty eating or drinking
• Typically resolves on its own within 7-14 days

Recognizing the Symptoms of Herpetic Stomatitis

Identifying the symptoms of herpetic stomatitis is crucial for prompt diagnosis and management. The onset of symptoms typically occurs 3-7 days after exposure to the virus.

Do symptoms appear suddenly or gradually? Herpetic stomatitis symptoms often develop rapidly, with fever and mouth pain being the initial indicators.

Common Symptoms Include:

1. Fever (often high, around 101-104°F)
2. Irritability and restlessness
3. Difficulty eating or drinking
4. Swollen, red gums
5. Small, painful blisters on the lips, tongue, cheeks, and gums
6. Ulcers forming as blisters rupture
7. Swollen lymph nodes in the neck
8. Excessive drooling (especially in young children)
9. Bad breath

Is herpetic stomatitis always painful? While discomfort levels can vary, most individuals experience significant pain, particularly when eating, drinking, or speaking.

Diagnosing Herpetic Stomatitis: What to Expect

Accurate diagnosis of herpetic stomatitis is essential for appropriate treatment and management. Healthcare providers typically rely on a combination of clinical examination and patient history to make a diagnosis.

How do doctors diagnose herpetic stomatitis? The primary method of diagnosis is through visual inspection of the mouth and throat, along with an assessment of symptoms and medical history.

Diagnostic Process:

• Physical examination of the mouth and throat
• Review of symptoms and their duration
• Assessment of fever and general health status
• In some cases, a swab test of the lesions may be performed to confirm HSV presence

Are blood tests necessary for diagnosing herpetic stomatitis? In most cases, blood tests are not required for diagnosis, as the clinical presentation is often sufficient.

Treatment Options for HSV-1 Mouth Ulcers

While herpetic stomatitis typically resolves on its own within 1-2 weeks, various treatment options can help manage symptoms and promote healing.

What is the primary goal of herpetic stomatitis treatment? The main objectives are to alleviate pain, prevent dehydration, and support the body’s natural healing process.

Common Treatment Approaches:

1. Pain management:
   • Over-the-counter pain relievers (acetaminophen or ibuprofen)
   • Topical anesthetics for localized pain relief
2. Hydration support:
   • Encouraging fluid intake
   • In severe cases, intravenous fluids may be necessary
3. Antiviral medications:
   • Acyclovir or valacyclovir may be prescribed in severe cases or for immunocompromised patients
4. Nutritional support:
   • Soft, cool foods to minimize discomfort while eating
5. Oral hygiene:
   • Gentle brushing and rinsing to prevent secondary infections

Do antibiotics help treat herpetic stomatitis? Antibiotics are not effective against viral infections like herpetic stomatitis and are only prescribed if a secondary bacterial infection develops.

Preventing the Spread of HSV-1 and Recurrent Outbreaks

While it’s not always possible to prevent initial HSV-1 infection, certain measures can help reduce the risk of transmission and recurrent outbreaks.

How can the spread of HSV-1 be minimized? Practicing good hygiene and avoiding direct contact with infected individuals during active outbreaks are key preventive strategies.

Prevention Strategies:

• Frequent handwashing, especially after touching the mouth or face
• Avoiding sharing utensils, towels, or personal items
• Refraining from kissing or close contact during active outbreaks
• Maintaining overall health through proper nutrition and stress management
• Using sunscreen on the lips, as UV exposure can trigger outbreaks

Can vaccines prevent herpetic stomatitis? Currently, there is no vaccine available to prevent HSV-1 infection or herpetic stomatitis. Research is ongoing to develop effective vaccines.

Managing Herpetic Stomatitis in Children

Herpetic stomatitis can be particularly challenging in young children due to their inability to communicate discomfort effectively and potential resistance to treatment.

How can parents help children cope with herpetic stomatitis? Providing comfort, ensuring adequate hydration, and maintaining good oral hygiene are crucial aspects of managing the condition in children.

Tips for Caring for Children with Herpetic Stomatitis:

1. Offer frequent sips of water or ice pops to prevent dehydration
2. Provide soft, cool foods that are easy to swallow
3. Use a soft-bristled toothbrush for gentle cleaning
4. Apply lip balm to prevent cracking and further discomfort
5. Distract the child with quiet activities to take their mind off the discomfort
6. Administer pain relief medications as recommended by a healthcare provider

Should children with herpetic stomatitis stay home from school or daycare? Yes, children should be kept home until fever subsides and mouth sores begin to heal to prevent transmission to others.

Complications and When to Seek Medical Attention

While most cases of herpetic stomatitis resolve without complications, it’s important to be aware of potential issues that may require medical intervention.

What are the potential complications of herpetic stomatitis? Dehydration is the most common complication, particularly in young children. In rare cases, the infection can spread to other areas of the body.

Signs That Warrant Immediate Medical Attention:

• Persistent high fever (above 103°F)
• Signs of dehydration (dry mouth, decreased urination, lethargy)
• Difficulty breathing or swallowing
• Symptoms persisting beyond two weeks
• Spread of lesions to other parts of the body
• Severe pain that interferes with eating or drinking

Can herpetic stomatitis lead to long-term health issues? Generally, herpetic stomatitis does not cause long-term health problems. However, the virus remains dormant in the body and may cause recurrent outbreaks.

Living with HSV-1: Long-term Management and Outlook

For individuals who have contracted HSV-1, understanding how to manage the virus long-term is essential for minimizing outbreaks and maintaining overall health.

How often do HSV-1 outbreaks typically occur? The frequency of outbreaks varies among individuals, with some experiencing recurrences several times a year, while others may have infrequent or no recurrences.

Strategies for Long-term Management:

1. Identifying and avoiding personal triggers (stress, certain foods, lack of sleep)
2. Maintaining a healthy lifestyle to support immune function
3. Using antiviral medications prophylactically if outbreaks are frequent
4. Practicing good oral hygiene
5. Being mindful of potential transmission to others, especially during active outbreaks

Does having HSV-1 affect overall life expectancy? HSV-1 infection does not typically impact life expectancy in healthy individuals. However, it can cause more severe complications in immunocompromised people.

Living with HSV-1 requires awareness and proactive management, but with proper care and attention, most individuals can lead normal, healthy lives with minimal disruption from the virus. By understanding the nature of herpetic stomatitis, recognizing its symptoms, and knowing how to manage outbreaks, those affected by HSV-1 can effectively mitigate its impact on their daily lives.

What You Need to Know About Herpes Mouth Sores

Choose an AuthorAaron Barber, AT, ATC, PESAbbie Roth, MWCAdam Ostendorf, MDAdriane Baylis, PhD, CCC-SLPAdrienne M. Flood, CPNP-ACAdvanced Healthcare Provider CouncilAila Co, MDAlaina White, AT, ATCAlana Milton, MDAlana Milton, MDAlecia Jayne, AuDAlessandra Gasior, DOAlex Kemper, MDAlexandra Funk, PharmD, DABATAlexandra Sankovic, MDAlexis Klenke, RD, LDAlice Bass, CPNP-PCAlison PeggAllie DePoyAllison Rowland, AT, ATCAllison Strouse, MS, AT, ATCAmanda E. Graf, MDAmanda GoetzAmanda Smith, RN, BSN, CPNAmanda Sonk, LMTAmanda Whitaker, MDAmber Patterson, MDAmberle Prater, PhD, LPCCAmy Coleman, LISWAmy Dunn, MDAmy E. Valasek, MD, MScAmy Fanning, PT, DPTAmy Garee, CPNP-PCAmy Hahn, PhDAmy HessAmy Leber, PhDAmy LeRoy, CCLSAmy Moffett, CPNP-PCAmy Randall-McSorley, MMC, EdD CandidateAnastasia Fischer, MD, FACSMAndala HardyAndrea Brun, CPNP-PCAndrea M. Boerger, MEd, CCC-SLPAndrea Sattler, MDAndrew AxelsonAndrew Kroger, MD, MPHAndrew SchwadererAngela AbenaimAngela Billingslea, LISW-SAnn Pakalnis, MDAnna Lillis, MD, PhDAnnette Haban-BartzAnnie Drapeau, MDAnnie Temple, MS, CCC-SLP, CLCAnthony Audino, MDAnup D. Patel, MDAri Rabkin, PhDAriana Hoet, PhDArielle Sheftall, PhDArleen KarczewskiAshlee HallAshleigh Kussman, MDAshley Ebersole, MDAshley EcksteinAshley Kroon Van DiestAshley M. Davidson, AT, ATC, MSAshley Minnick, MSAH, AT, ATCAshley Overall, FNPAshley Parikh, CPNP-PCAshley Parker MSW, LISW-SAshley Parker, LISW-SAshley Tuisku, CTRSAsuncion Mejias, MD, PhDAurelia Wood, MDBailey Young, DOBecky Corbitt, RNBelinda Mills, MDBenjamin Fields, PhD, MEdBenjamin Kopp, MDBernadette Burke, AT, ATC, MSBeth Martin, RNBeth Villanueva, OTD, OTR/LBethany Uhl, MDBethany Walker, PhDBhuvana Setty, MDBill Kulju, MS, ATBlake SkinnerBonnie Gourley, MSW, LSWBrad Childers, RRT, BSBrandi Cogdill, RN, BSN, CFRN, EMT-PBrandon MorganBreanne L. 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Baxter, CPNPCheryl Gariepy, MDChet Kaczor, PharmD, MBAChris Smith, RNChristina Ching, MDChristina DayChristine Johnson, MA, CCC-SLPChristine Mansfield, PT, DPT, OCS, ATCChristine PrusaChristopher Goettee, PT, DPT, OCSChristopher Iobst, MDChristopher Ouellette, MDCindy IskeClaire Kopko PT, DPT, OCS, NASM-PESCody Hostutler, PhDConnor McDanel, MSW, LSWCorey Rood, MDCorinne Syfers, CCLSCourtney Bishop. PA-CCourtney Hall, CPNP-PCCourtney Porter, RN, MSCrystal MilnerCurt Daniels, MDCynthia Holland-Hall, MD, MPHDana Lenobel, FNPDana Noffsinger, CPNP-ACDane Snyder, MDDaniel Coury, MDDaniel DaJusta, MDDaniel Herz, MDDanielle Peifer, PT, DPTDavid A Wessells, PT, MHADavid Axelson, MDDavid Stukus, MDDean Lee, MD, PhDDebbie Terry, NPDeborah Hill, LSWDeborah Zerkle, LMTDeena Chisolm, PhDDeipanjan Nandi, MD MScDenis King, MDDenise EllDennis Cunningham, MDDennis McTigue, DDSDiane LangDominique R. Williams, MD, MPH, FAAP, Dipl ABOMDonna M. Trentel, MSA, CCLSDonna Ruch, PhDDonna TeachDoug WolfDouglas McLaughlin, MDDrew Duerson, MDEd MinerEdward Oberle, MD, RhMSUSEdward Shepherd, MDEileen Chaves, PhDElise Berlan, MDElise DawkinsElizabeth A. Cannon, LPCCElizabeth Cipollone, LPCC-SElizabeth Zmuda, DOEllyn Hamm, MM, MT-BCEmily A. Stuart, MDEmily Decker, MDEmily GetschmanEmma Wysocki, PharmD, RDNEric Butter, PhDEric Leighton, AT, ATCEric Sribnick, MD, PhDErica Domrose, RD, LDEricca L Lovegrove, RDErika RobertsErin Gates, PT, DPTErin Johnson, M.Ed., C.S.C.S.Erin Shann, BSN, RNErin TebbenFarah W. Brink, MDGail Bagwell, DNP, APRN, CNSGail Besner, MDGail Swisher, ATGarey Noritz, MDGary A. Smith, MD, DrPHGeri Hewitt, MDGina Hounam, PhDGina McDowellGina MinotGrace Paul, MDGregory D. Pearson, MDGriffin Stout, MDGuliz Erdem, MDHailey Blosser, MA, CCC-SLPHanna MathessHeather Battles, MDHeather ClarkHeather Yardley, PhDHenry SpillerHenry Xiang, MD, MPH, PhDHerman Hundley, MS, AT, ATC, CSCSHiren Patel, MDHoma Amini, DDS, MPH, MSHoward Jacobs, MDHunter Wernick, DOIbrahim Khansa, MDIhuoma Eneli, MDIlana Moss, PhDIlene Crabtree, PTIrene Mikhail, MDIrina Buhimschi, MDIvor Hill, MDJackie Cronau, RN, CWOCNJacqueline Wynn, PhD, BCBA-DJacquelyn Doxie King, PhDJaime-Dawn Twanow, MDJames Murakami, MDJames Popp, MDJames Ruda, MDJameson Mattingly, MDJamie Macklin, MDJane AbelJanelle Huefner, MA, CCC-SLPJanice M. 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Day, CPNP-PCKelly Pack, LISW-SKelly Tanner,PhD, OTR/L, BCPKelly Wesolowski, PsyDKent Williams, MDKevin Bosse, PhDKevin Klingele, MDKim Bjorklund, MDKim Hammersmith, DDS, MPH, MSKimberly Bates, MDKimberly Sisto, PT, DPT, SCSKimberly Van Camp, PT, DPT, SCSKirk SabalkaKris Jatana, MD, FAAPKrista Winner, AuD, CCC-AKristen Armbrust, LISW-SKristen Cannon, MDKristen E. Beck, MDKristen Martin, OTR/LKristi Roberts, MS MPHKristina Booth, MSN, CFNPKristina Reber, MDKristol Das, MDKyle DavisLance Governale, MDLara McKenzie, PhD, MALaura Brubaker, BSN, RNLaura DattnerLaurel Biever, LPCLauren Durinka, AuDLauren Garbacz, PhDLauren Justice, OTR/L, MOTLauren Madhoun, MS, CCC-SLPLauryn RozumLee Hlad, DPMLeena Nahata, MDLelia Emery, MT-BCLeslie Appiah, MDLinda Stoverock, DNP, RN NEA-BCLindsay Kneen, MDLindsay Pietruszewski, PT, DPTLindsay SchwartzLindsey Vater, PsyDLisa GoldenLisa M. 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Matson, MDSteven Ciciora, MDSteven CuffSuellen Sharp, OTR/L, MOTSusan Colace, MDSusan Creary, MDSwaroop Pinto, MDTabatha BallardTabbetha GrecoTabi Evans, PsyDTabitha Jones-McKnight, DOTahagod Mohamed, MDTamara MappTammi Young-Saleme, PhDTerry Barber, MDTerry Bravender, MD, MPHTerry Laurila, MS, RPhTheresa Miller, BA, RRT, RCP, AE-C, CPFTThomas Pommering, DOThomas SavageTiasha Letostak, PhDTiffanie Ryan, BCBA Tim RobinsonTimothy Cripe, MD, PhDTracey L. Sisk, RN, BSN, MHATracie Rohal RD, LD, CDETracy Mehan, MATravis Gallagher, ATTrevor MillerTyanna Snider, PsyDTyler Congrove, ATVanessa Shanks, MD, FAAPVenkata Rama Jayanthi, MDVidu Garg, MDVidya Raman, MDW. Garrett Hunt, MDWalter Samora, MDWarren D. Lo, MDWendy Anderson, MDWendy Cleveland, MA, LPCC-SWhitney McCormick, CTRSWhitney Raglin Bignall, PhDWilliam Cotton, MDWilliam J. Barson, MDWilliam Ray, PhDWilliam W. Long, MD

