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How antivirals work. Antiviral Drugs: How They Work, Treatment Options, and Eligibility Criteria

How do antiviral drugs combat viral infections. Who is eligible for antiviral treatment against COVID-19. What are the available antiviral treatment options for COVID-19. Where can patients access antiviral medications for COVID-19. How effective are antivirals in treating respiratory diseases.

Understanding the Mechanism of Antiviral Drugs

Antiviral drugs play a crucial role in combating viral infections, including COVID-19. These medications work by supporting the immune system’s fight against viruses, primarily by inhibiting viral replication within the body. This reduction in viral load aims to alleviate symptoms and accelerate recovery.

How do antiviral drugs specifically target viruses? Antivirals interfere with various stages of the viral life cycle, such as:

  • Preventing viral entry into host cells
  • Inhibiting viral protein synthesis
  • Blocking viral genome replication
  • Impeding the release of new viral particles

By targeting these specific processes, antiviral medications can significantly reduce the severity and duration of viral infections, including respiratory diseases like COVID-19.

COVID-19 Antiviral Treatment Options

For individuals diagnosed with mild to moderate COVID-19 and at high risk for severe illness, several antiviral treatments have received emergency use authorization from the FDA. These options include:

1. Paxlovid (nirmatrelvir/ritonavir)

Paxlovid is an oral antiviral medication suitable for adults and children aged 12 and older, weighing at least 88 lbs. It must be administered within five days of symptom onset. Patients with severe kidney or liver disease are not recommended for this treatment.

Is Paxlovid associated with any specific side effects? Some patients may experience a phenomenon known as “COVID-19 rebound,” characterized by a recurrence of symptoms and a positive test result within 2-8 days of completing the Paxlovid course. In such cases, continued symptom monitoring and additional isolation periods are advised.

2. Lagevrio (molnupiravir)

Lagevrio is prescribed for adults 18 years and older. Like Paxlovid, it is an oral medication that must be taken within five days of symptom onset. It is not recommended during pregnancy or while breastfeeding.

3. Veklury (remdesivir)

Veklury can be prescribed for individuals over 28 days old. Unlike the other options, it is administered via intravenous infusion (IV) at a treatment center for three consecutive days. Treatment must begin within seven days of symptom onset. Veklury is also used for hospitalized COVID-19 patients.

Eligibility Criteria for Antiviral Treatment

Who qualifies for antiviral treatment against COVID-19? The FDA has authorized emergency use of antiviral medications for patients who meet the following criteria:

  • Test positive for COVID-19
  • Experience mild to moderate COVID-19 symptoms at home
  • Are at high risk for severe illness that may result in hospitalization

What factors contribute to being considered high-risk for severe COVID-19? Individuals may be classified as high-risk if they:

  • Are 50 years or older
  • Are unvaccinated
  • Are current or former smokers
  • Are overweight
  • Have been diagnosed with chronic lung, heart, or kidney disease
  • Are diabetic
  • Are pregnant
  • Are immunocompromised

Understanding your risk status is crucial, as it allows for prompt action upon testing positive for COVID-19, potentially reducing the likelihood of developing severe illness requiring hospitalization.

Accessing Antiviral Treatment

Where can patients obtain antiviral medications for COVID-19? Antiviral treatments require a prescription from a healthcare provider. If you are at high risk for severe COVID-19 and test positive, it’s essential to contact your healthcare provider immediately.

Can pharmacists prescribe antiviral medications? In some cases, pharmacists may be authorized to prescribe antiviral medications directly. If you have difficulty scheduling an appointment with your primary care provider, consult your pharmacist about treatment options.

What are Test to Treat locations? These are specialized clinics designed to:

  1. Confirm your COVID-19 diagnosis
  2. Review your medical history
  3. Prescribe appropriate treatment

Test to Treat locations offer a convenient one-stop solution for diagnosis and treatment initiation.

When should treatment begin? For optimal effectiveness, antiviral treatment should commence within five days of symptom onset. Prompt action is crucial in maximizing the benefits of these medications.

The Impact of Antiviral Treatment on Respiratory Diseases

How effective are antivirals in treating respiratory diseases? Antiviral treatments can significantly boost the immune system’s response when administered promptly at the onset of symptoms for various infectious respiratory diseases. These medications can help:

  • Reduce the severity of symptoms
  • Shorten the duration of illness
  • Prevent complications
  • Decrease the risk of hospitalization

While antivirals are not a cure for viral infections like COVID-19, they play a crucial role in managing symptoms and improving patient outcomes. It’s important to note that even while undergoing antiviral treatment, patients remain contagious and should continue to follow isolation guidelines to prevent virus transmission.

The Role of Antivirals in COVID-19 Management

How do antivirals contribute to the overall management of COVID-19? Antiviral medications serve as a critical tool in the fight against COVID-19, particularly for high-risk individuals. These treatments:

  • Reduce viral load in the body
  • Alleviate symptom severity
  • Accelerate recovery time
  • Lower the risk of hospitalization and severe complications

By targeting the virus directly, antivirals complement other COVID-19 management strategies, such as vaccination and non-pharmaceutical interventions. Their use in high-risk populations helps to reduce the burden on healthcare systems and improve individual patient outcomes.

