Viral Hepatitis Overview and HAV Details

Spread through fecal-oral route, direct contact, or contaminated water/food.

Infected individuals (with or without symptoms).

Virus found in feces two weeks after infection until two weeks after symptoms appear, but decreases after jaundice appears.

Virus is most infectious in the weeks before jaundice and decreases sharply after jaundice.

Orpharynx, salivary glands, intestines, and liver hepatocytes.

Less frequent and milder in children than adults; 40-50% infected with no symptoms.

Proteins assembled into capsids that create new virions.

Fecal-oral route, meaning contamination of food or water.

Viral replication within the liver cells.

Viral presence in the blood (viremia) from 2 weeks post-infection to 2 weeks after symptom onset.

Immune response to viral antigens on the liver cells leads to damage.

The immune system combats the infection, with IgM antibodies appearing during infection/excretion and lasting 6 months ; IgG appears later and protects against reinfection.

The time between infection and the appearance of symptoms (15-45 days, average 21 days).

The period before jaundice, showing nonspecific symptoms (3-5 days).

Most HAV infections are asymptomatic; symptomatic cases may present non-specific symptoms (fever, body aches).

Liver damage affects metabolic processes-lipids, proteins, carbohydrates, and electrolytes.

Generally good with no risk of becoming chronic. The virus usually clears within a few weeks or months.

A rare form of hepatitis A characterized by intense, prolonged jaundice with a green tint. Occurs in 4-10% of adult cases.

Extremely rare, more common in adults, characterized by massive liver necrosis, coagulation disorders, and neuropsychiatric disturbances.

No known teratogenic risk for the fetus. Infection in the last trimester may infect the fetus but usually without symptoms.

Individuals with HIV do not seem to develop more severe symptoms compared to the general population, but may experience persistent elevated transaminases.

May have a more severe course compared to individuals without pre-existing liver disease. Fulminant hepatitis is more common in this group.

Based on epidemiological, clinical, and laboratory data. This includes contact history, absence of prior infection, vaccination status, travel history, clinical symptoms, and laboratory tests.

Similar across various types of acute hepatitis. These changes are more extensively discussed for hepatitis A, with only specific differences highlighted for other types of hepatitis.

A syndrome characterized by damage to liver cells, often seen in hepatitis A and B, leading to increased transaminases (ALT and AST) in the blood.

ALT levels are significantly higher in acute hepatitis A compared to other hepatitis types (B, C, or E).

A syndrome characterized by the buildup of bilirubin in the blood due to problems with bile flow, leading to jaundice.

Increased bilirubin levels (both direct and indirect) in the blood, with jaundice being obvious at levels above 4-5 mg/dl.

A syndrome characterized by impaired bile flow, leading to high levels of bilirubin, GGT, ALP, and cholesterol in the blood.

A predominantly cholestatic syndrome suggests a non-viral cause, as it implies a blockage in bile flow rather than cell damage.

Leukocyte count can be normal or low with lymphocytosis and neutropenia. In rare cases, atypical lymphocytes can be present in blood.

Severe damage to the liver affecting its functions, including protein synthesis, detoxification, and metabolism, resulting in decreased serum protein levels, increased ammonium, and impaired bilirubin conjugation.

The initial stage of HBV infection characterized by active viral replication within the liver, but with minimal damage to liver cells and no noticeable symptoms.

The immune system recognizes HBV proteins and attacks infected liver cells, leading to symptoms like jaundice and inflammation.

Destruction of infected liver cells due to the immune response. This process is mediated by cytotoxic T lymphocytes (CTLs) and NK cells.

A person who has persistent HBV infection, often with ongoing viral replication and the potential for liver damage.

The process where HBV DNA becomes incorporated into the host's genome, potentially leading to viral reactivation later.

Replication of HBV can occur in tissues and organs outside the liver, but these sites typically do not result in inflammation.

The type of immune response determines the severity of the infection and the likelihood of chronic HBV infection.

The only antibodies that offer protection against Hepatitis B infection are those directed against the Hepatitis B surface antigen (HBsAg).

Certain mutations in the pre-core region of the HBV genome are associated with a higher likelihood of severe and rapid forms of the disease, including fulminant hepatitis.

The time between HBV infection and the appearance of symptoms is typically 60-90 days, but can range from 45-180 days. Factors influencing the duration include the amount of virus received, the transmission route, other infections, and the virus's properties.

This phase precedes jaundice and lasts for 2-3 weeks. Symptoms are usually similar to other types of acute viral hepatitis. Specific signs include pseudorheumatoid syndrome and skin syndrome.

Symptoms like fever, cough, headache, muscle aches, and weakness are rarely seen at the beginning of HBV infection. It is more typical of the onset of hepatitis A.

This syndrome, also known as papular acrodermatitis, is commonly observed in children with HBV infection. It involves a rash of red-pink bumps (papules) primarily on the face, trunk, and generalized lymph node swelling.

Clinically, the jaundice (yellowing of the skin and whites of the eyes) associated with HBV is typically more intense, longer lasting, and fluctuates in severity. It often comes with other symptoms like tender liver enlargement, right upper abdominal discomfort, and sometimes spleen swelling and lymph node enlargement.