Your Canker Sore or Cold Sore? – Cleveland Clinic

Many people confuse canker sores with cold sores or they assume they’re the same thing, but they’re not.

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First, these mouth sores show up in different places: Canker sores appear inside your mouth, but cold sores happen outside, says dentist Todd Coy, DMD.

Also, while canker sores are not contagious, cold sores involve a very contagious virus. You risk passing cold sores along when you kiss someone, drink out of the same container or share silverware with other people.

What you need to know about canker sores

While the cause of a canker sore is often hard to pinpoint, stress is one possible cause. Or they may sometimes develop after a mouth injury — such as when you accidentally bite your lip or tongue, says Dr. Coy.

Acidic fruits and vegetables, including lemons, oranges, pineapples, apples, tomatoes and strawberries, can trigger canker sores or make them worse. It also may surprise you to learn that nonsteroidal anti-inflammatory drugs, such as ibuprofen, sometimes cause canker sores.

You may have common canker sores if you notice a painful sore or sores on the inside your mouth, your tongue, soft palate (the back portion of the roof of your mouth), or inside your cheeks.

Treating canker sores: Use salt water

Canker sores will usually go away by themselves after a week or so, but they can make it difficult to eat or talk, so you may want to seek relief in the meantime.

“Rinsing your mouth out with highly concentrated salt water several times a day is one of the easiest ways to reduce the pain and inflammation caused by canker sores,” says Dr. Coy.

Mix about 1 teaspoon of salt into a half-cup to a cup of warm water. Swish the solution around in your mouth, but then spit it out (don’t swallow it).

How are cold sores different?

Cold sores (also called fever blisters) show up as groups of painful, fluid-filled blisters, typically under the nose, around the lips or under the chin. The herpes simplex virus (HSV type 1) causes them. While HSV type 1 is closely related to the virus that causes genital herpes, HSV type 2, it’s not the same.

Symptoms of a cold sore outbreak may include a tingling sensation on your lips, followed by emerging small, fluid-filled blisters. The blisters may ooze, and then scab over.

HSV type 1 flare-ups often emerge at the same place every time there is an outbreak. Other symptoms may include fever, sore throat or swollen lymph nodes.

If you suspect that you have cold sores, avoid sharing cups or utensils with others. You should also avoid kissing while you have open sores as HSV type 1 is most often spread when someone is having an outbreak. It is much less likely but still possible to pass the virus along to others when you don’t have signs or symptoms, says Dr. Coy.

“Stress is one of the primary triggers of cold sore outbreaks because it decreases your body’s resistance to disease,” he says. “Changes in weather, particularly exposure to sunlight, can also cause outbreaks. ”

Symptoms are typically most severe during an initial outbreak, and lessen somewhat during subsequent flare-ups, he says.

How to soothe a cold sore

Cold sores typically stick around for about two weeks, but there are steps you can take to shorten flare-ups:

• Apply ice to the sore to reduce swelling and pain.
• Use a topical numbing medicine to reduce pain and soften scabs.
• Apply an over-the-counter topical cream, such as Abreva, to help promote healing.
• Talk with your dentist or physician about prescription antiviral medications.

If you have had cold sores in the past, it’s a good idea to wear lip balm with an SPF of 30 to help protect your lips against sun exposure, which may cause outbreaks, says Dr. Coy.

Kids Health Information : Herpes simplex gingivostomatitis

Herpes simplex gingivostomatitis (jin-juh-voe-sto-ma-tie-tis) is inflammation of the gums and lips caused by the herpes virus – the same virus that later causes cold sores. This inflammation damages the skin, resulting in painful ulcers in the mouth and blisters on the lips.

Infections in children are common, and they often go unnoticed. However, about one in four children will develop mouth ulcers after their first infection. Your child may have a fever and become irritable, then a day or two later develop blisters on their lips and ulcers on
their gums. These are painful and often lead to drooling and a refusal to eat or drink. Your child may then become dehydrated.

Signs and symptoms of gingivostomatitis

If your child has been infected with herpes simplex gingivostomatitis, they may show no symptoms. If they do have symptoms, they may include:

• fever
• irritability
• painful mouth ulcers and lip blisters
• poor appetite or reluctance to drink.

The ulcers/blisters usually take 10 to 14 days to go away. The blisters never leave scars.

Care at home

Encourage your child to drink their normal amount of fluids to prevent them becoming dehydrated. There’s no need to worry about them not eating, but it is important that they get enough fluids.

Signs that your child is mildly dehydrated include:

• dizziness or light-headedness
• nausea or headaches
• dark yellow or brown wee (urine should be pale yellow)
• not going to the toilet much (in younger children, fewer wet nappies or nappies not as wet/heavy as usual)
• dry lips, tongue, mouth or throat.

If your child is showing these signs, encourage them to drink more. This can be in the form of water, milk, jelly, icy poles or oral rehydration solutions.

It is important to reduce the pain caused by the blisters so that your child is more likely to want to drink. Give your child pain relief medication (paracetamol or ibuprofen) – see our fact sheet
Pain relief for children. The pain usually goes away after three to four days.

No other medications are needed, because antibiotics and antiviral medications do not work and are of no use in treating this condition.

When to see a doctor

If your child is refusing to drink and you think they may be dehydrated, take them to your GP or to your nearest hospital emergency department.

Signs of severe dehydration include:

• not passing urine
• being pale and losing weight
• dry lips and mouth
• sunken eyes
• cold hands and feet
• no tears when they cry.

Call an ambulance if it is difficult to wake your child up.

See your GP if your child’s pain is not relieved with medication. The doctor may prescribe a numbing gel, which can safely be swallowed. Also see the GP if your child is becoming increasingly unwell, with high fever or vomiting.

A rare but serious complication of herpes simplex infection is inflammation of the brain (encephalitis). Symptoms include confusion, significant behaviour change and being very drowsy. If your child has herpes simplex gingivostomatitis and is showing these symptoms, call an ambulance
immediately.

Key points to remember

• Herpes simplex gingivostomatitis is a very common condition.
• Infection can often go unnoticed, but symptoms may include painful mouth blisters.
• Encourage your child to drink plenty of fluids to avoid dehydration.
• The only medications that should be used are pain relievers.

For more information

Common questions our doctors are asked

Once my child has had gingivostomatitis can she get it
again? 

Once someone has been infected with the herpes simplex virus, the virus will
stay in their body for life. Your child may have other episodes of herpes
reactivation (when the virus affects the body again), but the first instance is
usually the worst, and they may not experience symptoms such as painful
blisters again. Future episodes of herpes is often referred to as cold sores.

How can I get more fluids into my child?

Offer small amounts to drink often. Gastrolyte, HYDRAlyte,
Pedialyte and Repalyte are different types of oral rehydration fluid that can
be used to replace fluids and body salts. These are the best option if your
child is becoming dehydrated. They are also available as icy poles, which
children are often happy to have.

Developed by The Royal Children’s Hospital General Medicine and Infectious Diseases departments. We acknowledge the input of RCH consumers and carers.

Reviewed May 2018.

Kids Health Info is supported by The Royal Children’s Hospital Foundation. To donate, visit

www.rchfoundation.org.au.

Herpes Can Happen to Anyone

June 2018

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Share Facts, Not Fears

Did you know that the virus that causes “cold sores” or “fever blisters” on or around the mouth can also infect other areas of the body? The infection is caused by the herpes simplex virus. And it’s very common.