Monitoring and Follow-up During Antiviral Treatment

What should patients expect during antiviral treatment for COVID-19? While undergoing antiviral therapy, it’s crucial to:

  1. Continue monitoring symptoms closely
  2. Maintain self-isolation for at least 10 days after symptom onset
  3. Avoid using fever-reducing medications during the isolation period
  4. Contact healthcare providers if symptoms worsen or new concerns arise

Healthcare providers may schedule follow-up appointments to assess treatment efficacy and monitor for any potential side effects or complications. In the case of COVID-19 rebound following Paxlovid treatment, additional monitoring and isolation may be necessary.

How long should patients continue antiviral treatment? The duration of treatment varies depending on the specific antiviral medication prescribed. For example:

  • Paxlovid is typically taken for 5 days
  • Lagevrio is usually prescribed for 5 days
  • Veklury is administered for 3 consecutive days

It’s essential to complete the full course of treatment as prescribed, even if symptoms improve before the medication is finished.

Antiviral Resistance and Future Developments

Can viruses develop resistance to antiviral drugs? Like bacteria developing antibiotic resistance, viruses can potentially evolve to resist antiviral medications. This phenomenon occurs when a virus mutates in a way that makes the antiviral less effective or ineffective.

How does the medical community address antiviral resistance? To combat antiviral resistance, researchers and healthcare professionals:

  • Continuously monitor viral strains for signs of resistance
  • Develop new antiviral drugs targeting different aspects of viral replication
  • Explore combination therapies to reduce the likelihood of resistance
  • Emphasize proper use and completion of antiviral treatments

What future developments can we expect in antiviral treatments? The field of antiviral research is rapidly evolving, with ongoing efforts to:

  1. Discover new antiviral compounds
  2. Improve existing antiviral medications
  3. Develop broad-spectrum antivirals effective against multiple viral families
  4. Explore novel delivery methods for enhanced efficacy
  5. Investigate the potential of antiviral prophylaxis for high-risk individuals

These advancements aim to expand our arsenal against viral infections, including emerging threats and potential future pandemics.

The Importance of Comprehensive COVID-19 Management

While antiviral treatments play a crucial role in managing COVID-19, they are just one component of a comprehensive approach to controlling the pandemic. Other essential elements include:

  • Vaccination programs to prevent infection and reduce severity
  • Non-pharmaceutical interventions like mask-wearing and social distancing
  • Regular testing and contact tracing
  • Public health education and awareness campaigns
  • Ongoing research into virus behavior and treatment options

How do these elements work together to combat COVID-19? By combining multiple strategies, we create a layered defense against the virus. Vaccination reduces the likelihood of infection and severe illness, while non-pharmaceutical interventions limit virus spread. Antiviral treatments provide an additional tool to manage cases that do occur, particularly in high-risk individuals.

What role does ongoing research play in COVID-19 management? Continuous scientific investigation is crucial for:

  1. Understanding virus mutations and their implications
  2. Developing new treatments and improving existing ones
  3. Refining public health strategies based on emerging data
  4. Preparing for potential future variants or pandemics

This research ensures that our approach to managing COVID-19 remains dynamic and responsive to new challenges as they arise.

Global Access to Antiviral Treatments

How does access to antiviral treatments vary globally? While antiviral medications have shown promise in managing COVID-19, their availability and accessibility differ significantly across countries and regions. Factors influencing global access include:

  • Economic disparities between nations
  • Manufacturing and distribution challenges
  • Regulatory approval processes in different countries
  • Healthcare infrastructure variations
  • Intellectual property rights and licensing agreements

What efforts are being made to improve global access to antivirals? Various initiatives aim to enhance equitable access to antiviral treatments worldwide:

  1. International collaborations for research and development
  2. Technology transfer agreements to boost manufacturing capacity
  3. Donation programs from pharmaceutical companies
  4. Advocacy for patent waivers or voluntary licensing
  5. Funding mechanisms to support low- and middle-income countries

These efforts are crucial in ensuring that the benefits of antiviral treatments reach populations globally, contributing to a more effective and equitable response to the COVID-19 pandemic.

The Future of Antiviral Therapies

As we look beyond the current pandemic, how might antiviral therapies evolve? The lessons learned from COVID-19 are likely to accelerate advancements in antiviral research and development. Future directions may include:

  • Development of universal antivirals effective against multiple viral families
  • Integration of artificial intelligence in drug discovery and design
  • Exploration of combination therapies for enhanced efficacy
  • Investigation of antiviral prophylaxis strategies for high-risk populations
  • Advancements in delivery methods, such as inhalable or long-acting formulations

How might these advancements impact future pandemic preparedness? The ongoing research and development in antiviral therapies could significantly enhance our ability to respond to future viral threats. By having a diverse arsenal of antiviral treatments readily available, we may be better equipped to:

  1. Rapidly deploy effective treatments in the early stages of an outbreak
  2. Mitigate the severity and spread of viral infections
  3. Reduce the economic and social impact of potential pandemics
  4. Protect vulnerable populations more effectively
  5. Complement vaccination strategies for comprehensive disease management

These advancements, combined with improved global health infrastructure and surveillance systems, could significantly enhance our collective resilience against future viral threats.

