What are the characteristics of inactive Hepatitis B carriers. How does chronic Hepatitis B infection progress. What factors influence the natural history of Hepatitis B. How is Hepatitis B transmitted. What are the global health impacts of HBV infection.

The Global Impact of Hepatitis B Virus Infection

Hepatitis B virus (HBV) infection represents a significant global health challenge. With an estimated 400 million HBV carriers worldwide, the impact of this virus on public health cannot be overstated. Approximately 15-40% of individuals with chronic HBV infection are at risk of progressing to cirrhosis and end-stage liver disease, highlighting the potential severity of this condition.

The prevalence of HBV varies significantly across different regions. It is particularly endemic in:

• Asia
• Micronesia
• Sub-Saharan Africa
• Certain populations in Australia and New Zealand
• Parts of South America
• The Middle East
• Arctic regions

In the United States alone, an estimated 1.25 million people are positive for hepatitis B surface antigen (HBsAg), indicating active infection. This widespread prevalence underscores the importance of understanding the virus, its transmission, and its potential long-term effects on human health.

The Complex Natural History of Hepatitis B

The natural history of hepatitis B is intricate and influenced by various factors. These include:

1. Age at infection
2. Viral factors (HBV genotype, viral mutations, level of HBV replication)
3. Host factors (gender, age, immune status)
4. Exogenous factors (concurrent infection with other hepatotropic viruses, alcohol consumption)

The clinical spectrum of HBV infection is broad, ranging from subclinical to acute symptomatic hepatitis during the acute phase. In rare cases, it can even lead to fulminant hepatitis. During the chronic phase, manifestations can vary from an inactive HBsAg carrier state to chronic hepatitis, cirrhosis, and its complications.

Understanding this complex natural history is crucial for effective disease management and the development of improved therapeutic strategies. However, several factors complicate our ability to fully define the natural course of chronic hepatitis B:

• The indolent (slow-progressing) nature of the disease
• Lack of symptoms during early stages
• Heterogeneity of the disease presentation and progression

Hepatitis B Virus: Structure and Genomic Organization

HBV belongs to the Hepadnaviridae family of viruses. Its genome consists of a relaxed circular, partially double-stranded DNA of approximately 3,200 base pairs. The genetic structure of HBV is compact and efficient, with four partially overlapping open reading frames encoding various viral proteins:

1. Envelope (pre-S/S) proteins: Large, middle, and small surface glycoproteins
2. Core (precore/core) proteins: Precore polypeptide (modified into HBeAg) and nucleocapsid core protein (HBcAg)
3. Polymerase protein: Functions as both reverse transcriptase and DNA polymerase
4. X protein: A potent transactivator potentially involved in hepatocarcinogenesis

This genomic organization allows the virus to efficiently produce all necessary components for its replication and survival within host cells.

Transmission Routes of Hepatitis B Virus

HBV transmission occurs through several routes, primarily:

• Parenteral exposure
• Intimate personal contact
• Perinatal transmission

Individuals at higher risk of contracting HBV include:

1. Intravenous drug users
2. Children of HBV-positive mothers
3. Men who have sex with men
4. Patients on hemodialysis
5. Those exposed to blood or blood products

Understanding these transmission routes is crucial for implementing effective prevention strategies and identifying high-risk populations for screening and vaccination programs.

The Inactive HBsAg Carrier State: Characteristics and Prognosis

Inactive carriers form the largest group among chronic HBV infected patients, with an estimated 300 million people worldwide falling into this category. The inactive HBsAg carrier state is characterized by:

• Absence of HBeAg
• Presence of anti-HBe antibodies
• Undetectable or low levels of HBV DNA in PCR-based assays
• Repeatedly normal ALT levels
• Minimal or no necroinflammation, slight fibrosis, or even normal histology on liver biopsy

It’s important to note that inactive cirrhosis may be present in patients who experienced active liver disease during the replicative phase of infection.

The prognosis for inactive HBsAg carriers is generally favorable. Long-term follow-up studies, some extending up to 18 years, have shown that the vast majority of these carriers experience sustained biochemical remission and have a very low risk of developing cirrhosis or hepatocellular carcinoma (HCC).

Potential Risks and Complications

Despite the generally benign prognosis, inactive HBsAg carriers are not entirely free from risks:

1. Rare occurrences of liver cancer development, even in non-cirrhotic patients
2. Spontaneous reactivation of hepatitis B in approximately 20-30% of carriers during follow-up
3. Potential for progressive hepatic damage or even hepatic decompensation in cases of multiple reactivation episodes or sustained reactivation

Reactivation of Hepatitis B in Inactive Carriers

Reactivation of hepatitis B in inactive carriers is a significant concern that requires careful monitoring. Why does reactivation occur in some inactive carriers? While the exact mechanisms are not fully understood, several factors may contribute:

• Changes in the host immune system
• Viral mutations
• External factors such as immunosuppressive therapies

The frequency of reactivation events can vary, but studies suggest that approximately 20-30% of inactive carriers may experience spontaneous reactivation during long-term follow-up. How does reactivation impact liver health? The consequences of reactivation can be significant:

1. Single reactivation episodes may cause temporary liver inflammation
2. Multiple reactivation episodes can lead to cumulative liver damage
3. Sustained reactivation may result in progressive hepatic damage
4. In severe cases, hepatic decompensation can occur

These potential outcomes underscore the importance of regular monitoring for inactive HBsAg carriers, even when they appear clinically stable.