Most people with herpes infection don’t even know it. They may not have symptoms or not notice them.

For people who do have symptoms, a herpes infection may show up as one or more blisters. These can be on or near the mouth, eyes, genitals, or rectum. After the blisters break, they turn into sores or ulcers. These sores are painful and take about a week to heal.

Once someone is infected with herpes simplex, the virus goes into hiding and stays in the body for the rest of their lives. The virus can re-emerge at any time and cause an outbreak. Some people have outbreaks several times per year. Tingling or burning in the area can signal that an outbreak is looming.

There are two types of herpes simplex viruses: HSV-1 and HSV-2. HSV-1 is often transmitted during childhood. You can get it from close contact with someone who has the infection. For example, a family member with a cold sore may kiss a child. HSV-1 is the main cause of herpes of the mouth or eyes. Although it’s possible for HSV-2 to infect the mouth or eyes, it’s usually found in the genital area.

There’s no cure for herpes. But anti-herpes medicine can speed healing of the sores. If taken every day, this medicine can also lower the risk of future outbreaks.

“It’s the first episode that is particularly important to treat,” says Dr. Jeffrey I. Cohen, a herpes infection expert at NIH. That’s because the first outbreak is often the most severe. In addition to sores, you may have a fever and body aches. Also, the nearby lymph nodes might be swollen and painful.

A doctor may suspect a diagnosis of herpes from looking at a sore. But lab tests on a sample taken from the sore is needed to confirm the diagnosis. A blood test for HSV-1 and HSV-2 is also available to confirm if someone has been infected.

Researchers are working to develop herpes vaccines. “There are two different types of vaccines being developed for herpes virus,” Cohen explains. “One is a vaccine that would prevent infection in people who have not been infected with the virus. ” Cohen’s research team at NIH is working on this type of vaccine.

“The other type of vaccine is for people who are already infected,” he says. “The idea is that we could boost their immune system so that they have fewer recurrences.”

The fact that most people don’t know that they’re infected makes vaccines especially important.

When someone is diagnosed with herpes, they may feel anger, sadness, or shame. They also may fear rejection by romantic partners.

Keep in mind that herpes outbreaks can be managed. People can lower the risk of infecting someone else by avoiding direct contact during an outbreak. For those with genital herpes, using anti-herpes medicine every day and condoms during sexual activity also reduces the risk of infection for a romantic partner.

Talk with your doctor if you have questions about preventing or managing herpes. And help fight the stigma of herpes by sharing the facts in the Wise Choices box.

Genital herpes: Can you get it during oral sex with someone who gets cold sores?

Ask anyone who gets cold sores and they’ll tell you how unpleasant these little sores and blisters can be.

Key points:

• The same virus that causes cold sores can also cause genital herpes and it can happen even if there are no symptoms
• Previously HSV type 1 was common near the mouth and HSV type 2 mostly affected the genitals
• But HSV type 1 is now also common near the genitals

Cold sores, which usually appear on your lips or the skin around your mouth, are also known as oral herpes and are caused by the herpes simplex virus (HSV). This virus is also responsible for blisters and sores in the genital area, known as genital herpes.

So if you have cold sores, is it possible to give your partner genital herpes?

Unfortunately, the short answer is yes, according to sexual health physician Terri Foran.

To understand why — the first thing you need to know is that there are two types of HSV. In the past, HSV type 1 (HSV-1) was most commonly seen on the lips (usually as cold sores), while HSV type 2 (HSV-2) preferred the genital area.

However, in recent years doctors have seen more cases of genital herpes caused by HSV-1.

If you have oral HSV-1 and your partner doesn’t, you can spread it through any type of sexual contact where the mouth comes into contact with their mouth or their genitals — and sometimes the buttocks and legs as well. This explains why some people have the same type of herpes on both their lips and their genitals.

More alarmingly, Dr Foran said you don’t even need to have any outward sign of cold sores to spread the virus. Perfectly normal looking skin can still shed lots of viral particles — sometimes even more than when the blisters are actually present.

Who gets herpes?

Lots of people have cold sores, and lots of people have oral sex — so why don’t more of us get genital herpes?

The reason is because during childhood, most of us (perhaps 80 per cent) are exposed to type 1 of the herpes virus, Dr Foran said.

“Some people never have any symptoms [and] become completely immune. In others, the virus quietly hangs around in the spinal nerves, only to erupt months or years later,” she said.

It’s also important to know that only 1 to 2 per cent of the population actually get the typical oral blisters that most of us would call cold sores.

“It’s actually much more common, especially if you have had the virus for a while, to get a split in the skin or some irritation in the same spot,” Dr Foran said.

The good news is, often people who have already been exposed to oral HSV-1 in the past, build up an immunity which stops them getting type 1 genitally.

“Unfortunately they can still pick up HSV-2,” Dr Foran said. “Thankfully whether you have type 1 or type 2 genital herpes, it tends to be less severe and less frequent over time and that means you are less likely to infect a partner.”

Although exposure to HSV-1 during childhood is common, Dr Foran said there was evidence that in the last 20 years, exposure rates had dropped. There are lots of theories as to why, including a change in hygiene practices and maybe less chance of exposure with smaller family groups.

But what this means is that now nearly 80 per cent of genital herpes diagnosed in those under 20 turns out to be HSV-1 — presumably spread through oral sex.

“And we are also seeing more genital HSV-1 even in older age groups,” Dr Foran said.

Interestingly, the first attack of genital HSV-1 is usually more severe than genital HSV-2, but it comes back much less often.

How can you protect yourself?

If one of you gets cold sores and the other doesn’t (or isn’t sure), what steps can you take to protect each other?

Unfortunately, most people spread the HSV-1 virus to a partner, infecting their lips, genitals or both, simply because they have no symptoms themselves and therefore no idea that they carry the infection.

Quiz: What do you know about STIs?

How much do you know about STIs and practising safe sex?

Read more

For those who do get symptoms, there may be tell-tale signs like redness, tingling and itching even before the blisters actually erupt.

“From these early symptoms and until the blisters are completely healed, it is important to give oral sex a miss, or to use a condom or a latex dental dam (for women) to protect your partner during oral sex,” Dr Foran said.

And if you don’t have a dam, Dr Foran said, you can cut the end off a condom and cut up the middle to give you a sheet of latex that you can use as a do-it-yourself dam.

“The flavoured ones taste much better!” she said.

If frequent cold sores are a problem, there are now effective treatments available for controlling the symptoms.

“Some of these can actually stop an attack in its tracks if taken early enough,” Dr Foran said.

But unfortunately, there is no evidence that the use of these treatments lessens the risk of spreading the virus to a partner — and there is no cure yet for either type of HSV, though scientists are hard at work on a vaccine.

Putting it into perspective

According to Dr Foran, many of us carry HSV on the lips or the genitals without ever knowing it — and without ever passing it on to anyone else.

“But there is still a lot of confusion about this virus and many people are unaware that the same virus that causes cold sores can cause genital herpes as well,” she said.

“It just goes to show that safer sex is still important — and that goes for oral sex as well.”

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Herpes Simplex – an overview

Herpes Simplex

Herpes simplex outbreak may be followed by a prodrome of malaise, fever, and regional lymphadenopathy before the appearance of grouped vesicles on an erythematous base. The vesicles are typically quickly broken and become ulcerated in appearance, with each vesicle usually less than several millimeters in size. True first-time infections tend to present more severely than secondary presentations of previously infected individuals, with a prodrome present in 80% of cases.

The lesions can be in any location around the genitals or rectum, on the proximal thighs and buttocks, inside the vagina, and in and around the mouth. The lesions are most often painful, particularly when on mucosal surfaces, or itchy. In women, herpes simplex can present with cervicitis-like symptoms with bleeding and discharge and cervical ulcerations on examination, or simply mucopurulent cervicitis. Herpetic lesions around the urethra tend to be extremely painful and can make urination difficult. Rectal HSV can be confused with irritation, perianal fissure, and even candidiasis because of its often beefy-red appearance and itching.

Vesicles typically appear 6 days after infection and can last up to 2 weeks in an initial infection. Subsequent outbreaks tend to have a shorter duration and to be less uncomfortable for patients. Confirmation of infection is helpful, but the diagnosis can be made primarily on the clinical appearance of the exanthema. Vigorous sample collection from an ulcer (which the patient may not appreciate) to be sent for PCR identification and typing is the most readily available method of laboratory diagnosis. Serum antibody testing is not useful in the initial HSV diagnosis because antibody levels will not be appreciable early in infection. The appearance of convalescent immunoglobulin G (IgG) and IgM levels several weeks after a suspected outbreak might help to support the diagnosis of HSV infection.

The value of screening for HSV immunity is debatable and should generally not be recommended for asymptomatic individuals. In addition, the USPSTF recommends against screening asymptomatic pregnant women for HSV to prevent transmission to the newborn. Given that many patients with HSV infection never manifest symptoms, the value of knowing that one is HSV seropositive is questionable. In addition, HSV-1 and HSV-2, although classically oral and genital, respectively, can “mix and match” based on sexual practices. It is often confusing for asymptomatic individuals to know that they have HSV antibody (Do I have cold sores? Do I have genital herpes? How should this change the way I live my life?). In monogamous couples with one partner known to be HSV positive and the other with unknown status, testing of the latter may indicate suppressive therapy in the seropositive partner if the other is found to be negative.

Regular barrier method use decreases transmission of herpes in both men and women, with patients using condoms 100% of the time having a 30% reduction in HSV acquisition from those who never use condoms (Martin et al., 2009). Serodiscordant couples may also decrease transmission through antiviral suppressive therapy to the HSV-positive partner (Table 16-8).

Cold Sores vs. Canker Sores | How to Tell the Difference

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Canker sores and cold sores are both types of mouth sores – and both can be painful and aggravating to deal with. Yet the two are very different. If you have a mouth sore it’s important to know which one you are suffering from so you can treat it successfully and recover faster.

There are several ways to tell the difference between a cold sore and a canker sore. Knowing what to look for means you can be sure of which one you have.

What Is a Canker Sore?

A canker sore – also known as an aphthous ulcer – is a type of mouth sore that forms on the soft tissues in your mouth, such as on or under your tongue and inside your cheeks or lips.ⁱ

Cankers are typically shallow, round or oval ulcers that vary in size. They may appear whitish or yellowish with a red border.ⁱⁱ Canker sores tend to be painful, making it difficult to eat and talk, and large ones can take a while to heal.ⁱⁱⁱ

They are typically caused by trauma, such as aggressive tooth brushing, eating sharp-edged foods such as potato chips, or orthodontic braces and wires that rub against the inner cheek. Other triggers for canker sores include stress, diseases of the immune system and vitamin deficiencies. Canker sores are not contagious.

What Is a Cold Sore?

Cold sores are small, fluid-filled blisters that usually form along the borders of the lips, and sometimes on the face. They are caused by certain strains of the herpes simplex virus (usually HSV-1), and many people experience a burning, itching or tingling sensation before the actual sore appears.^iv

Cold sores can take up to seven to 10 days to heal completely^vi, but you may be able to get rid of your cold sore in as few as 2½ days* with an antiviral topical cream such as Abreva^® Cream, which is available over the counter. Compare Abreva^® Cream to other cold sore treatments.

