HBcAg (core antigen) is a hepatitis B viral protein. It is an indicator of active viral replication; this means the person infected with Hepatitis B can likely transmit the virus on to another person (i.e. the person is infectious).
HBeAg is the extracellular form of HBcAg, hence why the presence of both are markers of viral replication, and antibodies to these antigens are markers of a decline in replication.
Multiple protein products can be produced from the same DNA sequence. When "ORF Core" and "Pre C" are translated together, the result is "HBeAg".
Whereas HBcAg is considered "particulate" and it does not circulate in the blood, it is readily detected in hepatocytes after biopsy. "HBeAg" is considered "nonparticulate" or "secretory".
Both HBeAg and HBcAg are made from the same reading frame, but HBeAg is secreted from cells and accumulates in serum as an immunologically distinct soluble antigen. HBeAg is secreted and found in the serum of patients and serves as a marker of active replication in chronic hepatitis. Although the function of HBeAg is not clearly understood, one study demonstrated that it downregulated Toll-like receptor 2 expression on hepatocytes and monocytes leading to a decrease in cytokine expression. HBeAg is dispensable for replication, as mutant viruses with defects in the pre-C region are both infectious and pathogenic.
- Kimura T, Rokuhara A, Matsumoto A et al. (May 2003). "New enzyme immunoassay for detection of hepatitis B virus core antigen (HBcAg) and relation between levels of HBcAg and HBV DNA". J. Clin. Microbiol. 41 (5): 1901–6. doi:10.1128/JCM.41.5.1901-1906.2003. PMC 154683. PMID 12734224.
- Cao T, Meuleman P, Desombere I, Sällberg M, Leroux-Roels G (December 2001). "In vivo inhibition of anti-hepatitis B virus core antigen (HBcAg) immunoglobulin G production by HBcAg-specific CD4(+) Th1-type T-cell clones in a hu-PBL-NOD/SCID mouse model". J. Virol. 75 (23): 11449–56. doi:10.1128/JVI.75.23.11449-11456.2001. PMC 114731. PMID 11689626.
- "TSRI - News and Publications". Retrieved 2009-01-03.
- Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 7th ed. page 2062
- Chen X (May 2014). "Tapasin modification on the intracellular epitope HBcAg18-27 enhances HBV-specific CTL immune response and inhibits hepatitis B virus replication in vivo.". Lab Invest. 94 (5): 478–90. doi:10.1038/labinvest.2014.6. PMID 24614195.
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