Diagnostic Approaches for Identifying Inactive HBsAg Carriers

Accurate diagnosis of the inactive HBsAg carrier state is crucial for appropriate patient management. What diagnostic criteria are used to identify inactive carriers? The diagnosis typically involves a combination of serological, virological, and biochemical markers:

• HBsAg positivity for at least 6 months
• HBeAg negativity
• Presence of anti-HBe antibodies
• Persistently normal ALT levels (tested multiple times over at least 1 year)
• HBV DNA levels below 2000 IU/mL

In some cases, a liver biopsy may be performed to assess the degree of liver inflammation and fibrosis. However, non-invasive methods such as transient elastography (FibroScan) are increasingly being used to assess liver fibrosis without the need for biopsy.

Challenges in Diagnosis

Diagnosing the inactive carrier state can be challenging due to several factors:

1. Fluctuations in HBV DNA levels
2. Intermittent ALT elevations
3. The need for long-term follow-up to confirm the stability of the inactive state

Therefore, regular monitoring is essential to distinguish true inactive carriers from patients with active chronic hepatitis B who may have temporarily low viral loads or normal ALT levels.

Management Strategies for Inactive HBsAg Carriers

While inactive HBsAg carriers generally have a favorable prognosis, they still require appropriate management and follow-up. What are the key components of managing inactive carriers? The management strategy typically includes:

1. Regular monitoring of liver function tests (ALT levels)
2. Periodic assessment of HBV DNA levels
3. Screening for hepatocellular carcinoma, especially in high-risk groups
4. Counseling on lifestyle factors (alcohol avoidance, maintaining a healthy diet)
5. Vaccination against hepatitis A, if not already immune

How often should inactive carriers be monitored? The frequency of follow-up can vary based on individual risk factors, but generally:

• ALT and HBV DNA levels should be checked every 6-12 months
• Liver ultrasound for HCC screening should be performed every 6 months in high-risk patients (e.g., those with cirrhosis or a family history of HCC)

Is antiviral treatment necessary for inactive carriers? In most cases, antiviral treatment is not recommended for inactive carriers due to their low risk of disease progression. However, treatment may be considered in certain situations:

1. Evidence of significant liver fibrosis or cirrhosis
2. Family history of HCC
3. Extrahepatic manifestations of HBV infection
4. Planned immunosuppressive therapy

The decision to initiate treatment should be made on an individual basis, considering the potential benefits and risks of long-term antiviral therapy.

Prevention Strategies and Vaccination for Hepatitis B

Prevention plays a crucial role in controlling the spread of HBV infection. What are the primary prevention strategies for hepatitis B? The most effective approach involves a combination of:

1. Universal vaccination
2. Screening of blood products
3. Implementation of safe injection practices
4. Promotion of safe sex practices

Vaccination is the cornerstone of HBV prevention. How effective is the hepatitis B vaccine? The vaccine is highly effective, with a protective efficacy of over 95% in preventing HBV infection and its chronic consequences. It is typically administered as a series of three doses over a 6-month period.

Vaccination Recommendations

Who should receive the hepatitis B vaccine? Vaccination is recommended for:

• All infants, starting at birth
• Children and adolescents who were not vaccinated at birth
• Adults at increased risk of HBV infection, including:
  • Healthcare workers
  • People with multiple sexual partners
  • Injection drug users
  • Travelers to HBV-endemic areas
  • People with chronic liver disease or HIV infection

In many countries, universal vaccination programs have significantly reduced the incidence of new HBV infections, particularly among children and young adults.

Future Directions in Hepatitis B Research and Management

As our understanding of HBV infection continues to evolve, several areas of research hold promise for improving the management of chronic hepatitis B and inactive carriers. What are some of the key areas of focus for future research?

1. Development of novel antiviral therapies aimed at achieving functional cure
2. Identification of biomarkers to predict disease progression and HCC risk
3. Improved strategies for preventing mother-to-child transmission
4. Development of therapeutic vaccines to boost immune control of HBV
5. Understanding the mechanisms of HBV reactivation in inactive carriers

How might these advances impact the management of inactive carriers? Future developments could lead to:

• More accurate risk stratification tools
• Personalized monitoring and treatment strategies
• Potential interventions to prevent reactivation
• Improved methods for achieving HBsAg clearance, even in inactive carriers

As research progresses, the goal is to further reduce the global burden of HBV infection and improve outcomes for all individuals affected by this virus, including the large population of inactive carriers.

Hepatitis B Virus: Inactive carriers

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• v.2; 2005
• PMC1253537

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Virol J. 2005; 2: 82.