Antivirals | American Lung Association

If you are at risk for serious illness from COVID-19 and just tested positive, you should discuss treatment options with your healthcare provider, including taking antivirals.

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Treating COVID-19

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If you test positive for COVID-19 and are at increased risk for severe illness — including people with chronic lung disease, adults 65 and over, or people who currently or used to smoke cigarettes, there are treatment options available. Talk with your healthcare provider right away because treatments taken when your symptoms are mild may keep them from becoming severe. Your healthcare provider can help determine which treatment is the best option for you. Visit our website for more information.

What to Expect

Antiviral medications can help your immune system fight back by helping stop the virus from multiplying your body. This lowers the amount of virus in your body with the goal of you having less severe symptoms and recovering more quickly. Antiviral therapy is not a cure for COVID-19. You are still contagious and can spread the virus to others. Be sure to monitor your symptoms and continue to self-isolate until 10 days have passed without using fever reducing medications, and your COVID-19 symptoms are improving.

What are My Treatment Options?

If you are recovering at home from mild-to-moderate COVID-19, you may qualify for one of these antiviral treatments depending on your age, health history and how long you’ve had symptoms. The following treatments are authorized for emergency use by the Food and Drug Administration: 

  • Paxlovid (nirmatrelvir/ritonavir): May be prescribed for adults and children who are at least 12 years old and weigh at least 88 lbs. It is not recommended for people with serious kidney or liver disease. This treatment is taken by mouth (as a pill) and must be given within five days after the first symptoms of COVID-19 appear.
    • COVID-19 rebound is a recurrence of symptoms and a positive test after a negative result within 2-8 days of having finished Paxlovid. In these instances, continued monitoring of symptoms and additional periods of isolation are recommended.
  • Lagevrio (molnupiravir): May be prescribed for adults 18 years and older. It is not recommended during pregnancy or when breastfeeding. This treatment is taken by mouth (as a pill) and must be given within five days after the first symptoms of COVID-19 appear.
  • Veklury (remdesivir): May be prescribed for anyone over 28 days old. This treatment is administered via intravenous infusion (IV) at a treatment center for three consecutive days and must begin within seven days after the first symptoms of COVID-19 appear. This medication is also given to individuals hospitalized by COVID-19.

Talk with your healthcare provider about your treatment options. Based on your health history and symptoms, they can help you begin treatment if that is the best course of action. If antiviral medications are determined not to be the best treatment option for you, you may be recommended supportive care at home unless your symptoms worsen.  

Who is eligible?

Antiviral medication to treat COVID-19 is authorized for emergency use by the Food and Drug Administration (FDA) and used for patients who:

  • test positive for COVID-19, 
  • are experiencing mild-moderate COVID-19 symptoms at home, and
  • are high risk for severe illness that may result in hospitalization

Knowing if you are high-risk for severe illness from COVID-19 allows you to act quickly if you test positive for COVID-19 so you are less likely to develop severe illness requiring hospitalization. You may be high-risk if you are:

  • 50 years or older, 
  • unvaccinated,
  • a current or former smoker, 
  • overweight, 
  • diagnosed with chronic lung, heart, or kidney disease, 
  • diabetic, 
  • Pregnant, or 
  • immunocompromised

Where do I get antiviral treatment?

Antiviral medications require a prescription from a healthcare provider. If you are high risk for severe illness from COVID-19 and test positive, speak with your healthcare provider right away. You may also be prescribed antiviral medications directly from your pharmacist. Speak with your pharmacist if you have trouble getting in to see your primary care provider right away. Your symptoms must have started no later than within the last five days to begin treatment.

You can also visit a Test to Treat location, a clinic that is set up to confirm your COVID-19 diagnosis, review your medical history and prescribe appropriate treatment. If you still have questions about treatment, contact our Lung HelpLine staff at 800-LUNGUSA.

Antiviral treatment can boost your immune system if taken promptly at the onset of symptoms of some infectious respiratory diseases. Learn more about when to contact your healthcare provider how this treatment can help you feel better faster.

Antiviral medications can be effective in treating viral infections if used promptly when symptoms, such as fever, aches and cough, first appear. Pregnant women are one group at higher risk for severe illness from respiratory infections due to changes in the body caused by pregnancy. Early treatment is important because a serious respiratory illness may be harmful to your developing baby. It is important to call your doctor right away – within 48 hours of when symptoms begin.

While anyone may consider taking an antiviral, people at high-risk for severe illness are specifically recommended to do so. Your doctor may ask you to come in to test for what type of illness is making you sick. They may prescribe antiviral treatment with the goal to make you feel less sick and for a shorter length of time.ng an antiviral, people at high-risk for severe illness are specifically recommended to do so.