*Median healing time 4.1 days. 25% of users healed within 2½ days when used at first sign.

Canker Sore vs. Cold Sore

While these two types of mouth sore are often confused, they differ in several ways.

Cause

^v

A key difference between cold sores and cankers is that cold sores are contagious as they are caused by a virus, whereas canker sores are not. Various triggers can lead to the reactivation of the virus that results in an outbreak of cold sores. Triggers vary from person to person but include stress, fatigue, sunlight exposure, hormone fluctuations and illnesses such as colds and flu. You can’t develop a cold sore unless you have been infected with the virus first.

Canker sores can be caused by a number of factors, such as stress, nutrient deficiency and injury to the inside of the mouth.

Location

Canker sores are found only inside the mouth – on the inner cheek, lips or tongue – whereas cold sores are experienced on the lip area, from the outer to the inner edges, but rarely inside the mouth.

Appearance

A canker sore may appear like a whitish lesion or patch, with an inflamed reddish edge. It is always found within the soft moist tissues of your mouth. A cold sore appears as a blister or cluster of blisters around your lip area: on the corners, outer edges or on the lip itself.

How it Spreads

A canker sore can’t be spread from person to person or within your mouth. While you may experience one or more canker sores at one time, it’s likely they have been triggered by the same thing. The herpes simplex virus, which causes cold sores, is highly contagious. It is easily transmitted to others by touching, kissing, through oral sex or by sharing items such as glasses, forks, lipsticks and lip balm.

Stages of Development

Although a canker sore may develop gradually, you will likely notice it all of a sudden as it starts to hurt when you touch it with your tongue, toothbrush or with food. Most canker sores will heal without scarring within 1 to 2 weeks.ⁱ

A cold sore may be felt before it’s visible. You may experience a tingling, burning or itching sensation in the area where a cold sore blister then appears. The blister is usually red with an uneven and inflamed surface. Once the blister has formed, it often crusts over, weeps liquid and then eventually heals. Cold sores may take up to two weeks to heal completely.^vi Using a specially formulated cold sore cream such as Abreva^® Cream early on in this process can reduce the healing process to just a few days. *

*Median healing time 4.1 days. 25% of users healed within 2½ days when used at first sign.

Canker Sore vs. Cold Sore – Next Steps

While there are many differences between canker sores and cold sores, they are both painful and irritating to experience. Cold sores, however, can also make you feel uncomfortable or unhappy about your appearance. Using a cream such as Abreva^® Cream as soon as you feel a cold sore coming on will speed your recovery, helping your lips to look healthy again sooner.

SOURCES

Clicking any of the links below takes you to an external website that is independently operated and not managed by GSK. GSK assumes no responsibility for the content on the website. If you do not wish to leave this website, do not click on the links below.

^i. Canker sore. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/canker-sore/symptoms-causes/syc-20370615. Accessed 11/13/19.

^ii. A Detailed Guide to Canker Sores: Causes, Prevention, Remedies, Treatment, and More. Everyday Health. https://www.everydayhealth.com/canker-sore/. Accessed 11/13/19.

^iii. Canker Sores. PeaceHealth. https://www.peacehealth.org/medical-topics/id/zd1065. Accessed 11/13/19.

^iv. Cold sore. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/cold-sore/symptoms-causes/syc-20371017. Accessed 11/13/19.

^v. What’s the Difference Between Canker Sores and Cold Sores? Healthline. https://www.healthline.com/health/canker-sore-vs-cold-sore. Accessed 11/13/19.

^vi. Cold sore. NHS Inform. https://www.nhsinform.scot/illnesses-and-conditions/mouth/cold-sore. Accessed 10/12/19.

90,000 Symptoms and treatment of herpes stomatitis in children and adults

The causative agent of herpes stomatitis is the human herpes simplex DNA virus. There are two flavors of this virus. Herpes simplex virus 1 (HSV-1), as a rule, is associated with the oral cavity, and herpes simplex virus 2 – with the genital area.

Cause and symptoms of stomatitis

The symptoms of this virus are usually hidden, and the child and his parents are not aware that he is infected with this virus.The virus is very easily transmitted even if there are no symptoms. The transfer of oral fluid, such as saliva, can also lead to infection of the virus from one person to another.

When symptoms are present, they include fever, feeling unwell, drooling from the mouth, dysphagia (also known as difficulty swallowing), and mouth ulcers and sores (according to National Institutes of Health data ) . A child’s gums may turn red, swollen, sore to touch, and bleed.

Making a diagnosis

As a rule, the doctor can detect herpes stomatitis during a visual examination, although he can send the patient for tests to confirm his diagnosis, notes Aga Khan University Hospital .

Stomatitis treatment

After the herpes virus has entered the human body, it remains there for life. As a rule, manifestations of the disease are rare.For healthy people, this virus is not a serious problem or something noticeable. Because stomatitis is self-limiting, it can be treated with over-the-counter pain and fever medications for children. The child also needs to drink plenty of fluids during the onset of the herpes stomatitis virus, especially if he has no appetite. The situation usually resolves in two weeks or less.

Herpes simplex virus 1 recurrence does not necessarily occur in all people infected with the virus.Sometimes, if the manifestations of the virus are frequent, the doctor may prescribe antiviral drugs such as acyclovir, in tablets or in the form of an ointment, but this is not a medicine, but a means to limit the duration of the disease.

To prevent stomatitis, it is always necessary to take good care of oral hygiene. Brush your teeth twice a day with quality toothpaste.

Herpes Simplex Virus 1/2, IgG

This is the detection of immunoglobulins G to the herpes simplex virus of the first and second types, which are indicators of the presence of a herpes virus infection.

Synonyms Russian

Herpes virus, herpes simplex virus of the first and second types, determination of herpes by IgG antibodies.

English synonyms

Herpes Simplex Virus, Type 1 and Type 2, HSV-1 or HSV-2 IgG, HSV-1, HSV-2, HHV1, HHV2.

Research method

Solid phase chemiluminescent enzyme immunoassay (“sandwich” method).

Which biomaterial can be used for research?

Venous, capillary blood.

How to properly prepare for the study?

Do not smoke for 30 minutes prior to examination.

General information about the study

The most common types of viruses are the first and the second. They are contagious and cause small blisters to form on the mucous membranes, which burst to form open wounds. In HSV-1, blisters appear mainly around the mouth and in the mouth, while HSV-2 usually affects areas around the genitals.

Herpes simplex virus can be contracted through skin contact, contact with vesicles, and sometimes even in the absence of visible lesions.

Sexually transmitted HSV-2 is more often transmitted, however, HSV-1 herpes infection can occur, for example, through oral sex. According to the WHO, from 50% to 80% of the adult population of developed countries are infected with herpes of the first type and about 20% with herpes of the second type. Because symptoms are often subtle, 90% may not even be aware of their infection.

In the case of primary infection, painful blisters usually form at the site of infection after two weeks, which usually disappear after four weeks. They appear on the genitals, around the anus, on the buttocks, or on the thighs, after which they can burst. In addition, flu-like symptoms such as chills and sore throat may occur.

However, bubbles are not always formed with herpes. Sometimes the manifestations of the disease are so weak that they go unnoticed or are mistaken for something else, such as insect bites or allergies. After entering the body and spreading the herpes virus is in a latent form. With stress or other diseases that lead to a decrease in immunity, it can be reactivated. In most cases, herpes simplex is harmless to health, but it can cause serious illnesses: neonatal herpes (if the child becomes infected during childbirth from a mother infected with genital herpes) and encephalitis. They can lead to serious, incurable neurological diseases and even death.

The following factors increase the risk of contracting herpes:

• diseases in which the immune system is suppressed (e.g. HIV / AIDS),
• organ transplants.

There are antiviral drugs that suppress the spread of herpes, as well as shorten the duration of the acute phase of the viral infection and alleviate the symptoms of the disease.

Antibodies are produced to fight infection. The formation of IgG to the herpes simplex virus begins a few days after the appearance of IgM.The concentration of IgG in the blood first increases for several weeks, then falls, and then stabilizes. When re-infected with herpes, it increases much faster – already in the first days of infection. After a disease, small amounts of IgG remain in a person until the end of life, which, however, does not provide one hundred percent protection against re-infection.

What is the research used for?

• As an auxiliary study to confirm the diagnosis of symptoms of herpes lesions (ulcers, vesicles on the mucous membranes) or neonatal herpes.
• For screening specific groups of people, such as those who are sexually active, potential recipients with the AIDS virus, or those who have had previous exposure to HSV infection.

When is the study scheduled?

• When examining persons in contact with patients with HSV.
• During preparation for and during pregnancy monitoring.

What do the results mean?

Reference values ​​

S / CO ratio (signal / cutoff): 0 – 0. 9.

A positive result means the presence of IgG antibodies to HSV-1 or HSV-2, which indicates either active or previous herpesvirus infection.

A negative result indicates a low likelihood of an acute herpesvirus infection, and also that the body has not previously been in contact with the herpes simplex virus. However, immediately after infection, when sufficient antibodies have not yet developed, the result may be false negative.In this case, an additional IgM test and retesting for IgG after a few weeks is recommended.

What can influence the result?

Reducing the concentration of antibodies are capable of:

• antiviral therapy,
• immunodeficiency.

Herpes Simplex Virus 1/2, DNA [real-time PCR]

A study to identify the causative agent of herpesvirus infection of the 1st and 2nd types (Herpes Simplex Virus 1/2), during which using the polymerase real-time chain reaction (RT-PCR) is determined by the genetic material (DNA) of the herpes simplex virus.

Synonyms Russian

Herpes virus, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), determination of herpes by DNA.

Synonyms English

Herpes Simplex Virus, Type 1 and Type 2, HSV-1 or HSV-2 IgM or IgG, HSV-1, HSV-2, HHV1, HHV2.

Research method

Real-time polymerase chain reaction.

Which biomaterial can be used for research?

Smear from the pharynx (oropharynx), prostate secretion, the first portion of morning urine, scraping from the rectum, saliva, scraping from erosive and ulcerative elements, urogenital scraping, ejaculate, venous, capillary blood, cerebrospinal fluid.

General information about the study

By PCR it is possible to detect even a small amount of viral particles in biological material. It allows you to identify herpes viruses, regardless of the time of infection, even in the period when antibodies have not yet formed.

The most common are the 1st and 2nd types of herpes. Both are contagious and cause small vesicles (vesicles) to appear on the mucous membranes, which burst to form open wounds.In HSV-1, vesicles appear around the mouth and in the mouth, while HSV-2 usually affects areas around the genitals.

Herpes simplex virus can be transmitted through skin contact if there are vesicles on the skin, and sometimes in the absence of visible lesions on it. HSV-2 is often referred to as a sexually transmitted disease, but HSV-1 herpes can also be contracted through, for example, oral sex. According to the WHO, from 50% to 80% of the adult population of developed countries are infected with herpes type 1 and about 20% – type 2.Since type 2 symptoms are subtle, 90% of those infected with it may not be aware of their infection.

In the case of primary infection, painful blisters usually form at the site of infection after two weeks, which usually disappear after four weeks. They appear on the genitals, around the anus, on the buttocks, or on the thighs, after which they can burst. In addition, you may experience flu-like symptoms such as chills and sore throat.