Published online 2005 Sep 28. doi: 10.1186/1743-422X-2-82

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Inactive carriers forms the largest group in chronic HBV infected patients. Around 300 million people are inactive carriers The inactive HBsAg carrier state is diagnosed by absence of HBeAg and presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based assays, repeatedly normal ALT levels, and minimal or no necroinflammation, slight fibrosis, or even normal histology on biopsy. Inactive cirrhosis may be present in patients who had active liver disease during the replicative phase of infection. The prognosis of the inactive HBsAg carrier state is usually benign. Long-term follow- up (up to 18 years) of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma (HCC). Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state. In addition, approximately 20 to 30% of persons in the inactive HBsAg carrier state may undergo spontaneous reactivation of hepatitis B during follow-up. Multiple episodes of reactivation or sustained reactivation can cause progressive hepatic damage and even hepatic decompensation. Introduction

Hepatitis B virus (HBV) infection and its sequelae are major global health problems [1]. It is estimated that 400 million people worldwide are HBV carriers [2]. The natural history of hepatitis B is complex and is influenced by many factors, including age at infection, viral factors (HBV genotype, viral mutations, level of HBV replication), host factors (gender, age, and immune status), and exogenous factors such as concurrent infection with other hepatotropic viruses or alcohol. The clinical spectrum of HBV infection ranges from subclinical to acute symptomatic hepatitis or, rarely, fulminant hepatitis during the acute phase and from the inactive hepatitis B surface antigen (HBsAg) carrier state to chronic hepatitis, cirrhosis, and its complications during the chronic phase [3,4]. Approximately 15 to 40% of people who develop chronic HBV infection are expected to progress to cirrhosis and end-stage liver disease [1]. Difficulties in defining the natural history of chronic hepatitis B include the indolent course of the disease, the lack of symptoms during the early stages, and the heterogeneity of the disease. Understanding the natural history and prognosis of hepatitis B is the basis for disease management and for designing better therapeutic strategies.

HBV belongs to the family hepdnaviruses. The HBV genome is a relaxed circular, partially double stranded DNA of approximately 3,200 base pairs. There are four partially overlapping open reading frames encoding the envelope (pre-S/S), core (precore/core), polymerase, and X proteins [5]. The pre-S/S open reading frame encodes the large, middle, and small surface glycoproteins. The precore/core open reading frame is translated into precore polypeptide which is modified in to a soluble protein, the hepatitis B e antigen (HBeAg), and the nucleocapsid core protein hepatitis B core antigen (HBc Ag) [5]. The polymerase protein functions as reverse transcriptase as well as DNA polymerase. The X protein is a potent transactivator and may play role in hepatocarcinogenesis.

Hepatitis B is spread predominantly parenterally, through intimate personal contact, and perinatally. Individuals at risk are intravenous drug users, children of mothers with HBV, men who have sex with men, patients on hemodialysis and those exposed to blood or blood products [6,7]. Approximately 5% of the world’s populations are carriers of HBV, defined as being positive for hepatitis B surface antigen. HBV is endemic in many areas of the world, such as Asia, Micronesia, and sub-Saharan Africa as well as in certain populations in Australia, New Zealand, South America, the Middle East and the Arctic. An estimated 1.25 million people in the United States are positive for hepatitis B surface antigen. Fifteen percent to forty percent of these carriers may develop hepatitis B-related sequelae in their lifetimes [8-10].

Perinatal infection of infants from infected mothers and horizontal infection early in childhood from exposure to HBsAg-positive family members are the main routes of HBV transmission in highly endemic areas, such as Southeast Asia, Africa, the Pacific Islands, and the Arctic. In regions of low endemicity, such as Western countries, hepatitis B is primarily a disease of adolescents and adults as a result of high-risk sexual behavior and injection drug use. HBV infection is a dynamic process with replicative and nonreplicative (or low replicative) phases based on virus-host interaction. The presence of circulating HBsAg, hepatitis B e antigen (HBeAg), and high levels of serum HBV DNA characterizes the immunotolerant phase. This first phase is seen in patients with perinatal infection and often lasts for decades. During this phase patients have no symptoms, normal or slightly increased serum alanine aminotransferase (ALT) levels, and minimal histological activities, which imply that there is a lack of or a very weak immune response against the infected hepatocytes.

Experimental results in transgenic mice suggested HBeAg induces a state of immunological tolerance to HBV in neonates [11]. During the course of chronic HBV infection, for unknown reasons, the tolerogenic effect is and patients may enter the immunoactive phase, which is associated with a decrease in HBV DNA concentrations and increased ALT levels and histologic activity, reflecting immune-mediated lysis of infected hepatocytes. This second phase has a variable duration from months to years. The third low or nonreplicative phase occurs seroconversion from HBeAg to antibody to HBeAg. This phase is usually preceded by a marked reduction of serum HBV DNA to levels that are not detectable by hybridization techniques, followed by normalization of ALT levels and resolution of liver necroinflammation. In many patients, serum HBV DNA remains detectable by the sensitive technique of polymerase chain reaction (PCR). This phase is also referred as the inactive HBsAg carrier state [3,4]. The inactive carrier state may for a lifetime, but a proportion of patients may undergo subsequent spontaneous or immunosuppressioninduced reactivation of HBV replication with reappearance of high levels of HBV DNA with or without HBeAg seroreversion and a rise in ALT levels [3]. For reasons that are not yet known, replication-competent HBV variants with mutations in the precore or core promoter regions preventing or down-regulating HBeAg production may be selected during or after HBeAg seroconversion.

