| Summary: | The presence of hepatitis B virus genome in HBsAg-negative subjects is known as “occult infection” from HBV. Patients with occult infection may express markers of previous exposure to B virus (anti-HBs and / or anti-HBc positive). 20% is negative for all HBV markers except for the presence of HBV-DNA. Occult infection is associated with a strong suppression of viral replication that is responsible for both HBsAg negativity and the very low or undetectable HBV-DNA in serum but seen in the liver tissue. The pathogenesis of occult infection is considered multifactorial. Infection by mutants of HBV (HBsAg mutants), suppression of viral replication and expression of genes of HBV, HBV-DNA integration into the host genome, infection of HBV in mononuclear peripheral blood, abnormalities of the immune response, interference with other virus. HBV DNA with high sensitivity and specificity, can shorten the “window period” elapses between exposure to infection and responsiveness to the serological test.The presence of mutant HBV amino acid substitution of the determinant “a” gene “S” epitope of the surface protein of the virus, causes conformational changes that alter the binding with the specific antibody. Aim of this work is to assess negative or borderline subjects of HbsAg, with moderate increases of transaminase levels but - positive to HBV DNA test. The serological markers of HBV were determined with Architect (Abbott).The HBV-DNA was evaluated in Real-Time PCR Cobas TaqMan 48 (Roche) a quantitative test that detects the viral concentration. 15350.12 (0.07%) were positive for HBV-DNA test., 3 positive for HBsAg, 9 negative HBV markers showed anti-HBc reactivity in all 12 anti-HBe in 3, 4 anti-HBs with a titer of 13UI/ml.Le ALT were altered only for 2 to 12 and was detected viremia below the sensitivity test (<6 IU / ml).These data allow to draw some considerations: - Screening tests for infection with HBV do not show the “window period”.The slow replication of HBV with low viremia in the initial phase involves the impossibility of identifying HBsAg in serological screening, but detected by molecular biology tests. - The “window period”, the carrier state immunosilent chronic, low levels of viral proteins do not detect the infection. - Data in literature indicate the presence of different mutant strains of HBV characterized by altered expression of the antigenic determinant “a” of HbsAg. - The majority of screening tests for detection of HBsAg using monoclonal antibodies for the identification of the determinant “a” is needed to identify the different mutants using a mixture of monoclonal antibodies capable of recognizing even the most conserved regions.The gold standard methods to detect the mutant viruses are the techniques of molecular biology and the direct sequencing.
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