Acute Viral Hepatitis (HAV, HBV, HCV)

Hepatitis A virus (HAV) is a picovirus primarily transmitted via the fecal-oral route. HAV replicates in the liver and is shed in high concentrations in feces from 2-3 weeks before to 1 week after the onset of clinical illness. IgM antibody develops within a week of symptom onset, peaks around three months, and is usually no longer detectable after six months. The presence of IgM antibody to HAV is diagnostic of acute HAV infection.

Hepatitis B surface antigen (HBsAg) is a distinctive serological marker of acute or chronic hepatitis B infection. HBsAg is the first antigen to appear following infection with HBV and is generally detected 1-10 weeks after the onset of clinical symptoms. HBsAg assays are routinely used to diagnose suspected HBV infection and monitor the status of infected individuals to determine whether the infection has resolved or the patient has become a chronic carrier of the virus. In patients that recover from HBV infection, HBsAg is undetectable 3-5 months after the onset of infection. In patients with chronic infection, HBsAg remains detectable for life.

Anti-HBc IgM increases rapidly, peaks during the acute infection stage of HBV infection, and then falls to a relatively low level as the patient recovers or becomes a chronic carrier. Anti-HBc IgM is useful in the diagnosis of acute HBV infection even when HBsAg concentrations are below the sensitivity of the diagnostic assay.

Detection of both HCV antibody and HCV RNA indicates current HCV infection. Detection of HCV antibody in the absence of HCV RNA is consistent with the absence of current HCV infection. Repeat HCV RNA testing is recommended if the person tested is suspected to have had HCV exposure within the past 6 months or has clinical evidence of HCV disease.