Patients who become HBsAg negative and develop antibody to HBsAg (anti-HBs) are diagnosed as having resolved hepatitis B [3,4]. This is an uncommon phenomenon in chronic HBV infection. During stage HBV DNA may still be detectable by PCR in serum and more often in the liver.[12] In rare cases severe immune suppression, such as cancer chemotherapy or after organ transplantation, HBV can be reactivated in patients with resolved hepatitis B [13].

HBeAg positive Chronic Hepatitis

Patients with HBeAg-positive chronic hepatitis B usually present in the third or fourth decade of life. Men outnumber women, [14,15] liver damage ranges from mild (24 to 42%) to moderate or severe chronic hepatitis (44 to 63%) or active cirrhosis (10 to 24%) [16-20]. Chronic hepatitis B tends to be milder in children. Nevertheless, severe liver disease including cirrhosis may occur in a small proportion of patients during childhood [21,22]. A key event in the natural history of HBeAg positive chronic hepatitis is HBeAg seroconversion. Several studies have shown that seroconversion with marked reduction of HBV replication is associated with biochemical and histologic remission of inflammatory activity in the majority of patients [23-25]. Regression of fibrosis occurs gradually months to years after HBeAg seroconversion.[26] In longitudinal studies the observed probability of clearing HBeAg was about 50% and 70% within 5 and 10 years of diagnosis, respectively [23,27-29]. Most studies have found that the mean annual rate of spontaneous HBeAg seroconversion ranges from 8 to 15% in children or adults with elevated ALT [3,4,23-25,29-31,31]. Among Asian, most of whom have normal ALT, spontaneous HBeAg seroconversion occurs at a very low rate, less than 2% during the first 3 years of age and 4 to 5% in children older than 3 years [32]. Several determinants for HBeAg seroconversion have been reported, including gender, age, ALT level, and more recently HBV genotypes. Older carriers and females are more likely to clear HBeAg [33].

Frequent acute exacerbation of hepatitis, reflecting immune-mediated lysis of HBV-infected hepatocytes with ALT elevations to more than 10 times ULN and more than twice the baseline value and with HBV DNA levels rising before and falling during the flare, precede seroconversion of HBeAg to anti-HBe. These exacerbations usually last 2 to 4 months [34]. In some cases these spontaneous flares of hepatitis are not followed by subsequent HBeAg seroconversion and can be viewed as an abortive attempt at seroconversion. These flares of hepatitis are usually asymptomatic and frequently unrecognized, but some are accompanied by symptoms of acute hepatitis and rarely, primarily in patients with cirrhosis or advanced fibrosis, may lead to hepatic decompensation and even death due to massive necrosis [34].

HBsAg-negative chronic hepatitis

The diagnosis of HBeAg-negative chronic hepatitis B is based on the presence of HBsAg for more than 6 months, undetectable HBeAg, presence of anti-HBe, detectable serum HBV DNA exceeding 10⁵ to 10⁶ copies/mL, increased ALT levels, and hepatic necroinflammation on histology. Other causes of liver disease, such as superinfection with other hepatitis viruses, alcohol abuse, hepatotoxic drug use, and autoimmune or metabolic liver disease, should be excluded [3,4]. The atypical serological profile is related to the predominance of HBV variants, which are unable to express HBeAg. The most frequent variant has a G-to-A change at nucleotide 1896 (G1896A), which creates a stop codon in the precore region of the HBV genome and completely abolishes the production of HBeAg [35]. Other variants include changes in the start codon of the precore region or a two-nucleotide substitution (A1762T, G1764A) in the core promoter region, which reduces precore messenger RNA synthesis and HBeAg production [36].

Patient with HBeAg negative are older than patients with HBeAg-positive chronic hepatitis (median 40, range 36–45 years). Males predominate and data indicate that liver disease is more active and advanced, minimal or mild chronic hepatitis is infrequent, and severe necroinflammation is seen in more than 50% patients at diagnosis [37-39]. In reports from Mediterranean area, 29 to 38% had cirrhosis at presentation. The older age and the high rate of advanced liver damage at presentation suggest that HBeAg-negative chronic hepatitis represents a late phase in the natural history of chronic HBV infection rather than de novo infection with HBV variants that do not produce HBeAg. To further support this concept, a recent long-term study reported that HBeAg-negative chronic hepatitis accumulated over time after HBeAg seroconversion with a cumulative incidence of approximately 25% after 16 years of follow-up [40]. Thus, the increasing prevalence of HBeAg-negative. Fluctuation in level of viremia and ALT are more common and sustained response is rare. Delayed spontaneous HBsAg clearance has been estimated to occur at a low rate of 0.5% per year [40].