Once taken, antiviral medications work quickly to boost the immune system. In the airways of your lungs, where the respiratory infection is occurring, the virus is attacking healthy cells and creating copies of itself that further spread the infection while your immune system is working to stop the viral spread. Antivirals work by halting the attack, so the virus is unable to attach to a healthy cell or copy itself. This stops your illness from spreading so your body can focus on healing and recovery. Antivirals only work if taken as soon as possible. If you are in a high-risk group, make a plan with your doctor to connect quickly when you become ill with a respiratory infection so you can get tested, treated, and begin the healing process before serious damage is done. Learn more at Lung.org.

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Page last updated: February 7, 2023

A review: Mechanism of action of antiviral drugs

1.
Balloux F, van Dorp L. (2017) Q&A: What are pathogens,
and what have they done to and for us?
BMC Biology
15: 1–6. [PMC free article] [PubMed] [Google Scholar]

2.
Champe HRAPC, Fisher BD. (2007) Lippincott’s Illustrated Reviews:
Microbiology.
Philadelphia:Lippincott
Williams & Wilkins. [Google Scholar]

3.
Saxena SK, Saxena S, Saxena R, et al. (2010) Emerging
trends, challenges and prospects in antiviral therapeutics and drug
development for infectious diseases. Electronic
Journal of Biology
6: 26–31. [Google Scholar]

4.
De Clercq E, Li G. (2016) Approved antiviral drugs over
the past 50 years. Clinical Microbiology
Reviews
29: 695–747. [PMC free article] [PubMed] [Google Scholar]

5.
He H. (2013) Vaccines and antiviral
agents. Current Issues in Molecular Virology: Viral
Genetics and Biotechnological Applications
2013: 239–250. [Google Scholar]

6.
Parks JM, Smith JC. (2020) How to discover antiviral
drugs quickly. The New England Journal of
Medicine
382(23):
2261–2264. [PubMed] [Google Scholar]

7.
Shin W-J, Seong BL. (2019) Novel antiviral drug
discovery strategies to tackle drug-resistant mutants of influenza virus
strains. Expert Opinion on Drug Discovery
14: 153–168. [PubMed] [Google Scholar]

8.
Asiri YI, Alsayari A, Muhsinah AB, et al. (2020)
Benzothiazoles as potential antiviral agents.
Journal of Pharmacy and Pharmacology
72: 1459–1480. [PMC free article] [PubMed] [Google Scholar]

9.
Ryu W-S. (2017) Virus life
cycle. Molecular Virology of Human Pathogenic
Viruses
2017: 31–45. [Google Scholar]

10.
Connolly SA, Jackson JO, Jardetzky TS, et al. (2011) Fusing
structure and function: a structural view of the herpesvirus entry
machinery. Nature Reviews Microbiology
9: 369–381. [PMC free article] [PubMed] [Google Scholar]

11.
Balfour HH., JR (1983) Resistance of herpes simplex
to acyclovir. Annals of Internal Medicine
98: 404–406. [PubMed] [Google Scholar]

12.
Fyfe J, Keller P, Furman P, et al. (1978)
Thymidine kinase from herpes simplex virus phosphorylates the
new antiviral compound, 9-(2-hydroxyethoxymethyl) guanine.
The Journal of Biological Chemistry
253: 8721–8727. [PubMed] [Google Scholar]

13.
Derse D, Cheng Y, Furman P, et al. (1981)
Inhibition of purified human and herpes simplex virus-induced
DNA polymerases by 9-(2-hydroxyethoxymethyl) guanine triphosphate. Effects
on primer-template function. The Journal of
Biological Chemistry
256:
11447–11451. [PubMed] [Google Scholar]

14.
Furman PA, St, Clair M, Spector T. (1984) Acyclovir triphosphate is a
suicide inactivator of the herpes simplex virus DNA
polymerase. The Journal of Biological
Chemistry
259: 9575–9579. [PubMed] [Google Scholar]

15.
de Miranda P, Blum MR. (1983) Pharmacokinetics of acyclovir
after intravenous and oral administration. The
Journal of Antimicrobial Chemotherapy
12: 29–37. [PubMed] [Google Scholar]

16.
Balfour HH, Jr, Chace BA, Stapleton JT, et al. (1989) A
randomized, placebo-controlled trial of oral acyclovir for the prevention of
cytomegalovirus disease in recipients of renal allografts.
The New England Journal of Medicine
320: 1381–1387. [PubMed] [Google Scholar]

17.
Fletcher C, Englund J, Edelman C, et al. (1991)
Pharmacologic basis for high-dose oral acyclovir prophylaxis
of cytomegalovirus disease in renal allograft recipients.
Antimicrobial Agents and Chemotherapy
35: 938–943. [PMC free article] [PubMed] [Google Scholar]

18.
Meyers JD, Wade JC, Mitchell CD, et al. (1982)
Multicenter collaborative trial of intravenous acyclovir for
treatment of mucocutaneous herpes simplex virus infection in the
immunocompromised host. The American Journal of
Medicine
73: 229–235. [PubMed] [Google Scholar]

