EBV VCA IgA (антитела IgA к капсидному антигену вируса Эпштейна-Барр)

Epstein–Barr virus (EBV) viral capsid antigen (VCA) IgG with avidity testing supports laboratory confirmation of EBV infection in patients with suspected infectious mononucleosis. The VCA IgG avidity index helps distinguish recent primary infection from past infection and assists in staging an ongoing illness. Results are interpreted alongside other EBV serologic markers (VCA IgM, early antigen IgG, and EBNA IgG) to corroborate the phase of infection, including patterns seen with chronic infectious mononucleosis. The assay also contributes evidence when assessing the etiologic role of EBV in EBV-associated lymphoproliferative disorders and malignancies.

Epstein–Barr virus (EBV) is a DNA virus in the genus Lymphocryptovirus (subfamily Gammaherpesvirinae, family Herpesviridae). EBV expresses four principal antigens in a defined sequence: the early antigen (EA), the viral capsid antigen (VCA), the membrane antigen (MA), and the Epstein–Barr nuclear antigen (EBNA). Each antigen elicits a corresponding antibody response that aids in clinical staging. EBV primarily infects epithelium of the upper respiratory and gastrointestinal tracts and B lymphocytes; infection of B cells can lead to immortalization. EBV is linked to infectious mononucleosis as well as certain cancers, including Burkitt lymphoma and nasopharyngeal carcinoma. Seroprevalence is high worldwide; in Russia, up to 50% of children younger than 5 years and approximately 95% of adults show evidence of prior infection. Humans with active disease or asymptomatic carriage serve as reservoirs. Virus is shed in saliva during the prodrome, throughout acute illness, and for up to 6 months during convalescence. Transmission occurs via droplets, close contact, sexual exposure, blood transfusion, and other parenteral routes. In immunocompetent hosts, primary infection may be silent or subclinical and then persist latently. High inoculum or impaired immunity can lead to viremia and acute disease. Although more than 70 virus‑specific proteins are expressed during replication, a smaller set of immunodominant targets is used clinically to define infection stage; the most informative markers include VCA IgM and IgG, EA IgG, and EBNA IgG. Serologic kinetics provide context for interpretation. VCA‑IgG typically appears 1–4 weeks after symptom onset, is detectable at the beginning of illness, peaks by the second month, and then persists for life, indicating prior infection and immunity; persistent high titers may be seen in chronic‑phase disease. In young children (particularly under 7 years), VCA‑IgG may be absent. A negative VCA‑IgG result generally argues against past infection but does not exclude very early acute infection; repeat testing is appropriate when clinical suspicion remains. A single result should be interpreted in conjunction with clinical findings and additional laboratory data. IgG avidity reflects the overall binding strength between IgG antibodies and their target antigens and is reported as an avidity index (%). For EBV, IgG avidity testing is clinically applied to VCA‑specific IgG; avidity for other classes (eg, IgM) is not informative. Low avidity (<60%) indicates low‑maturity antibodies consistent with acute primary infection or a very recent primary infection. Borderline avidity (60–70%) represents a gray zone, often seen in late primary infection or early past infection. High avidity (>70%) points to past infection when VCA‑IgM is absent; high avidity in the presence of VCA‑IgM suggests either viral reactivation or a late primary infection. Over weeks, maturation of the humoral response leads to a progressive rise in the avidity index.