The time sequence, relative reactivity, and persistence of anti-HBc IgM were assessed in patients with HBsAg-positive viral hepatitis. A solid-phase immunoassay was developed using the IgM capture procedure with anti-p-coated polystyrene beads. HBcAg was purified from serum Dane particles and used as a probe with '261-labeled anti-HBc IgG. This immunoassay exhibited a pronounced prozoning phenomenon, and relative titers of sera differed widely depending upon the dilution of serum tested. When all sera were tested at 1:5,000 dilution, results were comparable in different patient groups.
Anti-HBc IgM persisted at detectable levels for up to 2 years, and it was necessary to establish relative titers to discriminate current from remote infections. A cut-off assay value was established, and in 12 cases of acute hepatitis B virus (HBV) infection, antibody exceeded this value for about 6 months after onset of HBs antigenemia. A similar profile of anti-HBc IgM persistence was observed in seven patients who developed an HBsAg chronic carrier state. Long-term viral replication did not sustain elevated IgM class-specific antibody levels.
The studies suggest that anti-HBc IgM analyses may be useful for differentiating recent and current HBV infections from remote infections, eliminating HBV as the agent for non-A, non-B hepatitis in asymptomatic HBsAg carriers, and detecting HBV as the etiologic agent during silent (HBsAg negative) infections.
Despite the availability of sensitive immunoassays for all serologic markers for diagnosing hepatitis B (HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-HBc), it is often difficult to differentiate acute, recent, or remote infections from chronic infections. All of these consequences of hepatitis B virus (HBV) infection may be characterized by persistence of the same set of markers (1). The ability to distinguish acute hepatitis B from non-A, non-B hepatitis in an asymptomatic HBsAg carrier is epidemiologically and clinically important, but is not resolvable with current HBV markers. Furthermore, in some cases of acute hepatitis B, HBsAg and HBeAg are transient and may be undetectable at first presentation. Under these circumstances, we would expect anti-HBc to be a primary marker for HBV exposure; however, the antibody is known to persist for many years, and its presence does not distinguish current from a past infection. A class of anti-HBc (IgG, IgM) has been distinguished by several immunoassay procedures and proposed as a serologic feature for differentiating sequential stages of HBV infections (2)(3).
Virus-specific IgM class antibody has been confirmed as a prominent early immune response in many viral