19.
Soul-Lawton J, Seaber E, On N, et al. (1995) Absolute
bioavailability and metabolic disposition of valaciclovir, the L-valyl ester
of acyclovir, following oral administration to humans.
Antimicrobial Agents and Chemotherapy
39: 2759–2764. [PMC free article] [PubMed] [Google Scholar]

20.
Erice A, Jordan MC, Chace BA, et al. (1987)
Ganciclovir treatment of cytomegalovirus disease in
transplant recipients and other immunocompromised hosts.
JAMA
257: 3082–3087. [PubMed] [Google Scholar]

21.
Anderson RD, Griffy KG, Jung D, et al. (1995)
Ganciclovir absolute bioavailability and steady-state
pharmacokinetics after oral administration of two 3000-mg/d dosing regimens
in human immunodeficiency virus—and cytomegalovirus-seropositive
patients. Clinical Therapeutics
17: 425–432. [PubMed] [Google Scholar]

22.
Boyd MR, Bacon TH, Sutton D, et al. (1987)
Antiherpesvirus activity of
9-(4-hydroxy-3-hydroxy-methylbut-1-yl) guanine (BRL 39123) in cell
culture. Antimicrobial Agents
Chemotherapeutics
31: 1238–1242. [PMC free article] [PubMed] [Google Scholar]

23.
Tyring S, Barbarash RA, Nahlik JE, et al. (1995)
Famciclovir for the treatment of acute herpes zoster: effects
on acute disease and postherpetic neuralgia: A randomized, double-blind,
placebo-controlled trial. Annals of Internal
Medicine
123: 89–96. [PubMed] [Google Scholar]

24.
Safrin S, Crumpacker C, Chatis P, et al. (1991) A
controlled trial comparing foscarnet with vidarabine for acyclovir-resistant
mucocutaneous herpes simplex in the acquired immunodeficiency
syndrome. The New England Journal of
Medicine
325: 551–555. [PubMed] [Google Scholar]

25.
Huggins JW, Hsiang CM, Cosgriff TM, et al. (1991)
Prospective, double-blind, concurrent, placebo-controlled
clinical trial of intravenous ribavirin therapy of hemorrhagic fever with
renal syndrome. The Journal of Infectious
Diseases
164: 1119–1127. [PubMed] [Google Scholar]

26.
Taylor K, Fritz K, Parmar M. (2020) Lamivudine.
In: StatPearls [Internet]. Treasure Island
(FL): StatPearls
Publishing. [Google Scholar]

27.
Dolin R, Reichman RC, Madore HP, et al. (1982) A
controlled trial of amantadine and rimantadine in the prophylaxis of
influenza A infection. The New England Journal of
Medicine
307: 580–584. [PubMed] [Google Scholar]

28.
Frediansyah A, Tiwari R, Sharun K, et al. (2020)
Antivirals for COVID-19: A critical review.
Clinical Epidemiology and Global Health
9: 90–98. [PMC free article] [PubMed] [Google Scholar]

29.
Jomah S, Asdaq SMB, Al-Yamani MJ. (2020) Clinical efficacy of
antivirals against novel coronavirus (COVID-19): A review.
Journal of Infection and Public Health
13(9):
1187–1195. [PMC free article] [PubMed] [Google Scholar]

30.
Saha A, Sharma AR, Bhattacharya M, et al. (2020) Probable
molecular mechanism of Remdesivir for the treatment of COVID-19: Need to
know more. Archives of Medical Research
51(6):
585–586. [PMC free article] [PubMed] [Google Scholar]

31.
Yavuz S, Ünal S. (2020) Antiviral treatment of
COVID-19. Turkish Journal of Medical
Sciences
50: 611–619. [PMC free article] [PubMed] [Google Scholar]

32.
Guan W-j, Ni Z-y, Hu Y, et al. (2020) Clinical
characteristics of coronavirus disease 2019 in China.
The New England Journal of Medicine
382: 1708–1720. [PMC free article] [PubMed] [Google Scholar]

33.
Grein J, Ohmagari N, Shin D. (2020) Original: Compassionate use
of remdesivir for patients with severe covid-19. The
New England Journal of Medicine
382: 2327–2336. [PMC free article] [PubMed] [Google Scholar]

34.
McCreary EK, Pogue JM. (2020) Coronavirus disease 2019
treatment: A review of early and emerging options.
Open Forum Infectious Diseases
7(4): ofaa105. [PMC free article] [PubMed] [Google Scholar]

35.
Rossignol J-F (2016) Nitazoxanide,
a new drug candidate for the treatment of Middle East respiratory syndrome
coronavirus. Journal of Infection and Public
Health
9: 227–230. [PMC free article] [PubMed] [Google Scholar]

36.
Jasenosky LD, Cadena C, Mire CE, et al. (2019) The
FDA-approved oral drug nitazoxanide amplifies host antiviral responses and
inhibits Ebola virus. iScience
19: 1279–1290. [PMC free article] [PubMed] [Google Scholar]

