ПЦР. Гепатит D, количественный (RNA HDV)

Hepatitis D Virus (HDV) Antibody, IgG and IgM testing is performed to qualitatively identify total HDV antibodies in individuals with confirmed hepatitis B surface antigen (HBsAg) positivity. The assay helps recognize HDV coinfection or superinfection in the setting of hepatitis B, supports differential evaluation of atypical or severe hepatitis, and informs prognosis in mixed viral hepatitis. A reactive HDV antibody result should be followed by HDV RNA testing to distinguish active replication from past or resolved infection; results are interpreted alongside HBV markers (HBsAg, anti-HBc, HBV DNA). Although primarily diagnostic, the test may be incorporated into longitudinal assessment in patients with documented HDV infection.

HDV is a defective virus with a circular single-stranded RNA genome that relies on hepatitis B virus for replication and envelopes itself with hepatitis B surface antigen (HBsAg). Approximately 5% of individuals with hepatitis B are coinfected with HDV. Three principal genotypes are described: genotype 1 is globally prevalent, genotype 2 is found in East Asia, and genotype 3 predominates in South America. The virus tolerates acidic conditions and elevated temperatures but is inactivated by alkaline environments. Transmission is primarily parenteral, mirroring HBV, with less common sexual and vertical routes. Populations at increased risk include people who inject drugs, organ recipients, patients receiving hemodialysis, and those undergoing frequent transfusions. HDV infection occurs only in the presence of acute or chronic HBV or HBsAg carriage and therefore represents a mixed infection. Replication of HDV can suppress HBV replication (viral interference), which may lower or obscure certain HBV serologic markers. Clinical syndromes differ by timing of acquisition. Coinfection (simultaneous HBV and HDV) has an incubation of 3–7 weeks and typically presents with acute onset of fever, nausea, anorexia, and jaundice. Biochemical activity is often biphasic, with an initial alanine/aspartate aminotransferase peak driven by HBV followed weeks later by a second peak associated with HDV; about 90% of coinfections resolve. Superinfection (HDV acquisition in a person with existing HBV) is associated with a substantially lower probability of recovery, reported in only 5%–10% of cases. Distinguishing coinfection from superinfection draws on clinical course and HBV serology: anti-HBc IgM supports coinfection, whereas anti-HBc IgG favors superinfection. HDV infection reduces the likelihood of a favorable antiviral response; about 5% of cases demonstrate rapidly progressive liver injury with fatal outcomes. Chronic hepatitis and cirrhosis increase the risk of hepatocellular carcinoma, although a direct causal link with HDV has not been proven. With advancing cirrhosis, HDV replication may decline. In recipients of livers from HDV-infected donors, a latent pattern can occur: if HBV is absent or suppressed by immunoprophylaxis, HDV replication may remain confined to affected hepatocytes without dissemination, and HDV RNA may be undetectable in blood. Analytically, HDV RNA becomes detectable by PCR within days of infection, whereas HDV antibodies appear weeks later; therefore, a nonreactive antibody result does not exclude very early infection. A reactive HDV antibody result warrants confirmation and staging with HDV RNA and correlation with HBV markers (HBsAg, anti-HBc, HBV DNA). As with other immunoassays, nonspecific reactivity can occur; when clinical suspicion persists despite a negative antibody result, alternative HDV-specific testing is recommended.