However, bubbles are not always formed with herpes.Sometimes the manifestations of the disease are so weak that they go unnoticed or are mistaken for something else, such as insect bites or allergies. After the infection enters the body and spreads, the herpes virus is in a latent form. With stress or other diseases that lead to a decrease in immunity, it can be reactivated. In most cases, herpes simplex is not dangerous to health, but it can cause serious illnesses: neonatal herpes (if the child becomes infected during childbirth from a mother infected with genital herpes) and encephalitis.They can lead to serious, incurable neurological diseases and even death. The following factors increase the risk of contracting herpes:

• diseases in which the immune system is suppressed (e.g. HIV / AIDS),
• organ transplants.

Currently, a cure for herpes is not possible, however, there are antiviral drugs that suppress its spread, as well as shorten the duration of the acute phase of viral infection and alleviate the symptoms of the disease.

What is the research used for?

• For the detection of genital herpesvirus infection in men and women and monitoring of its treatment.
• To test a woman for herpes before and during pregnancy (if there is a risk of infection).

When is the study scheduled?

• If necessary, confirm or deny the fact of genital herpes infection.

What do the results mean?

Reference values: negative.

Positive result

• The body is infected with a virus. The result is indicated in crosses, depending on the amount of genetic material identified during the study.

Negative

• Most often, the absence of infection of the genitals with the herpes virus.

What can influence the result?

• Antiviral therapy is able to reduce the amount of virus in epithelial cells, however, due to the high sensitivity of the PCR method, this rarely leads to false negative results.
• Errors at the stage of taking biological material, when a sufficient number of cells infected with the virus does not enter the sample for research, can lead to false negative indicators.

What is oral cancer?

This is the growth of malignant cells in any part of the mouth, which includes the lips, gums, tongue, cheeks, palate and tonsils.The most common sites for cancer are the lips, then the tongue and other sites. Symptoms vary with the site of the cancer, but usually include ulceration, which is initially painless. In later stages of development, cancer spreads to the lymph nodes in the neck or under the jaw.

What are the risk factors for developing oral cancer?

Among the factors provoking the development of oral cavity cancer, modern oncology gives the first place to carcinogens formed during the combustion of tobacco, the effect of the high temperature of a smoldering cigarette. Alcohol potentiates the effect of tobacco smoke carcinogens and doubles the likelihood of a smoker developing oral cancer.

Early diagnosis of oral cancer, hereditary predisposition (the presence of cancer of the oral cavity in the genus) and age over 40 also greatly increase the risk of developing oral cancer.

Carriage of the Human Papilloma Virus (the virus that causes cervical cancer in women) known as HPV 16 is a significant risk factor for developing oral cancer, as is the carriage of Herpes Simplex Virus (HSV-1).

Another risk factor is candidiasis, as well as sunlight (ultraviolet).

25% of patients with oral cancer did not have a single risk factor for developing cancer.

COMPLAINTS that may bother with the development of the disease:

1. The presence of long-term non-healing ulcers in the mouth (on the mucous membrane of the cheeks, tongue, floor of the mouth, tonsils)
2. Consistent oral pain,
3. Swelling or thickening of the cheek.
4. White or red spots on the gums, tongue, tonsils or oral mucosa,
5. Sensation of a foreign body when swallowing,
6. Difficulty chewing or swallowing,
7. Difficulty moving jaw or tongue,
8. Numbness of the tongue
9. The appearance of swelling in the neck.

The appearance of such complaints is a signal for an immediate visit to the doctor.

IMPORTANT TO REMEMBER!

The final diagnosis, on the basis of which the treatment tactics are determined, has the right to make only a doctor working in a specialized medical institution.Do not trust the opinions of acquaintances, relatives, or random people, this leads to a loss of time, misdiagnosis and, ultimately, to disappointing results.

Oral cancer prevention

• Tobacco products should be avoided.
• Avoid excessive alcohol consumption.
• Regular dental checks and periodic self-examinations of the mouth can help detect cancer early.

Doctor Khveskovets E.M.

What is oral herpes?

Oral herpes is an infection of the mouth caused by the herpes simplex virus. Symptoms appear in the form of sores on the lips, often colloquially called herpes, and in some cases, ulcers on the mucous membranes of the mouth. These mouth ulcers are usually fluid-filled blisters that will eventually burst.

The herpes virus is extremely common; Health professionals say the percentage of people who have experienced some form of herpes infection by the time they reach adulthood is close to 100%.There are actually two different types of herpes simplex virus (HSV) called HSV-1 and HSV-2 respectively. HSV-1 is the most common of the two viruses, but they are very similar, causing the same symptoms in an infected person. Both types of virus can also cause a concomitant infection, genital herpes.

In addition to the main symptoms of sores on the lips and bladders, sometimes additional symptoms occur with herpes infection of the oral cavity. These symptoms can include swollen gums, fever, headache, and dehydration.Young children are especially prone to these unpleasant symptoms and often have severe mouth pain that can make it difficult to eat.

Oral herpes is highly contagious. It can be transmitted by kissing other skin contact, or by separating objects that come into contact with the mouth, such as a toothbrush or lipstick. In addition, the virus can be transmitted from the mouth to the genitals or vice versa during oral sex.

When a person contracts oral herpes, the virus usually goes through three stages.When a person becomes infected for the first time, viruses enter the oral cavity and begin to multiply. This is called a primary infection and can be accompanied by sores and other symptoms. Alternatively, it can occur without any symptoms, in which case it is called an asymptomatic infection.

In the second stage of infection, the virus migrates from the mouth to the nerve tissue of the spine. Here, the virus continues to multiply for a certain period and then becomes inactive. This stage of infection is called latency, and the infected person will usually continue to host the virus on an ongoing basis.

Herpes sores appear from time to time. It usually happens when an infected person is under stress, physically or mentally. This stage is called relapse and is likely to recur as the virus alternates between being stuck and active.

OTHER LANGUAGES

90,000 Herpes simplex is … What is Herpes simplex?

Herpes simplex (ancient Greek ἕρπης, lat. herpes simplex ) is a creeping, spreading skin disease) – a viral disease with a characteristic rash of grouped vesicles on the skin and mucous membranes.It is caused by two types of herpes viruses: HSV-1 and HSV-2. The most common form of infection is labial (labial). The visible symptoms of the labial form are often referred to as “colds” such as “cold sores”. In second place in terms of frequency of occurrence is genital herpes, which mainly affects the genital area. HSV-1 usually causes infections of the mouth, neck, face, eyes, and central nervous system, while HSV-2 is characterized by anogenital lesions. However, both types of the virus can cause damage to both sites, for example, after infection with orogenital forms of sexual intercourse.Several types of herpes viruses affect a wide variety of sites.

There are also other forms of viral lesions: herpetic felon, lat. herpes gladiatorum , which occurs in wrestling athletes, ocular herpes (keratitis), forms of herpetic encephalitis, meningitis, neonatal herpes, and Bell’s palsy is also thought to be caused by this virus.

It should be noted that other members of the family Herpesviridae , such as shingles caused by the varicella-zoster virus, cause similar symptoms.In addition, differential diagnosis also involves consideration of other diseases of the hands, feet, mucous membranes of the mouth, characterized by similar injuries.

There is currently no cure for herpes. Available drugs only suppress the multiplication of the virus, but do not remove fragments of viral DNA from neurocytes. Therefore, there is always the possibility of relapse, especially with immunodeficiencies (for example, with HIV infection or tumors). After a few years, relapses begin to be asymptomatic, although the person is contagious to others.Treatment with antiviral drugs can suppress the activity of the virus and relieve symptoms. Vaccines under development have not been proven effective in clinical trials.

Transmission routes

Herpes simplex virus is most easily transmitted through direct contact with damaged tissues or body fluids of the host. Transmission can also occur transcutaneously (through the skin) during periods of asymptomatic virus carriage. Barrier methods are the most reliable and nevertheless, they only reduce the likelihood of transmission, not excluding it.Oral herpes is easily diagnosed only if there are external manifestations – wounds or ulcers. In the early stages, there are no symptoms of the disease and herpes can only be diagnosed by laboratory methods.

In an external environment at room temperature and normal humidity, the herpes simplex virus persists for a day, at a temperature of 50-52 ° C it is inactivated after 30 minutes, and at low temperatures (-70 ° C) the virus is able to remain viable for 5 days. On metal surfaces (coins, doorknobs, water taps), the virus survives for 2 hours, on wet sterile medical cotton and gauze – during the entire drying time (up to 6 hours) ^[1] .

Symptoms

Herpes simplex virus (HSV) causes several identical medical disorders. Infection of the skin, mucous membranes can cause lesions on the face and mouth (labial herpes), genitals, or hands (herpetic felon). More serious disorders occur when a virus infects the eyes (herpetic keratitis) or invades the central nervous system, damaging the brain (herpetic encephalitis). Patients with an immature immune system (newborns) or immunodeficiencies, such as organ transplant recipients with AIDS. Cognitive deficits that occur in patients with bipolar disorder and Alzheimer’s disease have also been associated with the virus, although this is primarily determined by the patient’s heredity.

After the initial infection, the herpes virus is permanently incorporated into the genome of the host cell and will never be eliminated by the immune system. It enters the nerve endings in the skin and travels along them to a sensitive neuron located in the ganglion ^[2] , where it enters the latent stage.

Antibodies generated by HSV-1 virus infection seem to relieve symptoms of subsequent HSV-2 infection, but even an asymptomatic patient is still infectious. Many have noted that pre-immunization with HSV-2 virus also relieves symptoms in people infected with HSV-1 virus. Infection with the HSV-2 virus is often asymptomatic, although transmission may persist for a long time. See pathogenesis for details.

Lost	Comments	Artwork
Herpetic gingivostomatitis	Herpetic gingivostomatitis often occurs after primary infection. In the future, herpes often recurs in a lighter labial form.
Labial herpes	Relapse occurs with repeated contact with the affected oral mucosa or skin.
Genital herpes	In the case of classic symptoms, typically presents as primary HSV-1 or HSV-2 genital infection in the form of clusters of inflamed papillae and vesicles on the outer surface of the genitals, resembling labial herpes.
Herpetic panaritium	Herpetic felon is a painful infection that often affects the phalanges of the fingers. Sometimes occurs on the nail roll.
Herpes gladiatorum	People involved in contact sports such as wrestling, rugby, and football sometimes develop an HSV-1 disease known as herpes gladiatorum, presenting with ulcers on the face, ears, and neck. Symptoms include fever, headache, sore throat and tonsils.Eyes or eyelids are sometimes affected.
Herpetic keratoconjunctivitis	The primary infection is usually swelling of the conjunctiva, eyelids (conjunctivitis), accompanied by small, white, itchy lesions on the cornea.
Herpetic encephalitis	A herpetic brain infection suspected to be caused by retrograde transmission of the virus along the trigeminal axon to the brain. HSV is the most common cause of viral encephalitis.The virus accumulates primarily in the temporal lobes. [3]
Herpetic meningitis	Mollaret meningitis, most often caused by HSV-2; one of the types of recurrent viral meningitis.
Neonatal herpes simplex	Neonatal herpes simplex, a rare but difficult infection, is usually transmitted from mother to newborn.
Herpes with immunodeficiency	In patients with weakened immune systems, herpes can cause unusual skin lesions. One of the most common manifestations is clean, elongated erosions on the skin folds, similar to knife cuts. [4]
Herpetic sycosis	Herpetic sycosis is a recurrent or primary herpes that affects the hair follicles. [5] : 369
Herpetic eczema	Herpes infection in patients with chronic atopic dermatitis may cause eczema-like rashes. [5] : 373
Herpetic esophagitis	Herpetic esophagitis is characterized by painful or difficult swallowing. Often proceeds against the background of immunodeficiencies (for example, HIV / AIDS), or in the post-transplant period.