37.
Choy K-T, Wong AY-L, Kaewpreedee P, et al. (2020)
Remdesivir, lopinavir, emetine, and homoharringtonine inhibit
SARS-CoV-2 replication in vitro. Antiviral
Research
178: 104786. [PMC free article] [PubMed] [Google Scholar]

38.
Bell WR, Chulay JD, Feinberg JE. (1997) Manifestations resembling
thrombotic microangiopathy in patients with advanced human immunodeficiency
virus (HIV) disease in a cytomegalovirus prophylaxis trial (ACTG
204). Medicine
76: 369–380. [PubMed] [Google Scholar]

39.
Renis HE. (1969) In vitro antiviral activity
of calcium elenolate. Antimicrobial Agents and
Chemotherapy
9: 167. [PubMed] [Google Scholar]

40.
Stark J, Heath R, Oswald N, et al. (1970) A trial
of chemoprophylaxis of natural influenza infection with UK
2371. Thorax
25: 649–655. [PMC free article] [PubMed] [Google Scholar]

41.
Takemoto K, Liebhaber H. (1961) Virus-polysaccharide
interactions: I. An agar polysaccharide determining plaque morphology of EMC
virus. Virology
14: 456–462. [PubMed] [Google Scholar]

42.
Leinbach SS, Reno JM, Lee LF, et al. (1976)
Mechanism of phosphonoacetate inhibition of
herpesvirus-induced DNA polymerase.
Biochemistry
15: 426–430. [PubMed] [Google Scholar]

43.
Overby L, Duff R, Mao J-H. (1977) Antiviral potential of
phosphonoacetic acid. Annals of New York Academy of
Sciences
284: 310. [PubMed] [Google Scholar]

44.
Jamieson A, Gentry G, Subak-Sharpe J. (1974) Induction of both thymidine
and deoxycytidine kinase activity by herpes viruses.
The Journal of General Virology
24: 465–480. [PubMed] [Google Scholar]

45.
Kit S, Leung WC, Trkula D, et al. (1974) Gel
electrophoresis and isoelectric focusing of mitochondrial and viral-induced
thymidine kinases. International Journal of
Cancer
13: 203–218. [PubMed] [Google Scholar]

46.
Cheng Y-C, Domin BA, Sharma RA, et al. (1976)
Antiviral action and cellular toxicity of four thymidine
analogues: 5-Ethyl-, 5-vinyl-, 5-propyl-, and
5-allyl-2′-deoxyuridine. Antimicrobial Agents and
Chemotherapy
10: 119–122. [PMC free article] [PubMed] [Google Scholar]

47.
Declercq Et, Torrence P. (1978) Nucleoside analogs with
selective anti-viral activity. Journal of
Carbohydrates-Nucleosides-Nucleotides
5: 187–224. [Google Scholar]

48.
Cheng YC. (1977) A rational approach to the
development of antiviral chemotherapy: Alternative substrates of herpes
simplex virus type 1 (HSV-1) and type 2 (HSV-2) thymidine kinase
(TK). Annals of New York Academy of
Sciences
284: 594–598. [PubMed] [Google Scholar]

49.
Goswami BB, Borek E, Sharma OK, et al. (1979) The
broad spectrum antiviral agent ribavirin inhibits capping of
mRNA. Biochemical Biophysical Research
Communications
89: 830–836. [PubMed] [Google Scholar]

50.
Adams B, Morgan M, Muthukrishnan S, et al. (1978) The
effect of “cap” analogs on reovirus mRNA binding to wheat germ ribosomes.
Evidence for enhancement of ribosomal binding via a preferred cap
conformation. The Journal of Biological
Chemistry
253: 2589–2595. [PubMed] [Google Scholar]

51.
Lodish HF, Rose J. (1977) Relative importance of
7-methylguanosine in ribosome binding and translation of vesicular
stomatitis virus mRNA in wheat germ and reticulocyte cell-free
systems. The Journal of Biological
Chemistry
252: 1181–1188. [PubMed] [Google Scholar]

52.
Bergmann J, Lodish H. (1979) Translation of capped and
uncapped vesicular stomatitis virus and reovirus mRNA’S. Sensitivity to
m7GpppAm and ionic conditions. The Journal of
Biological Chemistry
254: 459–468. [PubMed] [Google Scholar]

53.
Contreras A, Carrasco L. (1979) Selective inhibition of
protein synthesis in virus-infected mammalian cells.
Journal of Virology
29: 114–122. [PMC free article] [PubMed] [Google Scholar]

How antivirus works

Antivirus is a program that scans for viruses, trojans, worms, backdoors and other unwanted software on the user’s computer. As a rule, antiviruses are developed for the Windows OS family, which, as it were, hints at the following features of this operating system: a) greater prevalence, b) greater vulnerability to attacks, c) greater prospects for the antivirus market due to high commercialization, d) alas, low computer literacy its users.

There are paid and free antiviruses. We will not talk in detail about the pros and cons of both categories here, I will only note that everything is not as simple as it might seem at first glance.