Inactive HBsAg Carrier State

Inactive carriers forms the largest group in chronic HBV infected patients. Around 300 million people are inactive carriers The inactive HBsAg carrier state is diagnosed by absence of HBeAg and presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based assays, repeatedly normal ALT levels, and minimal or no necroinflammation, slight fibrosis, or even normal histology on biopsy [3,4]. Inactive cirrhosis may be present in patients who had active liver disease during the replicative phase of infection. The prognosis of the inactive HBsAg carrier state is usually benign. Long-term follow- up (up to 18 years) of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma (HCC) [40-42]. Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state [40-43]. In addition, approximately 20 to 30% of persons in the inactive HBsAg carrier state may undergo spontaneous reactivation of hepatitis B during follow-up [29,33,34,40]. Multiple episodes of reactivation or sustained reactivation can cause progressive hepatic damage and even hepatic decompensation. HBV reactivation is usually asymptomatic but on occasion can mimic acute viral hepatitis [44]. Acute flares of hepatitis should be differentiated from superinfection with other hepatotropic viruses. As many as 20 to 30% of these acute exacerbations may be caused by superinfection with HDV, HCV, or hepatitis A virus and can be associated with an increased risk of fulminant hepatic failure [44]. Some carriers eventually become HBsAg negative and develop anti-HBs. The incidence of delayed HBsAg clearance has been estimated to be 1 to 2% per year in Western countries, where HBV infection is usually acquired in adulthood, but a lower rate from 0.05 to 0.8% per year in endemic areas, where HBV infection is mostly acquired perinatally or in early childhood. Clearance of HBsAg has been reported to be higher in women than in men and in older than younger carriers. Prognosis is improved by loss of HBsAg as liver disease is usually inactive and nonprogressive, but HBsAg clearance does not completely prevent occurrence of decompensation or HCC in patients who have already developed cirrhosis [45,46].

Change in the terminology of HBV carriers

HBV infection is termed as chronic if it continues to be HBsAg +ve for ≥6 months. Chronic HBV infection is a dynamic process with a wide spectrum of spectrum of affliction. On one hand patients are asymptomatic with no clinical evidence of liver diseases, while on other being end-stage cirrhosis and hepatocellular carcinoma. For many decades the patients were considered to have a benign, non progression infection and were designated as hepatitis B “carriers”. Probably the word ‘carrier’ was mistakenly chosen for hepatitis B as in true sense, a carrier is an individual who (i) harbors a specific infectious agent (ii) has no discernible clinical disease and (iii) serves as a potential source of infection. For this infection the second and third points should be looked at carefully. One the basis of Asian collaborative survey the term ‘carrier’ was replaced by the term ‘chronic hepatitis B virus infection’ [47,48]. Later on for this infection the term ‘Inactive HBsAg carrier’ was adopted [49].

Differentiation from chronic HBsAg negative hepatitis B, requires serial testing of ALT and HBV DNA for one year before designating carrier state [49]. In subject with inactive carrier state testing of HBV DNA and liver biopsy are not recommended. Treatment is not recommended as there is no evidence that available therapy affects HBsAg status. Family screening with HBsAg and anti-HBs, if negative vaccinate them and success of vaccination should be confirmed with anti-HBs testing. Protected sexual intercourse until partner has developed protective antibodies. The offspring need active and passive vaccination [4,47]. Use of alcohol should be avoided, possibility of reactivation or super infection by other viruses and advised if there is jaundice, malaise or increased fatigue. Regular follow-up at every 6–12 months intervals with ALT [4]. If the age of the patient is more than 50 yrs family history of HCC-AFP and ultrasonography every 6–12 monthly should be done. Universal precaution should be taken while treating these patients in the hospital. They should not be allowed to donate the blood or organ or semen. For pregnant women vaccinate the new born at birth with active and passive immunization with in 12 hours of the birth, close monitoring required if undergoing chemotherapy or immunosuppressive medication.

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Articles from Virology Journal are provided here courtesy of BioMed Central

Chronic phase of hepatitis C

After six months 70% to 85% of those infected will have failed to clear the virus spontaneously. After this period the hepatitis C virus enters what is known as the ‘chronic phase’. This is when hepatitis C becomes a chronic or long-term infection. The diagnosis is confirmed when over a six month period hepatitis C RNA viral presence is detectable on at least two occasions.

A diagnosis of chronic hepatitis C means the battle between the virus and the immune system that occurs during the acute stage has finally been won by the virus. It is now highly unlikely that the virus can be cleared without treatment.

How the disease then progresses varies significantly from person to person. After many years some people will have minimal liver damage with no scarring while others can progress to cirrhosis (extensive scarring of the liver) within less than ten years. On average it takes about twenty years for significant liver scarring to develop.
It is still not known whether chronic hepatitis C infection inevitably leads to cirrhosis. At present it is thought that this is a very likely outcome, although for some people it may take at least 50 years or more. They may well die of other unrelated diseases or conditions before cirrhosis develops. The rate of progression of liver damage cannot be accurately determined by liver enzyme levels, viral load or by genotype.

The symptoms experienced and the damage done to the liver vary dramatically from person to person. Some people will have few, if any, symptoms for many years. While for others the symptoms can have quite noticeable effects on their health.

It was originally thought that the virus only infected liver cells. But recently it has become clear that hepatitis C also infects parts of the immune system, some blood cells and probably the brain. This means that hepatitis C is not just a liver disease but is a systemic disease prone to affecting other organs in the body.

