HDV RNA is detectable in the blood and liver at the time of onset of acute symptomatic disease. IgM anti-HDV is a reliable indicator of recent HDV exposure, but is frequently short-lived. Acute coinfection by HDV and HBV is associated with the presence of IgM against HDAg and HBcAg (denoting new infection with hepatitis B). With chronic delta hepatitis arising from HDV superinfection, HBsAg is present in serum, and anti-HDV antibodies (IgG and IgM) persist for months or longer. Because of its dependency on HBV, HDV infection is prevented by vaccination against HBV.
HEV is an enterically transmitted, water-borne infection that usually produces a self-limiting disease. The virus typically infects young to middle-aged adults. HEV is a zoonotic disease with animal reservoirs that include monkeys, cats, pigs, and dogs. Epidemics have been reported in Asia and the Indian subcontinent, sub-Saharan Africa, and Mexico, and sporadic cases are seen in Western nations, particularly where pig farming is common and in travelers returning from regions of high incidence. Of greater importance, HEV infection accounts for 30% to 60% of cases of sporadic acute hepatitis in India, exceeding the frequency of HAV. A characteristic feature of HEV infection is the high mortality rate among pregnant women, approaching 20%. In most cases, HEV is not associated with chronic liver disease or persistent viremia. The average incubation period following exposure is 4 to 5 weeks.
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Discovered in 1983, HEV is an unenveloped, positive-stranded RNA virus in the Hepevirus genus. Virions are shed in stool during the acute illness. Before the onset of clinical illness, HEV RNA and HEV virions can be detected by PCR in stool and serum. The onset of rising serum aminotransferases, clinical illness, and elevated IgM anti-HEV titers are virtually simultaneous. Symptoms resolve in 2 to 4 weeks, during which time the IgM titers fall and IgG anti-HEV titers rise.
Clinicopathologic Syndromes of Viral Hepatitis
As already discussed, infection with hepatitis viruses produces a wide range of outcomes. Acute infection by each of the hepatotropic viruses may be symptomatic or asymptomatic. HAV and HEV do not cause chronic hepatitis, and only a small number of HBV-infected adults develop chronic hepatitis. In contrast, HCV is notorious for producing chronic infections. Fulminant hepatitis is unusual and is seen primarily with HAV, HBV, or HDV infections. Although HBV and HCV are responsible for most cases of chronic hepatitis, there are many other causes of similar clinicopathologic presentations, including autoimmune hepatitis and drugand toxin-induced hepatitis (discussed later). Therefore, serologic and molecular studies are essential for the diagnosis of viral hepatitis and for distinguishing between the various types.
Acute Asymptomatic Infection With Recovery. Patients in this group are identified incidentally on the basis of elevated serum transaminases or the presence of anti-viral antibodies. HAV and HBV infections, particularly in childhood, are frequently subclinical.
Acute Symptomatic Infection With Recovery. Whichever virus is involved, acute disease follows a similar course, consisting of: (1) an incubation period of variable length (see
Table 16.2 (3) a symptomatic icteric phase; and (4) convalescence. Peak infectivity occurs during the last asymptomatic days of the incubation period and the early days of acute symptoms.