If you look at the operation of the antivirus from the outside, it can easily be mistaken for a virus, but only with a plus sign. The methods of the antivirus work are monitoring network traffic, listening to ports, monitoring services, modifying and deleting files, collecting statistics and sending data to the software developer, a fair amount of computing power … Except that equipment failure is not enough! Of course, all this is aimed at the benefit of the user and in the name of saving his data, but the overall picture is at least curious. By the way, it is precisely because of this feature that it is highly recommended not to install two antiviruses on one machine at once. Not only is it rare for anyone to succeed without dancing with a tambourine, but the consequences of their joint “work” can be the most bizarre, even fatal for the OS.

The myth that many viruses are created by anti-virus companies themselves is firmly ingrained in the mass consciousness, a good article here will dot the “i” in this matter.

Different antiviruses deal with malware in different ways. All antiviruses can detect viruses, but, unfortunately, not all can be effectively treated. The antivirus may include several modules, depending on the release and what the antivirus developer is capable of. Modules can be as follows: an unwanted software search module, a module for analyzing suspicious program behavior (heuristic module), a quarantine module for isolating suspicious files, an update module for keeping up-to-date with new threats, a module for “healing” infected files, a firewall, aka a firewall, and some others.

Antivirus is not a panacea! This is one of the many “fighters” thrown into the battle with security threats in an endless war for information, and not the strongest. No antivirus provides 100% protection due to the peculiarities of its functioning.

Unfortunately, most of the work of the antivirus is aimed at eliminating the consequences of “unhygienic” risky, and sometimes, alas, simply illiterate user work on the Internet, with external data carriers and unknown applications.

Signature-based detection method

You have probably seen anti-virus messages, such as Kaspersky Anti-Virus, that anti-virus databases are outdated and need to be updated. What bases are we talking about?

Antivirus laboratory – developer of antivirus – detects the virus, analyzes it, and reveals the so-called signature. Virus signature (attack signature) is a special digital sign of a malicious program by which it can be “recognized” and unambiguously identified. These signatures are entered into a database whose updates are regularly downloaded by the user manually or according to a schedule. A message from the antivirus about the obsolescence of the virus database signals a weakening of protection and an increase in the likelihood of catching some kind of “fresh”.

Advantages of this method:

  1. Proven reliability. The method has been used for a long time and with success, we can say that this is the main method for detecting a virus.
  2. High performance.

Disadvantages:

  1. The problem of the avalanche increase in signatures. Both the increase in the number of new viruses and the ability to mutate in the “old” ones are to blame. As a result, the signature databases grow to indecent sizes, so the second advantage of the method is lost. The situation is resolved by special optimizations, when one signature describes many viruses at once, however, the problem of false positives arises, which reduces the first advantage.
  2. The problem of detecting new viruses. It is believed that the users themselves contribute too little to the growth of the virus database. That is, the detection of new viruses seems to be a problem for antivirus developers, which on the one hand seems fair, on the other hand, is a violation of the principle “security is everyone’s business.” Many antiviruses have a built-in “send for scan” function, which should be used without restriction. The main methods for solving the problem are the mutual exchange of information with other anti-virus offices, heuristic (that is, intelligent, using a special algorithm) search for viruses on the Internet, quick response during epidemics, and the consciousness of system engineers analyzing suspicious activity on the network.

Heuristic detection methods

Many anti-virus programs contain a module for the so-called heuristic detection of malicious programs. The essence of the method is to analyze the behavior of all running programs. If, during the operation of the system, “suspicious” behavior of the application is suddenly detected, that is, the program suddenly starts doing something that it did not do before, then an alarm is triggered and the heuristic module informs the user about a potential threat.

Advantages of the method:

  1. A very promising direction, in the future the capabilities of the heuristic module will increase and the computer and information will be better protected from unexpected and latest threats.
  2. The heuristic module can respond to threats that are not in the signature database.

Disadvantages of the method:

  1. False alarm for safe events. As a result, the user can turn off the heuristic module in annoyance, reducing protection.
  2. Due to the peculiarities of the heuristic module, there is a problem of excessive consumption of computing power. Simply put, the antivirus devours all the memory and the processor, as a result, not only you can’t play games, you can’t really work in Word. The result is the same – disabling the module and reducing protection.

Firewall or firewall

Firewall is designed to protect against network threats – from the local network and the Internet.

This module is by no means always included in the standard set of antiviruses; often the firewall is developed, supplied and sold as a separate program.

Many programs can use insecure methods to connect to remote computers or servers, leaving holes and vulnerabilities for outsiders to infiltrate.

The essence of the firewall is to control both incoming and outgoing traffic by limiting the ability to establish connections with certain remote resources. The most obvious method of protection is white and black lists of network resources.

“Black” list of network resources is a list, for example, of sites where you cannot go, but “white” list is a list of resources where only you can go. As you can see, the white list method is much more secure, but it also severely limits the capabilities of the user and programs.