Hepatitis C causes damage to the liver mainly in the form of inflammation, which then leads to scarring or fibrosis. How the virus affects the various functions of the liver is discussed in the section The Liver & hepatitis C.

Liver damage and fibrosis during the chronic stage

Hepatitis C results in the death of liver cells. It is uncertain whether the virus kills the cells or if it is the immune system’s response to invasion by the virus. At present it is thought that it is probably a combination of the two, but that the immune system’s response is what causes the most damage. The death of liver cells triggers the dispatching of inflammatory cells to the affected area. Inflammation leads to the enlargement of the liver (hepatomegaly) in over 60% of people infected with hepatitis C and can cause the fibroelastic sheath (Glisson’s capsule) surrounding the liver to stretch, which may be the cause of pain in the liver area.

Inflammation begins the processes that lead to fibrosis. Fibrosis is not a disease but is a condition caused by the body’s response to liver damage. Inflammation triggers a reaction by a group of cells in the liver called stellate (literally star-shaped) or fat cells. When the liver is functioning normally stellate cells store fat and vitamin A in the liver. They also help regulate the flow of blood through the liver. But when the liver is inflamed by the presence of hepatitis C, a reaction occurs amongst different liver cells. This leads stellate cells to dispense with vitamin A, altering their function.

Infected and inflamed liver cells release chemical signals called ‘cytokines’. These activate leukocytes (white blood cells) from outside the liver which travel to the area of infection. On arrival they team up with Kupffer cells (specialised white blood cells that neutralise and remove bacteria, viruses, parasites and tumour cells from the liver) and produce further chemical signals. These signals cause stellate cells to begin producing and laying down collagen fibres in the extra cellular matrix, which is the area between the cells.

Collagen is a fibrous protein which is fundamental to the formation of scar tissue. The body’s use of collagen in an area of injury is an attempt to limit the spread of infection to other cells. As an infection or injury resolves, the collagen matrix enclosing the injury is normally dissolved. The activated stellate cells then die off, allowing the tissue to return to normal.

In a chronic illness such as hepatitis C the collagen matrix grows too fast and cannot be properly dissolved. This results in a build-up of scar tissue around cells. Liver cells lose vital access to the blood carrying nutrients and oxygen and so die. A vicious circle results in which inflammation and fibrogenic cells stimulate each other leading to increased fibrosis.

Free Radicals and Fibrosis

A further possible cause of fibrosis is due to damage by free radicals. Free radicals are highly reactive chemical substances. They are the by-product of a cell’s normal reactions such as energy generation and the breakdown of fats. During these reactions oxygen is transformed into the free radical superoxide. Normally cells have mechanisms for protecting themselves from the dangers of free radicals. When too many are generated, or if they are not controlled properly, there is a danger that they will cause cell and tissue damage. 

Free radicals are of concern for people with hepatitis C for a number of reasons:
•    Chronic liver inflammation may lead to over-production of free radicals within the liver.
•    There is evidence that free radicals play a role in liver fibrosis. Free radicals can chemically alter fat in the body. This is called lipid peroxidation. The free radicals attack the cell membrane and can injure and eventually kill cells. If this happens to liver cells, this will lead to fibrosis.
•    If the liver function is already impaired and this has led to an overload of iron, the free radicals may interact with the iron causing further damage.

The liver is famed for its ability to regenerate, so why doesn’t liver regeneration prevent liver damage in hepatitis? In Greek mythology the liver’s self-healing ability was exploited by Zeus to punish Prometheus, the Titan God. Zeus, the king of the Gods, ordered Prometheus to be chained to a rock in the Caucasian mountains as a punishment for stealing the holy fire from Mount Olympus and sharing it with mankind. Zeus sent an eagle to the rock. By day the bird pecked away at Prometheus’s liver. By night as the eagle slept Prometheus’s liver grew back so that it was a fresh tasty meal again for the eagle the next morning.

Hepatitis C is usually characterised by a degeneration of the liver through slow but progressive scarring. So why can’t the liver repair itself in the presence of hepatitis C? The liver has two responses to harmful agents which are capable of damaging its cell structure. Either there is regeneration with complete restoration of the liver structure and function or there is sustained scarring of liver tissue leading to damage. When the liver is damaged by a single strong injury, regeneration is highly likely even if a large area is affected. But if the injury is repetitive as is the case with hepatitis C infection, the liver cannot effectively cope. It does not have the time and space to heal itself properly.

Hepatitis B often resolves without symptoms. How to protect yourself from it? — Meduza

1

What happened?

2019 marks 50 years since the invention of the hepatitis B vaccine. The authors of the idea are the discoverer of the virus, Baruch Blumberg (he later received the Nobel Prize in Physiology or Medicine for this discovery) and his colleague, microbiologist Irving Millman.

The vaccine, the basic principle of which was invented in 1969, was subsequently made from part of the outer shell (surface antigen) of the virus, which was obtained from the blood of donors and purified. Modern vaccines are produced in a completely different way – the necessary components are created by modified yeast or mammalian cell cultures.

2

Is hepatitis B jaundice?