Bell’s palsy

Although the exact etiology of Bell’s palsy as a form of facial nerve palsy is currently unknown, there is a theory that the paralysis may be caused by reactivation of the HSV-1 virus.At the moment, this theory is disputed, since viruses of the HSV group are found in many people without paralysis. In addition, patients with paralysis did not show a significant increase in the level of antibodies to HSV, and antiviral drugs do not improve the condition of such patients.

Alzheimer’s disease

HSV-1 appears to be one of the risk factors for Alzheimer’s disease. The nervous system of people with a certain genotype (carriers of the epsilon4 allele of apolipoprotein-E) is more susceptible to the pathogenic action of the virus, which increases the risk of developing Alzheimer’s disease.The virus interacts with components and receptors of lipoproteins. In the absence of this gene allele, the HSV-1 virus does not cause disease.

Viral DNA is localized in β-amyloid plaques, which is characteristic of Alzheimer’s syndrome. This suggests that the virus is the cause of their occurrence and, therefore, a significant etiological factor for the development of this disease.

Pathogenesis

The herpes virus is unable to penetrate through the intact stratum corneum of the skin, due to the absence of specific receptors on it. Herpes is transmitted by direct contact of damaged integuments with affected areas of the skin or with the biological fluids of an infected person. Transmission occurs between discordant partners: a person who has been ill (HSV-seropositive) can transmit the virus to a seronegative healthy person. The HSV-2 virus is transmitted exclusively by transcutaneous (through the skin).

After contact with a source of infection, viral particles that have got on the epithelium move with short interruptions through the skin or mucous membranes of the mouth or genitals.The virus enters cells through receptors such as nectin-1, HVEM, and 3-O sulfated heparan sulfate. The outer envelope of the virus fuses with the cell membrane. Further, the viral nucleocapsid is in the neuroplasm, where the release of viral DNA occurs. Then it is transported along the dendrites of nerve endings into the body of a sensitive neuron, located in the sensory ganglion, where they are embedded in its genetic apparatus forever. After the penetration of the virus, the process of its active reproduction in the cell begins – persistence.With labial lesions, the persistence of the virus in the neurocytes of the sensitive ganglia of the trigeminal nerve is characteristic, and with genital lesions, the lumbar.

In most people, the reproduction and shedding of the virus immediately after infection is asymptomatic. This can happen more than a week before or after the first symptoms appear in 50% of cases. The causative agent multiplies intensively in it, launching a lytic, productive type of infection. Focal degeneration of the epithelium occurs: the cells increase in size, then die, forming foci of necrosis.

Herpes viruses have cyclical periods of activity (bubbles containing viral particles form within 2–21 days) and periods of remission, during which the sores disappear. Genital herpes (HSV-2) is usually asymptomatic, although the virus multiplies and can be passed on to other people. This is most common with the HSV-2 virus. Recurrences of the disease are not determined in time, although some triggers of the disease have been identified. These factors include the effects of immunosuppressants (see below). With a relapse, the virus, which is in the latent stage, is activated, resulting in the formation of many infectious particles moving along the processes of the neuron, from which they subsequently pass into the epithelium of the skin and mucous membranes.Vesicles often reappear, accompanied by necrotic damage to the epithelium. The virus reproduction cycle is 10 hours. Over time, the body develops antiviral immunity and the frequency and severity of relapses decreases.

Carriage most often continues during the first 12 months after infection. The duration of such a carrier with immunodeficiencies (for example, with HIV infection) is longer. There is information that some people may have a shortened carrier, but there is no reliable information to confirm this. There is no visible significant difference in the number of asymptomatic carriers when comparing individuals with one to twelve annual relapses with those who did not.

After infection, the body begins to synthesize antibodies against a specific HSV-type virus, preventing the spread of the infection. In the case of infection with the HSV-1 virus, this seroconversion (production of antibodies) will protect the body from other infectious processes caused by this virus, such as genital herpes, herpetic keratitis and felon.

Antibodies that are produced after an initial herpes infection prevent infection with the same type of virus: people who have had HSV-1 orofacial herpes do not have panaritium or genital herpes caused by HSV-1.

In a monogamous marriage, a seronegative woman has a risk of infection from a seropositive man above 30% per year. During the first oral infection, production of protective antibodies will take 6 weeks, after which humoral immunity will be able to protect the body from repeated genital infection.

Diagnostics

Primary orofacial herpes is easily diagnosed in people who have not previously been sick and have not had contact with HSV-1 virus carriers. Such people usually develop several round, superficial ulcers in the corner of the mouth, accompanied by acute gingivitis. Adults with atypical symptoms are more difficult to diagnose. Prodromal symptoms, which appear even before the appearance of visible herpetic lesions, will make it possible to differentially diagnose symptoms of HSV-type virus infection from, for example, allergic stomatitis.If the disease does not manifest inside the mouth, primary orofacial herpes may be mistaken for impetigo or bacterial contamination. In addition, mouth ulcers (aphthae) can also look like oral herpes, but no blisters appear.

Genital herpes is more difficult to diagnose as most HSV-2 infected people do not have the “classic” symptoms. In addition, mycoses, atopic dermatitis, urethritis have similar symptoms, which complicates its diagnosis. Laboratory tests include: virological studies, RIF, PCR.Although these procedures are highly specific and provide high precision, they are too complex and expensive for ongoing clinical use.

Serological method. IgM serology does not discriminate between antibodies to HSV-1 and HSV-2 virus types. However, the new immuno-point glycoprotein G-specific HSV test provides more than 98% specificity and thus allows distinguishing between HSV-1 and HSV-2 types of herpes. Some foreign clinicians believe that the IgM test will soon be replaced by a new one.

Cytological method. In the scraping of the affected area of ​​the epithelium, stained according to Romanovsky – Giemsa, multinucleated cells with intracellular inclusions are found.

Virological method. Infect cell cultures and detect cytopathological action (CPE) in the form of giant multinucleated cells with inclusions that are destroyed. Identification is carried out in the reaction of neutralization of CPP, RIF with monoclonal antibodies. White plaques form on the chorionallantoic membrane of chicken embryos after 2-3 days.

Biological method. When viral material is applied to scarification of the cornea of ​​a rabbit, keratitis occurs, and encephalitis occurs in the brain of newborn mice.

Prevention of genital herpes

As with most STDs, women are more susceptible to herpes than men. In general, in a year without using antiviral drugs or condoms, the risk of HSV-2 transmission from man to woman is 8-11%. It is believed that this is due to the increased vulnerability of the mucous membranes at the points of contact.The risk of transmission from an infected woman to a man is 4–5%. Suppressive antiviral therapy reduces the risk by up to 50%. In addition, the use of antiviral drugs can prevent symptoms after infection in 50% of seropositive people. Condom use significantly reduces the risk of infection, and the risk is lower for women. The combined approach reduces risk by 75%.

It should be noted that the figures above are derived from clinical studies in subjects with frequent recurrent genital herpes (more than six cases per year). Individuals without symptoms or with a low relapse rate were excluded from these studies. Previous exposure to HSV-1 herpes reduces the risk of HSV-2 infection in women by a factor of three.

Asymptomatic carriers are unaware of the disease and can infect others.

In October 2011, it was reported that the anti-HIV drug Tenofovir, when applied topically as a vaginal gel, also prevents the transmission of the herpes virus.

Barrier method

Condom use reduces the risk of transmission by 30%.

Condoms provide moderate protection against HSV-2 for both men and women. The virus does not pass through the barrier made of synthetic material and, with regular use, the risk of infection is reduced by 30%. The female condom provides more complete protection, since, unlike the male, it prevents the male body from contacting the woman’s labia. However, in this case, free contact of the scrotum, anus, buttocks and thighs is possible – areas that can come into contact with ulcers or body fluids during coitus. Thus, an increase in the level of mechanical protection is advisable only up to a certain limit, beyond which sex ends.

Condoms and rubber dams (latex cunnilingus plates) are also effective for oral sex.

Parallel use of antiviral drugs provides additional protection.

Vaccine

Vaccines are currently undergoing clinical trials. After successfully completing clinical testing, they can be used to prevent transmission, prevent and treat herpes infections.

Antiviral drugs

Antiviral drugs can reduce acute virus shedding. It is believed that in treated patients, the viral particle shedding phase takes 10% of the days of the year, while in untreated patients it takes 20%.

Pregnancy

The risk of mother-to-child transmission is highest if the mother becomes infected immediately before childbirth (30 to 60%). If the infection is recurrent, the risk drops to 3%. In the absence of ulcers, the risk is less than 1%.

To prevent neonatal infections, pregnant women are advised to avoid unprotected orogenital contact with an HSV-1 seropositive partner during the last trimester of pregnancy. Seronegative mothers infected with HSV have a 57% risk of transmission due to the incomplete formation of an immune response – the synthesis of antibodies that are transmitted to the child even before birth and protect him for some time after. Therefore, a woman who is positive for HSV-1 and HSV-2 will transmit the infection with a 1-3% probability.Women who are seropositive for only one of the types of the virus are half as likely to be transmitted as those who are seronegative.

Mothers infected with HSV should avoid traumatic delivery procedures (eg forceps, vacuum extractors). If there is a high risk of infection, it may be advisable to use a caesarean section.

Treatment with antiviral drugs (starting at 36 weeks), such as acyclovir, reduces the likelihood of transmission, and therefore the need for a cesarean section.The safety of using other antiviral drugs during pregnancy is still being tested.

Treatment

There is currently no method to remove the virus from the body. Antiviral drugs only reduce the frequency, duration, and severity of relapses. Analgesics such as ibuprofen and paracetamol only reduce pain and fever. Local anesthetics such as prilocaine, lidocaine, benzocaine, or tetracaine also relieve itching and pain.

Treatment with antiviral drugs

Effective against herpes infections: acyclovir, valacyclovir, famciclovir, penciclovir.Acyclovir was discovered first, there are many generics of it.

It has been proven that acyclovir and valacyclovir are effective in the treatment of facial herpes (lips), including in cancer patients. The evidence to support the use of acyclovir in the treatment of primary herpetic gingivostomatitis is less strong.

Local application

When applied topically for the treatment of facial herpes, acyclovir, penciclovir, docosanol are effective. These drugs are approved for sale without a doctor’s prescription.

Alternative treatments

Alternative methods act indirectly, having only a tonic, anti-inflammatory effect. Echinacea preparations stimulate the immune system. Lysine, being an essential amino acid, is a plastic material for tissue regeneration. Zinc ointments, when applied to the skin, have an anti-inflammatory, antiseptic and drying effect, preventing the penetration of the virus and accelerating the healing of ulcers.This also includes aloe vera extract and propolis as natural anti-inflammatory agents.

Immunity

During primary infection, IgM antibodies are formed, with relapses – IgG and IgA. Due to the persistence of the virus in infected people, immunity is non-sterile and temporary – with a decrease in immunity, especially a deficiency of natural killer cells (NK), a relapse occurs. In addition, the herpes virus itself is capable of inducing immunodeficiency, one of the mechanisms of which is the stimulation of the synthesis of “ineffective” IgG antibodies, which suppress immunity and suppress NK.In people resistant to infection, immunity is carried out by the interferon system, natural killer and T-killer cells, as well as sIgA antibodies. 80-90% of adults have IgG antibodies to HSV-1. The level of immunity significantly affects the number and severity of relapses.

