Viral Hepatitis Overview

Systemic infections primarily affecting the liver due to inflammation.

A spherical RNA virus causing acute hepatitis, transmitted enterically.

Spread by the enteric route (through contaminated food or water).

Non-enveloped RNA virus with icosahedral symmetry, 27nm diameter.

Replicates strictly in the liver, and is found in liver, bile, and feces.

Thermostable and resistant to acid, and organic solvents.

Detection in the liver, bile, and feces by the end of the incubation period.

Boiling/intense chlorination/autoclaving/UV exposure/formaldehyde inactivates HAV.

Symptoms include fever, headache, muscle aches, loss of appetite, nausea, vomiting, abdominal pain, and bloating. These can be mild or severe, and often appear 1-2 weeks before jaundice.

The time between exposure to the virus and the onset of symptoms is usually 15-45 days, with an average of 21 days.

The period before jaundice occurs, lasting 3-5 days, marked by general infectious symptoms like fever, headache, and muscle aches.

The body's response includes: NK cells and cytotoxic T cells kill infected cells, IgM antibodies appear early, marking current infection, and IgG antibodies develop later, providing long-term protection.

The virus replicates in the liver, causing inflammation and damage. This can lead to increased levels of enzymes and electrolytes in the blood.

The infection affects various metabolic pathways, including lipid metabolism (increased triglycerides, decreased cholesterol), protein metabolism (decreased albumin and clotting factors, increased globulins), and glucose metabolism (irregular blood sugar).

Some people with HAV infection don't develop jaundice, especially children. They may experience milder symptoms or be asymptomatic.

Hepatitis A virus is transmitted through the fecal-oral route, primarily by ingestion of contaminated food or water.

Children often experience anicteric (without jaundice) and asymptomatic HAV infections, meaning they may not show clear symptoms.

Direct contact with an infected individual, contaminated water, or food are all ways HAV can spread.

The virus replicates in the oropharynx, salivary glands, bowel, and liver, with a particular focus on the liver cells.

No, there's no chronic excretion of HAV. Once the infection is cleared, you develop lifelong immunity.

The liver is the main target for HAV infection. The virus replicates there and causes inflammation leading to hepatitis A.

No, unlike some viruses, HAV does not directly destroy liver cells. It replicates inside them but doesn't cause cell death.

After replicating, the virus is released through the bile duct and ends up in the feces.

A syndrome in acute hepatitis characterized by increased liver enzyme levels (AST, ALT), particularly ALT, which is significantly higher in hepatitis A compared to other forms. These enzyme levels gradually decrease during recovery, not necessarily correlating with liver damage.

A syndrome in acute hepatitis marked by increased bilirubin levels, both direct and indirect, leading to jaundice. High and persistent bilirubin levels indicate a severe form, with lower average levels in hepatitis A compared to hepatitis B.

A syndrome associated with high serum bilirubin levels and elevated GGT, ALP, and cholesterol. It is characterized by impaired bile flow, and if more pronounced than hepatocytolysis, may suggest a non-viral cause for hepatitis.

Characterized by possible low or normal white blood cell count with a predominance of lymphocytes (lymphocytosis) and low neutrophil count (neutropenia). Sometimes, unusual lymphocytes with a lymphoblastoid appearance are observed in peripheral blood smears. Thrombocytopenia, hemolytic anemia, aplastic anemia, and pancytopenia may occur in severe cases.

A measure of the time it takes for blood to clot, specifically reflecting prothrombin activity. A decrease in PI or an increase in International Normalized Ratio (INR) indicates reduced prothrombin synthesis and a potential sign of liver damage and severe prognosis.

Elevated serum ammonia levels in hepatitis suggest impaired liver detoxification function. This can lead to neurological complications and represents a serious indicator of liver failure.

Reduced capacity of the liver to conjugate bilirubin, leading to increased unconjugated bilirubin levels. This is an indicator of impaired liver function with potential consequences for bilirubin metabolism.

Acute hepatitis is characterized by several syndromes, including Hepatocytolysis, Biliary Retention, Cholestatic, Hematological, and Liver Failure syndromes. Each reflects specific liver function disturbances and may indicate the severity of the disease.

Hypoalbuminemia and hypergammaglobulinemia are considered to be signs of chronic liver injury.

IgM anti-HAV antibodies are detectable since the clinical onset and up to 3-6 months later; they signal acute or recent infection.

IgG antibodies signify residual immunity post infection or post vaccination.

HAV antigen can be detected in stools by immune electron microscopy or in serum by ELISA.

In the prodromal period come into discussion, depending on the initial symptomatology: respiratory viruses, flu, food poisoning, biliary dyskinesias, cholecystitis, appendicitis, mental disorders, urticaria, acute articular rheumatism.

During the period of the condition, the differentiation must be made between the various types of jaundice: hemolytic jaundice, hepatocellular jaundice, obstructive jaundice.

Hepatocellular jaundice can occur in both infectious and non-infectious pathologies. a) Infectious: viral (cytomegalovirus, infectious mononucleosis, enteroviruses, arboviruses, herpes virus infection), bacterial (systemic salmonellosis, septicemia, typhoid fever, tuberculosis), spirochetes (leptospirosis, Lyme disease, secondary syphilis), brucellosis. b) Non-infectious: toxic hepatitis (mushrooms, carbon tetrachloride, white phosphorus, mercury, etc.), medicinal hepatitis (antidiabetic drugs, anesthetics, antimetabolites, isoniazid, antithyroid drugs, etc.), alcoholic hepatitis, genetic diseases (Rotor syndrome, Gilbert's disease, Crigler-Najjar syndrome)

Budd-Chiari syndrome – suprahepatic vein occlusion

During the incubation period (2-4 weeks), HBV replicates actively with minimal immune response and few symptoms. The body tolerates the virus.

The immune system reacts to HBV through cytotoxic T lymphocytes (CTLs), targeting viral proteins. This leads to symptoms of acute hepatitis and the virus may be cleared.

HBV doesn't directly damage liver cells; it's the host's immune response that causes the damage and symptoms. Cytotoxic T cells and NK cells target infected cells, leading to inflammation.

Some people don't clear the virus despite the immune response. They become chronic carriers and can shed HBsAg for years.

A strong immune response can lead to HBs seroconversion. HBsAg disappears, but HBV DNA remains in liver cells, potentially reactivating if immunosuppression occurs.

Lymph nodes and other organs act as a reservoir for HBV, potentially causing extrahepatic syndromes and post-transplant reactivation.

If the host is immunosuppressed (HIV infection, therapy), HBV can reactivate from its integration sites in the liver.