No. Jaundice is colloquially referred to as viral hepatitis A. Despite the fact that both diseases are caused by hepatitis viruses entering the body, they are transmitted and proceed in different ways. In some cases, only the symptoms are similar: yellowing of the skin and eyes – hence the confusion.

The hepatitis B virus is transmitted through blood and other bodily fluids. The infection affects the liver and can cause both acute and chronic illness. Moreover, the hepatitis B virus is considered oncogenic, that is, capable of leading to the development of liver cancer.

3

What are other symptoms of hepatitis B besides yellow eyes?

Dark urine, fatigue, nausea, vomiting, abdominal pain. Symptoms usually go away after 1-3 months. Such vivid manifestations occur in an acute form, but it happens that she has no obvious signs. In the chronic form, this happens even more often: if symptoms do occur, they are usually limited to fatigue. Of course, if chronic hepatitis did not eventually provoke the development of cirrhosis or other complications, then the symptoms can be quite obvious.

4

How do I know if I have hepatitis B or not?

According to blood tests. At the polyclinic at the place of residence, you can take an analysis for the determination of the surface antigen of the virus (HBsAg) free of charge. If the result is positive, this may indicate an acute or chronic infection.

But in some other countries, HBcAb is also immediately evaluated (this is an indicator of whether the body has reacted to the core of the hepatitis B virus or not). It happens that the analysis for HBsAg is negative, and for HBcAb it is positive. This may also mean that hepatitis B still exists.

5

If I don’t have hepatitis B, how can I continue to protect myself from it?

The first thing to do is to get vaccinated if you are not vaccinated. According to the World Health Organization (WHO), the modern vaccine is very effective and safe. According to a study conducted in Alaska, protective immunity after it can last 30 years or more.

In Russia, the hepatitis B vaccine is included in the National Immunization Schedule: for the first time, a child is vaccinated at the maternity hospital, then a month later, and the third vaccination is given at six months. Thanks to this, there is less hepatitis B in Russia. However, some doctors, for not entirely scientific reasons, discourage parents from vaccinating their child at the maternity hospital.

Standard adult vaccination schedule: also 0-1-6 months. If you are under the age of 55, you can get vaccinated free of charge at a polyclinic at your place of residence.

An important “bonus” of vaccination is protection against hepatitis D virus (HDV), which can only multiply in the presence of hepatitis B virus (HBV). HDV-HBV coinfection is the most severe form of chronic viral hepatitis, leading to the fastest death from liver disease and hepatocellular carcinoma.

It is also important to use condoms to protect against hepatitis B if you do not know if your partner is sick, do not share a razor and toothbrush with anyone, be careful when choosing tattoo parlors and dental clinics (especially if you go there for anything). something more serious than a filling). In the latter case, it is important that the doctor wears gloves and changes them after each patient, that only disposable syringes are used, that each patient has their own instruments, and then they are processed. That is, if the doctor does not get new gloves or a syringe with you, this is a reason to be wary.

6

What if I was at risk of infection and I am not vaccinated?

See a doctor as soon as possible: he will decide whether you need to be vaccinated and administer immunoglobulin. If the vaccine is given, then it will need to be repeated after another 1, 2, and 12 months.

You need to check whether you managed to defend yourself after six months or earlier if suspicious symptoms appear. The incubation period for hepatitis B is approximately 45–180 days.

7

Alas, hepatitis B was found in me. Is he being treated?

Hepatitis B is usually self-limiting . The disease is divided into two stages: acute and chronic. In more than 95% of adults, the body copes with the virus on its own, and the disease does not become chronic. There is no specific treatment for acute hepatitis B. Medical care is mainly aimed at making the patient comfortable.

For the treatment of chronic hepatitis B, WHO recommends tenofovir or entecavir tablets. Both drugs are registered in Russia and included in the list of Vital and Essential Drugs (VED). The duration of the course of treatment is determined by the infectious disease specialist. The main criteria for prescribing therapy: the viral load must exceed 2000 IU / ml, and there are signs of inflammation in the liver. The therapy does not completely destroy the virus, but only suppresses its reproduction, so many patients are prescribed medication for life in order to avoid the development of cirrhosis or liver cancer. In some regions of Russia, programs are provided through which you can buy these medicines at a huge discount or receive them for free. But the good news is that there are more than 50 molecules in development today, and some of them may be able to completely cure a person of hepatitis B.

Aleksey Lakhov , Member of the Board of the Interregional Public Organization for Assistance to Patients with Viral Hepatitis “Together Against Hepatitis”

The author thanks Ekaterina Stepanova, an infectious disease specialist, for her help

symptoms, treatment, prevention – MEDSI

Hepatitis B is an infectious inflammatory disease of the liver. This disease appears due to the penetration of the hepatitis B virus into the blood and is a potential threat to the life of the patient, since its development can lead to cirrhosis or a cancerous tumor of the liver. Therefore, treatment of viral hepatitis B (B) should be started as early as possible.