Forecast

After the stage of active infection, the virus remains latently persistent in the sensitive ganglia and ganglia of the autonomic nervous system. The double-stranded strand of viral DNA is embedded in the cell genome, located in the nucleus of the neurocyte.No viral particles are produced in this phase. This is controlled by viral DNA, which contains two LAT transcripts. – transcripts associated with latency), which are contained in the set. ^[7] The gene encoding them partially overlaps with the super-early genes encoding proteins of the ICP0 type, but its transcription is carried out from the complementary DNA strand. With the deletion of this region of the genome, the resulting mutant viruses, which go into a latent state, and their ability to reactivate is reduced.Thus, LAT transcripts are used to maintain the latency state rather than to enter it. The mechanisms of the transitions themselves have not been sufficiently studied at the moment, respectively, drugs that can control the activity of viruses have not yet been created.

Many infected people relapse within the first year after the initial infection. ^[2] The relapse is preceded by a prodromal period, which includes such symptoms as: tingling (paresthesia), itching, pain in the area of ​​sensitive innervation of the lumbosacral nerve skin.The prodromal period can take from several hours to several days. Antiviral therapy started in the prodromal period reduces the severity and duration of symptoms. In any case, relapses pass much easier and stop within 5-10 days, even without special therapy. ^[2] Subsequent outbreaks, as a rule, are episodic, occurring on average 4-5 times a year, while special therapy is not being carried out.

As mentioned, the causes of reactivation (relapse) are not known, but some triggers are documented.Recent studies (2009) have shown that the vmw65 protein ( eng. ) plays a key role in the reactivation of the virus. ^[8] Changes in the immune system before menses may also stimulate HSV-1 activation. ^{[9] [10]}

Concurrent infections such as SARS and others that cause fever can also lead to relapses. Probably, it is because of this that the concept of “cold on the lips” arose.

Other indicated triggers include localized facial injuries to the lips, eyes or mouth, trauma, surgery, effects of radiation therapy, wind, exposure to UV radiation or sunlight. ^{[11] [12] [13] [14] [15]}

The frequency and severity of outbreaks varies widely from person to person. Some develop ulcers that do not heal for weeks, while others show only slight itching and burning for several days. There is some evidence that heredity affects the rate of relapse. In the region of chromosome 21, there is a zone that includes 6 genes, which is associated with the frequency of bursts.

Immunity to the virus is permanent.The severity and frequency of outbreaks decreases over time. After a few years, some people will not have any symptoms at all, although the virus will be secreted and able to be transmitted to others. In immunocompromised individuals, outbreaks will be more severe, longer, and more frequent; they are shown antiviral therapy. ^[16] Outbreaks may occur in former locations or in close proximity to nerve endings of infected ganglia. In the case of genital herpes, the rash appears in the same place or at the base of the spine, buttocks, or back of the thighs.Individuals infected with HSV-2 are at greater risk of contracting HIV through unprotected sex with an HIV-positive partner, ^[17] especially during HSV reactivation. ^[18]

Epidemiology

The worldwide prevalence of herpes simplex viruses ranges between 65% and 90%. ^[19] HSV-1 is more common than HSV-2, the frequency of which increases significantly with age. ^[19] The prevalence and incidence of infection is determined by the presence of virus-specific antibodies in susceptible organisms. ^[20]

For example, in the United States, 57.7% of people are infected with HSV-1-type virus ^[21] and 16.2% are infected with HSV-2. Among all HSV-2 seropositive people, only 18.9% are aware of their illness. ^[22]

The source of infection is a person with active herpes. The virus can be transmitted even if there are no visible symptoms. Routes of transmission – contact-household, airborne, sexual, transplacental (from mother to fetus). The main path is the contact one.The virus is found in saliva and body fluids. Infection occurs through kisses, dishes, towels, toys. Studies for the presence of specific antibodies confirm that HSV-1 infection usually occurs at an early age, and HSV-2 infection occurs after the onset of sexual activity. The contact pathway can be realized iatrogenically using non-sterile medical instruments (in dentistry and ophthalmology). With airborne transmission, herpes infection occurs in the form of ARVI. Children from 6 months to 3 years are more likely to be infected by contact and airborne droplets.There is a genetic predisposition to herpes infection, some people are resistant. The disease is often family in nature (parents-children). Moreover, the mother can be resistant, and the children become infected from the father.

History

Herpes has been known for over 2000 years. It is said that Emperor Tiberius banned kissing in Rome for a while due to the large number of infected people. Herpetic bubbles are also mentioned in the work of the 16th century Romeo and Juliet .In the 18th century, the disease was so widespread among prostitutes that it was called the “occupational disease of women.” ^[23]

The term herpes simplex (Herpes Simplex) appeared in the book by Richard Bolton. in 1713, where other terms related to the topic appeared.

The herpes virus could not be found until 1940. ^[23]

The beginning of antiherpetic therapy dates back to 1960, when drugs that interfere with the replication of viral DNA were first used.Treatment of fatal or disabling diseases such as encephalitis ^[24] keratitis ^[25] in immunocompromised patients (transplant recipients) ^[26] or herpes zoster has been performed. ^[27] The original preparations included: 5-iodine-2′-deoxyridine (idoxuridine), IUdR, or (IDU), as well as 1-β-D-arabinofuranosylcytosine or ara-C, ^[28] later trade names “cytosar” or “cytorabine”.Later they were used for local treatment of herpes simplex, ^[29] zoster, and chickenpox. ^[30] Different drug combinations led to different results ^[24] Administration of 9-β-D-arabinofuranozzinadenine (ara-A) or vidarabine (vidarabine) is significantly less toxic than Ara-C. Since the mid-1970s, it has been regularly used for neonatal antiviral therapy. Vidarabine was the first drug whose therapeutic dose for the treatment of life-threatening HSV was lower than the toxic one. Intravenous vidarabine was licensed by the Food and Drug Administration (FDA) in 1977. Other experimental antivirals: heparin, ^[31] trifluorothymidine (TFT), ^[32] Ribivarin, ^[33] interferon, ^[34] Virazole, ^[35] and 5-methoxymethyl-2′-deoxyuridine (MMUdR). ^[36] The introduction of 9- (2-hydroxyethoxymethyl) guanidine (acyclovir), late 1970, ^[37] was a significant achievement.In the 1980s, special studies were conducted to compare the effectiveness of acyclovir versus vidarabine. ^[38] Because of the lower toxicity and ease of control, acyclovir became the drug of choice and was licensed by the FDA in 1998. ^[39] using vidarabine. ^[39] On the other hand, acyclovir can inhibit the synthesis of antibodies and when it is used more than when using vidarabine, the increase in antibody titer slows down.

Scientific research

Researchers at the University of Florida have synthesized a hammerhead-type ribozyme that specifically cleaves the mRNA of the main HSV-1 genes. Hammerhead, which attacks mRNA of the UL20 gene, significantly reduces the level of ocular HSV-1-associated infections in rabbits and reduces the release of viral particles in vivo. ^[40] This approach uses specially synthesized RNA enzymes that suppress herpes simplex virus strains. The enzyme turns off a gene responsible for the synthesis of a protein involved in the maturation and release of viral particles from an infected cell.This technique has been shown to be effective in mice and rabbits, but more research is needed before humans can use it. ^[41]

Duke University is also developing a treatment for this virus. In the normal course of the pathological process, some of the viruses are always in a latent state inside the nerve cells. Researchers are trying to figure out how to simultaneously bring all host viruses into an active stage so that the entire population can be killed at once with conventional antiviral drugs.

A class of drugs called antagomir can serve this purpose. These are artificially synthesized oligonucleotides or short segments of RNA that are complementary to herpes mRNA. They can be designed in such a way that when attached to the mRNA, they will silence it, making the virus unable to remain latent. ^[42] Professor Cullen believes that a drug could be developed that can block the mRNA responsible for keeping the virus latent. ^[43]

There is also a Herpevac vaccine against HSV-2, currently in Phase III clinical trials at the US National Institutes of Health. ^[44] In 2010 it was announced that after 8 years of study, more than 8000 women in the US and Canada, despite early favorable interim reports ^[44] , had no positive results in the treatment of genital herpes. ^[45]

The dl5-29 (now known as ACAM-529) was developed in the laboratory of Harvard Medical School. replication-defective mutant virus , which has been shown to be successful in preventing HSV-2 / HSV-1 infections and in fighting the virus in infected animals.

A vaccine that causes replication damage has been shown to induce a strong HSV-2 specific antibody and T cell immune response; protects against infection with the wild HSV-2 virus; significantly reduces the likelihood of relapses; protects against HSV-1, and prevents the virus from returning to a virulent or latent stage. ^[46] The vaccine is currently being researched and developed by Accambis (acquired by Sanofi Pasteur).) Russian. September 2008), which was to introduce a new experimental drug in 2009. ^[47] However, the post-acquisition status of ACAM-529 is not entirely clear. According to Jim Tartaglia, a spokesman for Sanofi Pasteur, ACAM-529 is still under development, and clinical trials will not begin until 2012. ^[48]

The private company “BioVex” in March 2010 began the first phase of clinical trials of the ImmunoVEX vaccine. ^[49] The HSV-2 ICP0 live vaccine for attenuated HSV-2 viruses uses a fundamentally new approach explored by Dr. William Helford at Southern Illinois Medical University. ^[50]