Advantages of the firewall:

  1. Firewall settings allow you to ensure network interaction only with verified resources, cutting off all potentially dangerous and unverified ones.
  2. Can be installed on the network gateway of the local network, that is, on the server that “distributes” Internet access to computers, for example, schools, without wasting the computing resources of user machines.

Disadvantages of a firewall:

  1. The disadvantage of a firewall logically follows from its advantage: good knowledge of network protocols and features of network applications is required to properly configure a firewall. A firewall running at “default” settings does little to protect against anything.

How antivirus software works

Antivirus software is a powerful piece of software that is essential on computers. You may have ever wondered how antivirus programs detect viruses, what they do on your computer, and whether you need to perform regular system scans yourself.

Antivirus software is an integral part of a multi-layered security strategy—even if you’re an advanced computer user, a constant stream of vulnerabilities in browsers, extensions, and the operating system itself makes antivirus protection important.

On-access scan

Antivirus software runs in the background on your computer, checking every file you open. This is usually referred to as on-access scan, background scan, resident scan, real-time protection, or something else, depending on your antivirus program.

When you double-click an EXE file, it may appear that the program starts immediately, but it doesn’t. Your antivirus software first checks the program against known viruses, worms, and other types of malware. Your antivirus software also performs a “heuristic” scan, checking programs for types of misbehavior that might indicate a new, unknown virus.

Antivirus programs also scan other types of files that may contain viruses. For example, a .zip archive file may contain compressed viruses, or a Word document may contain a malicious macro. Files are scanned whenever they are used – for example, if you download an EXE file, it will be scanned immediately, even before you open it.

It is possible to use an antivirus without an on-access scan, but this is usually not a good idea – viruses that exploit software security holes will not be detected by the scanner. Once a virus has infected your system, it is much more difficult to remove it.

Full system scan

Due to on-access scanning, it is usually not necessary to run a full system scan. If you download a virus to your computer, your antivirus program will detect it immediately – you don’t need to run a manual scan first.

However, a full system scan can be useful for some things. A full system scan is useful when you’ve just installed an antivirus program – it ensures that there are no dormant viruses on your computer. Most antivirus software sets up a full system scan on a scheduled basis, often once a week. This ensures that the most recent virus definition files are used to scan your system for dormant viruses.

These full disk scans can also be useful when repairing your computer. If you want to recover an already infected computer, it’s a good idea to insert its hard drive into another computer and perform a full system virus scan (if not doing a full reinstall of Windows). However, you usually don’t need to run a full system scan yourself when the antivirus program is already protecting you – it always scans in the background and performs its own regular full system scan.

Virus definitions

Your antivirus software uses virus definitions to detect malware. That’s why it automatically downloads new updated definition files once a day or even more often. Definition files contain the signatures of viruses and other malware. When the antivirus program scans a file and finds that the file matches a known malware, the antivirus program stops the file from running, placing it in “quarantine”. Depending on your antivirus program’s settings, the antivirus program may automatically delete the file, or you may still be able to allow the file to run if you’re sure it’s a false positive.

Antivirus companies need to stay up to date with the latest malware by releasing definition updates that ensure malware is caught by their programs. Antivirus labs use a variety of tools to disassemble viruses, run them in sandboxes, and issue timely updates to keep users protected from new malware.

Heuristics

Antivirus programs also use heuristics and machine learning. Machine learning models are created by analyzing hundreds or thousands of pieces of malware to find common properties or behaviors. This combination allows the antivirus program to identify new or changed types of malware even without virus definition files. For example, if an antivirus program notices that a program running on your system tries to open every EXE file on your system, infecting it by writing a copy of the original program into it, the antivirus program may detect that program as a new, unknown type of virus.

No antivirus program is perfect. Overly aggressive heuristics or improperly trained machine learning models can inadvertently flag perfectly harmless software as malware.

False positives

Due to the amount of software it is possible that anti-virus programs may sometimes label a file as a virus when in fact it is a perfectly harmless file. This is known as a “false positive”. Sometimes antivirus companies even make mistakes, such as identifying Windows system files, popular third-party programs, or files in their own antivirus programs as viruses. These false positives can damage users’ systems – bugs like this usually make the news, like when Microsoft Security Essentials identified Google Chrome as a virus, AVG corrupted 64-bit versions of Windows 7, or Sophos identified itself as malware.

Heuristics can also increase the number of false positives. The antivirus may notice that the program behaves similarly to malware and mistakenly identify it as a virus.

Despite this, false positives are quite rare in normal use. If your antivirus says a file is malicious, you should generally trust it. If you’re not sure if a file is really a virus, you can try uploading it to VirusTotal (which is now owned by Google). VirusTotal scans the file with various antivirus products and tells you what each says about it.

Detection rate

Different antivirus programs have different detection rates, and both virus definitions and heuristics contribute to the discrepancy. Some antivirus companies may have better heuristics and release more virus definitions than their competitors, resulting in higher detection rates.

Some organizations regularly benchmark antivirus programs against each other, comparing detection rates in real-world conditions. AV-Comparitives regularly publishes studies that compare current virus detection rates. Discovery rates tend to fluctuate over time – there is no best product that consistently sits on top.