The latest research & treatment news about Hepatitis C infection, diagnosis, symptoms and treatment.

Hepatitis A and B diagnostics by means of viral antigens and antibodies

Hepatitis A

The incubation period of Hepatitis A is short, lasting usually from 2 to 16 weeks.

Acute Hepatitis A, which may proceed as an icteric or anicteric illness or as a subclinical disease, generally lasts 2-12 weeks. In a protracted form it may persist up to a maximum of about one year, but chronic courses or permanent carriers of the virus are unknown.

The patients stool is infectious already during the incubation period and for about 2 weeks at the onset of the acute disease. Fecal excretion of HAV lasts for a period of 1-8 weeks in total. Examinations of the feces for HAV antigen, however, are not easily practicable and for this reason are carried out only rarely.

IgM anti-HAV antibodies are detectable immediately after the onset of the disease and are characteristic of acute Hepatitis A. They can persist for some months, beyond the stages of illness and convalescence, which detracts somewhat from their diagnostic significance. Anti-HAV antibodies of the IgG-class are usually identifiable for the whole of a patient’s life upon restitution following the acute disease and are characteristic of immunity to the Hepatitis virus A.

Hepatitis B

The incubation period of Hepatitis B usually lasts from 2 to 4 months, although it may be very short (10 days) or extremly long (9 months). Yet before the outbreak of the acute disease HBs- and HBe-antigen are detectable in the patient’s serum.

The onset of acute hepatitis is characterized by the occurrence of anti-HBc antibodies which at first exclusively belong to the IgM class. From this time on anti-HBc antibodies will be detectable in the patient’s serum for the rest of his life, no matter whether there is an acute Hepatitis B, a form of persisting virus infektion or some naturally acquired immunity to HBV. The IgM anti-HBc antibodies are detectable not during acute hepatitis, but sometimes also for considerable lengths of time into the stage of immunity, and furthermore in many phases of chronic Hepatitis B virus infection, so that the qualitative identification of IgM anti-HBc is not sufficient for diagnosing acute Hepatitis B.

If this disease proceeds without any complications, seroconversion of HBe-antigens will occur within a period of 10 weeks, with anti-HBe antibodies appearing in the serum some time after or simultaneously with the disappearance of HBe-antigen.

Seroconversion of HBs-antigen to anti-HBs antibodies follows this event within a period of 6 months after the onset of the disease. In this process we usually find a “window-stage” of some weeks to some month’s duration, in which HBsAg is no longer and anti-HBs antibodies are not yet detectable . In some cases the HBeAg and/or HBsAg seroconversions will proceed without any window-stage, so that one serum sample may contain both HBe-antigen and anti-HBe (or HBs-antigen and anti-HBs) simultaneously.

The anti-HBs and anti-HBe antibodies—together with the anti-HBc antibodies—can persist for the whole of a patient’s life after resolution of the acute hepatitis and will be characteristic of the stage of immunity. In most cases, however, the anti-HBe antibodies are less long-lived, and the anti-HBs antibodies may also drop below the level where identification is possible after some years.

Injection of Hepatitis B hyperimmune globulin results in a transitory, active Hepatitis B vaccination in a lasting level of anti-HBs antibodies in the serum.

The most significant event indicating a chronic course of Hepatitis B is the absence of the HBsAg/anti-HBs seroconversion. If this phenomenon has not occured within 6 months after the onset of the disease, persistence of the Hepatitis B virus infection and the related clinical pictures (asymptomatic HBsAg carrier, chronic hepatitis, cirrhosis, or hepatoma) have to be reckoned with.

In the least favourable form of the disease HBe-antigen and IgM anti-HBc antibodies will be detectable in the patient’s serum for several years. Although the HBeAg/anti-HBe seroconversion is a favourable prognostic sign, even anti-HBe-positive chronic hepatitis may take a severe course. If the HBe-antigen phase is relatively short, we will mostly be confronted with the picture of an asymptomatic carrier, in which at last—in the stage of inapparent virus persistance—even HBsAg will no longer be detactable . The dissappearance of HBe-antigen does not always signal a favourable course of the disease; after a short period of anti-HBe-positive results HBeAg may reoccur and the disease be reactivated.