See also

Notes

1. ↑ http://www.rusmg.ru/php/content.php?id=8515&pr=print Genital herpes: modern problems and solutions
2. ↑ ^{1 2 3} Gupta R, Warren T, Wald A (December 2007).Genital herpes. Lancet 370 (9605): 2127-37. DOI: 10.1016 / S0140-6736 (07) 61908-4. PMID 18156035.
3. ↑ Herpes Encephalitis: eMedicine Radiology. Archived from the original on March 19, 2012.
4. ↑ Jocelyn A. Lieb, Stacey Brisman, Sara Herman, Jennifer MacGregor, Marc E. Grossman (2008). Linear erosive Herpes Simplex Virus infection in immunocompromised patients: the “Knife-Cut Sign”. Clin Infect Dis 47 (11): 1440-1441.DOI: 10.1086 / 592976. PMID 18937574.
5. ↑ ^{1 2} James, William D. Andrews’ Diseases of the Skin: clinical Dermatology. – Saunders Elsevier, 2006 .– ISBN 0-7216-2921-0
6. ↑ Warren Terri The Good News about the Bad News: Herpes: Everything You Need to Know. – New Harbinger Publications, 2009. – P. 28. – ISBN 1572246189
7. ↑ Stumpf MP, Laidlaw Z, Jansen VA (2002).”Herpes viruses hedge their bets.” Proc. Natl. Acad. Sci. U.S.A. 99 (23): 15234-7. DOI: 10.1073 / pnas.232546899. PMID 12409612.
8. ↑ How Herpes Re-rears Its Ugly Head – Science News. Archived from the original on March 19, 2012.
9. ↑ Myśliwska J, Trzonkowski P, Bryl E, Lukaszuk K, Myśliwski A (2000). “Lower interleukin-2 and higher serum tumor necrosis factor-a levels are associated with perimenstrual, recurrent, facial Herpes simplex infection in young women.” Eur. Cytokine Netw. 11 (3): 397-406. PMID 11022124.
10. ↑ Segal AL, Katcher AH, Brightman VJ, Miller MF (1974). “Recurrent herpes labialis, recurrent aphthous ulcers, and the menstrual cycle.” J. Dent. Res. 53 (4): 797-803. DOI: 10.1177 / 00220345740530040501. PMID 4526372.
11. ↑ Chambers A, Perry M (2008). “Salivary mediated autoinoculation of herpes simplex virus on the face in the absence of” cold sores, “after trauma.” J. Oral Maxillofac. Surg. 66 (1): 136-8. DOI: 10.1016 / j.joms.2006.07.019. PMID 18083428.
12. ↑ Perna JJ, Mannix ML, Rooney JF, Notkins AL, Straus SE (1987). “Reactivation of latent herpes simplex virus infection by ultraviolet light: a human model.” J. Am. Acad. Dermatol. 17 (3): 473-8. DOI: 10.1016 / S0190-9622 (87) 70232-1. PMID 2821086.
13. ↑ Rooney JF (1992). “UV light-induced reactivation of herpes simplex virus type 2 and prevention by acyclovir”. J. Infect. Dis. 166 (3): 500-6. DOI: 10.1093 / infdis / 166.3. 500. PMID 1323616.
14. ↑ Oakley C, Epstein JB, Sherlock CH (1997). “Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy.” Oral Surg Oral Med Oral Pathol Oral Radiol Endod 84 (3): 272-8. DOI: 10.1016 / S1079-2104 (97)
15. -5. PMID 9377190.
16. ↑ Ichihashi M, Nagai H, Matsunaga K (2004).”Sunlight is an important causative factor of recurrent herpes simplex.” Cutis 74 (5 Suppl): 14-8. PMID 15603217.
17. ↑ Martinez V, Caumes E, Chosidow O (2008). Treatment to prevent recurrent genital herpes. Curr Opin Infect Dis 21 (1): 42–48. DOI: 10.1097 / QCO.0b013e3282f3d9d3. PMID 18192785.
18. ↑ Sobngwi-Tambekou J (2009). Effect of HSV-2 serostatus on acquisition of HIV by young men: results of a longitudinal study in Orange Farm, South Africa. J Infect Dis 199 (7): 958-964. DOI: 10.1086 / 597208. PMID 19220143.
19. ↑ Koelle DM, Corey L (2008). Herpes Simplex: Insights on Pathogenesis and Possible Vaccines. Annu Rev Med 59 : 381-395. DOI: 10.1146 / annurev.med.59.061606.095540. PMID 18186706.
20. ↑ ^{1 2} Chayavichitsilp P, Buckwalter JV, Krakowski AC, Friedlander SF (April 2009).Herpes simplex. Pediatr Rev 30 (4): 119-29; quiz 130. DOI: 10.1542 / pir.30-4-119. PMID 19339385.
21. ↑ Smith JS, Robinson NJ (2002). Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review. J. Infect. Dis. 186 Suppl 1 : S3-28. DOI: 10.1086 / 343739. PMID 12353183.
22. ↑ Xu, Fujie; Fujie Xu, MD, PhD; Maya R. Sternberg, PhD; Benny J.Kottiri, PhD; Geraldine M. McQuillan, PhD; Francis K. Lee, PhD; Andre J. Nahmias, MD; Stuart M. Berman, MD, ScM; Lauri E. Markowitz, MD (2006-10-23). “Trends in Herpes Simplex Virus Type 1 and Type 2 Seroprevalence in the United States.” JAMA (AMA) 296 (8): 964-73. DOI: 10.1001 / jama.296.8.964. PMID 16926356.
23. ↑ Xu, F; MR Sternberg, PhD, SL Gottlieb, MD, SM Berman, MD, LE Markowitz, MD, Div of STD Prevention, National Center for HIV / AIDS, Viral Hepatitis, STD, and TB Prevention; SE Forhan, MD, LD Taylor, DrPH, EIS officers, CDC (23).Seroprevalence of Herpes Simplex Virus Type 2 Among Persons Aged 14–49 Years — United States, 2005-2008. Morbidity and Mortality Weekly Report (MMWR) 59 (15): 456-459. Retrieved April 12, 2011.
24. ↑ ^{1 2} John Leo . The New Scarlet Letter, Time .2 Aug 1982.
25. ↑ ^{1 2} Chow AW (March 1973).Cytosine Arabinoside Therapy for Herpes Simplex Encephalitis — Clinical Experience with Six Patients. Antimicrob. Agents Chemother. 3 (3): 412-7. PMID 47

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26. ↑ Kaufman HE, Howard GM (August 1962). “Therapy of experimental herpes simplex keratitis”. Invest Ophthalmol 1 : 561-4. PMID 14454441.
27. ↑ Ch’ien LT, Whitley RJ, Alford CA, Galasso GJ (June 1976). “Adenine arabinoside for therapy of herpes zoster in immunosuppressed patients: preliminary results of a collaborative study.” J. Infect. Dis. 133 Suppl : A184-91. PMID 180198.
28. ↑ McKelvey EM, Kwaan HC (November 1969). Cytosine arabinoside therapy for disseminated herpes zoster in a patient with IgG pyroglobulinemia. Blood 34 (5): 706-11. PMID 5352659.
29. ↑ Fiala M, Chow A, Guze LB (April 1972). “Susceptibility of Herpesviruses to Cytosine Arabinoside: Standardization of Susceptibility Test Procedure and Relative Resistance of Herpes Simplex Type 2 Strains. “ Antimicrob. Agents Chemother. 1 (4): 354-7. PMID 4364937.
30. ↑ Allen LB (June 1976). “Effect of 9-beta-D-arabinofuranosylhypoxanthine 5′-monophosphate on genital lesions and encephalitis induced by Herpesvirus hominis type 2 in female mice.” J. Infect. Dis. 133 Suppl : A178–83. PMID 6598.
31. ↑ Juel-Jensen BE (March 1970). Varicella and cytosine arabinoside. Lancet 1 (7646).DOI: 10.1016 / S0140-6736 (70)

    -9. PMID 41.

32. ↑ Nahmias AJ, Kibrick S (May 1964). INHIBITORY EFFECT OF HEPARIN ON HERPES SIMPLEX VIRUS. J. Bacteriol. 87 (5): 1060-6. PMID 4289440.
33. ↑ Allen LB, Sidwell RW (September 1972). “Target-Organ Treatment of Neurotropic Virus Diseases: Efficacy as a Chemotherapy Tool and Comparison of Activity of Adenine Arabinoside, Cytosine Arabinoside, Idoxuridine, and Trifluorothymidine. “ Antimicrob. Agents Chemother. 2 (3): 229-33. PMID 47
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    ↑ Allen LB, Wolf SM, Hintz CJ, Huffman JH, Sidwell RW (March 1977). “Effect of ribavirin on Type 2 Herpesvirus hominis (HVH / 2) in vitro and in vivo”. Ann. N. Y. Acad. Sci. 284 : 247-53. DOI: 10.1111 / j.1749-6632.1977.tb21957.x. PMID 212976.
    ↑ Allen LB, Cochran KW (November 1972). Target-Organ Treatment of Neurotropic Virus Disease with Interferon Inducers. Infect. Immun. 6 (5): 819-23. PMID 4404669.
    ↑ Sidwell RW, Huffman JH, Khare GP, Allen LB, Witkowski JT, Robins RK (August 1972). “Broad-spectrum antiviral activity of Virazole: 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide.” Science 177 (4050): 705-6. DOI: 10.1126 / science.177.4050.705. PMID 4340949.
    ↑ Babiuk LA, Meldrum B, Gupta VS, Rouse BT (December 1975). “Comparison of the Antiviral Effects of 5-Methoxymethyl-deoxyuridine with 5-Iododeoxyuridine, Cytosine Arabinoside, and Adenine Arabinoside.” Antimicrob. Agents Chemother. 8 (6): 643-50. PMID 1239978.
    ↑ O’Meara A, Deasy PF, Hillary IB, Bridgen WD (December 1979). “Acyclovir for treatment of mucocutaneous herpes infection in a child with leukaemia.” Lancet 2 (8153). DOI: 10.1016 / S0140-6736 (79) 92428-0.PMID 91931.
    ↑ Whitley R (February 1991). “A controlled trial comparing vidarabine with acyclovir in neonatal herpes simplex virus infection. Infectious Diseases Collaborative Antiviral Study Group. ” N. Engl. J. Med. 324 (7): 444-9. DOI: 10.1056 / NEJM1943240703. PMID 1988829.
    ↑ ^{1 2} Kimberlin DW (August 2001). “Safety and efficacy of high-dose intravenous acyclovir in the management of neonatal herpes simplex virus infections”. Pediatrics 108 (2): 230-8. DOI: 10.1542 / peds.108.2.230. PMID 11483782.
    ↑ Molecular Therapy Molecular Therapy – Abstract of article: 801. RNA Gene Therapy Targeting Herpes Simplex Virus. Nature.com (May 1, 2006). Archived from the original on March 19, 2012. Retrieved on April 12, 2011.
    ↑ University of Florida News – Potential new herpes therapy studied. News.ufl.edu (February 3, 2009). Archived from the original on March 19, 2012. Retrieved on April 12, 2011.
    ↑ Fox, Maggie . New approach offers chance to finally kill herpes, Reuters (2 July 2008). Retrieved April 12, 2011.
    ↑ Kingsbury, Kathleen . A Cure for Cold Sores ?, Time (2 July 2008). Retrieved May 4, 2010.
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    ↑ Harvard Medical School: from Herpes Vaccines , 15. April 2011
    ↑ BioVex commences dosing in Phase 1 study of ImmunoVEX live attenuated genital herpes vaccine. See also: Your partner has herpes – now the good news from New Scientist .
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    90,000 Herpes Labialis (Mouth Ulcer) – Cause, Image and Treatment.

    Herpes labial, also called mouth sores , herpes , herpes , herpes sores , is a form of viral herpes simplex infection that occurs on or around the lips .A herpes outbreak can last 2–3 weeks before the wounds gradually heal, but the virus will still be latent in the facial nerves – and can (in people with symptoms) infect up to 12 times a year in the worst case scenario. Infected people usually have 1 to 3 outbreaks during the year. Outbreaks seem to have escalated over the years. You may be completely asymptomatic, but once the herpes virus has taken over your body, it will never leave your body. Herpes outbreaks usually occur when the immune system is weakened. Especially during times of high stress, poor sleep, and possibly poor nutrition.

    – Is herpes contagious?

    Yes, the herpes simplex virus can be spread from person to person – for example, through close contact, lip contact or sexual intercourse.

    – How long does a herpes outbreak last?

    A herpes outbreak usually lasts no more than 2-3 weeks.

    – Can symptomatic herpes on the lips be treated?

    Yes, you can buy acyclovir at the pharmacy, which is applied directly to the affected area.Studies have shown that it clears infection up to 10% faster than natural healing. For more aggressive outbreaks, you can also get antiviral drugs prescribed by your GP.

    – Are there frequent outbreaks of herpes on the lips?

    Yes, a large US study found that among young adults, 33% of men and 28% of women had 2 to 3 outbreaks per year. So you are not alone in this, no.

    Les også : Lip pain? You should know this.