Symptoms of hepatitis B

Often, the disease is asymptomatic for a long time after infection. Therefore, you should pay attention and make an appointment with a doctor for such signs as:

• Constant nausea and unwillingness to eat, vomiting
• Fatigue, chronic fatigue
• Appearance of pain in the joints
• Heaviness and discomfort on the right under the ribs (in the area of ​​the liver)
• Dark urine and light stool
• Yellowing of the skin, sclera of the eyeballs
• Fever
• Headache

Some of these phenomena may turn out to be symptoms of other diseases, but in order to accurately determine the problem, it is necessary to pass a series of tests that only a qualified specialist can prescribe.

How can one get sick?

One of the dangerous features of this disease is its ubiquity. According to WHO data in April 2017, there are 257 million people in the world who are carriers of chronic hepatitis B.

The main ways of infection with this disease:

• Blood transfusion from an infected patient
• When using non-sterile instruments in hospitals, dentists, tattoo and piercing parlors
• When taking drugs with the same syringe by several people
• During unprotected intercourse with a carrier
• During childbirth

It is impossible to get infected with hepatitis B in a household way, provided that the skin and mucous membranes of a healthy person do not have violations (wounds, abrasions, etc.).

Hepatitis B testing

When undergoing an examination for the presence of this infection, the doctor directs the patient to several basic blood tests:

• Complete blood count
• Biochemical analysis for:
• Liver enzymes (ALT and AST) – in the presence of liver diseases, their concentration is increased
• Bilirubin – an increase in its concentration stains tissues yellow
• Albumin – its level decreases in chronic liver diseases
• ELISA (for virus antibodies):
• Anti-HBs – shows if there are protective antibodies in the blood
• Anti-HBcor – shows if a person has been infected in the past
• PCR (for virus antigens):
• HBsAg – displays whether the virus is currently in the blood

The doctor also directs the patient to an abdominal ultrasound of the abdominal cavity in order to examine the structures of the liver and the degree of their integrity and examine other organs for the presence of pathologies or disorders in them.

In some cases, the hepatologist may order a liver biopsy to obtain a sample of liver tissue and more accurately identify problems.

How contagious is the virus?

The hepatitis virus is extremely contagious for people who have not been vaccinated, because even without a favorable environment it does not die within seven days. In developed countries, children are vaccinated after birth through a three-dose vaccination. So they are protected until the age of 9-ty years.

In children infected with hepatitis under the age of one year, the probability of developing a chronic form of the disease is 80-90%, and in those infected up to 6 years – 30-50%.

In adults, the likelihood of hepatitis B becoming chronic is about 5%, of which 20-30% are at risk of developing cirrhosis or liver cancer.

What happens after the virus enters the bloodstream?

Together with blood cells, the virus reaches the liver, where it is introduced into its cells (hepatocytes). Upon reaching the nucleus of the hepatocyte, the virus changes its structure to its own. Then such infected cells begin to infect nearby healthy ones and in this way spread through the liver. This period can take from 3 to 6 months.

How does hepatitis B progress?

The incubation period can last up to six months. In some cases, the disease does not manifest itself in any way until serious violations occur in the structure of liver tissues. Standardly, the disease is manifested by a change in temperature (fever), nausea.

During the transition to the acute stage, the disease is accompanied by discomfort in the liver, joint pain, lightening of feces, darkening of urine and yellowing of the skin. This stage can last up to 3-4 months and end with either recovery or transition to chronic.

The chronic stage is not completely cured, but can be stopped in various ways that the doctor will prescribe. But in case of alcohol abuse and non-compliance with medical prescriptions, the disease can develop into pathologies such as malignant neoplasm (cancer) and cirrhosis (excessive growth of connective tissues).

When do the first signs of hepatitis B appear?

Initial symptoms in the form of headaches, fever and nausea may appear in the first 6 months from the moment of infection. Then more typical hepatitis symptoms may appear: discoloration of the skin, urine, feces.

How to cure the disease?

In the treatment of an acute form of hepatitis, it is important to adhere to bed rest and a diet with plenty of juices, glucose-containing drinks, mineral water, and sweet tea. This is necessary to make up for the loss of fluid in the body. In this case, the treatment is more aimed at maintaining the body in a stable state. In severe cases, additional treatments may be used.

If the disease has become chronic, then for its treatment antiviral drugs are used in the form of injections or tablets, which must be taken for a long time (in the case of injections, this period is no more than a year, and in the case of tablets – several years). In each case, the treatment program should be prescribed by a qualified hepatologist.

Modern treatment of hepatitis B (B) allows not only to stop the manifestations of a chronic condition, but also to stop the spread of cancer and cirrhosis and maintain the patient’s quality of life at the proper level.

Side effects

Modern drugs for the treatment of viral hepatitis B (B) have virtually no side effects. But the manifestation of ailments of the following nature is possible:

• Headache
• Temperature increase
• Weakness
• Discomfort in limbs

Less common are things like:

• Hair loss
• Weight changes
• Depression
• Problems with the functioning of the thyroid gland (with individual intolerance to drugs)

Also, the doctor may note a change in the content of leukocytes and platelets in the blood.

Effectiveness of treatment

Modern treatment of hepatitis B (B) in the acute form is very effective. In the chronic stage, a complete cure does not occur, but the disease is stopped, it is possible either to avoid complications such as cancer or cirrhosis, or to stop their development (if these pathologies have already appeared at the time of the start of treatment).