Hepatitis, literally an inflammation of the liver, has several causes, including viral infection. The most common viruses are hepatitis A (HAV), hepatitis B (HBV), and hepatitis C (HCV). There is also a lesser known, less common virus, hepatitis D (HDV). These viruses differ in their characteristics, modes of transmission, and incubation times. Although these pathogens have different antigenic properties, they produce clinically similar illnesses, ranging from asymptomatic to fulminant and fatal acute infections. Infection can vary from subclinical persistent illness to rapidly progressive chronic liver disease with cirrhosis and hepatocellular carcinoma.

While the pathogenesis behind viral hepatitis is not completely understood, it is known that the organisms target the hepatocytes. The pathology is not clear, but the hepatocytes are damaged in two distinct ways: direct action of the virus, as with HCV, or through a cell-mediated response to the virus, as with HBV. During the incubation and replication phases, viral markers, antigens, and later antibodies begin to develop. This is followed by associated inflammatory responses and liver-cell death. Depending on the severity of inflammation and liver-cell damage, the hepatocytes may regenerate or fibrous scar tissue can develop. Chronic inflammation is described as persistent inflammation and necrosis of the liver of six months’ duration or longer. This may lead to permanent liver fibrosis and cirrhosis as well as increased incidence of hepatocellular cancer.


Hepatitis A, also called “infectious hepatitis,” affects 1.4 million people annually worldwide.1 Although HAV is highly contagious, causing up to 65% of all viral hepatitis cases in the United States,2 it is the least serious of the four types. Infection is acute and self-limiting. Fulminant hepatic failure is rare. 

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Transmission is primarily through the fecal-oral route, usually from ingestion of contaminated water or shellfish. Sexual transmission mainly occurs in the homosexual population. Patients at high risk of acquiring HAV include those who travel to endemic regions, military personnel, food handlers, and children and staff in child-care facilities. Incidence is highest among children, with approximately 30% of reported cases occurring in those younger than 15 years.2 Very young children are usually asymptomatic, so the number of unreported cases could be even greater. 

Incubation lasts two to six weeks. This is followed by abrupt onset of symptoms, including fatigue, malaise, nausea, vomiting, anorexia, fever, and right upper-quadrant pain. Within a few days to one week, patients will notice dark urine, acholic stools, jaundice, and pruritus. Systemic symptoms resolve with the onset of jaundice. Jaundice and hepatomegaly occur in 70%-80% of symptomatic patients.1 Less common findings include splenomegaly, cervical lymphadenopathy, and arthritis. Patients with protracted illness often develop associated extrahepatic manifestations, such as vasculitis, arthritis, optic neuritis, transverse myelitis, thrombocytopenia, aplastic anemia, and red-cell aplasia.


If HAV infection is suspected, a hepatitis A antibody test (anti-HAV) should be ordered. It detects both immunoglobulin (Ig) G- and IgM-type antibodies. The IgM antibody develops approximately three to four weeks after exposure and usually appears in conjunction with symptom development. Its presence indicates an acute infection. Although IgM typically becomes undetectable approximately eight weeks following initial infection, it can be detected for up to 12 months. 

Presence of the IgG antibody indicates a previous HAV infection or vaccine-related immunity. Titers generally peak four to six weeks after exposure and remain elevated for life, providing immunity to infection.

Deciphering the viral hepatitis panel is often a challenging task. Unfortunately, there is no easy solution to this mystery other than memorizing the significance of each individual test. Table 1 provides a basic overview of common serologic tests not only for hepatitis A but also hepatitis B and C.


No specific medications or therapies are available to treat HAV infection. The standard of care consists of treating associated symptoms. During the acute phase, rest is recommended. Alcohol or other hepatotoxic substances, such as acetaminophen, can increase the impact of HAV on the liver and should be avoided. Liver function tests should be monitored.