” In addition, OBI can be serologically classified as seropositive OBI (e.g., hepatitis B virus core protein [anti-HBc] and/or hepatitis B virus surface protein [anti-HBs positive]) or seronegative OBI (anti-HBc and anti-HBs negative). Figure 1 summarizes the classification of OBI as suspected (based on indicative OBI markers) or confirmed OBI (based on definitive OBI markers: HBV DNA in liver tissue with or without detectable serum levels). It is important to exclude false OBI,
which is the result of infection by HBV variants with S-gene escape mutations that produce modified HBsAg molecules not recognized by some commercially available assays. False OBI is typically characterized by serum HBV DNA levels comparable to those RG7204 purchase usually
detected in the overt HBV infection, whereas true OBI p38 MAPK signaling is characterized by serum HBV DNA levels typically less than 200 IU/mL.1 Etiopathogenically, OBI is caused by persistent low-level replication of HBV resulting from host suppression of HBV replication or to mutant viral strains with defective replication or S-protein synthesis. Like overt HBV infection, OBI can be associated with integration of HBV sequences into the host genome.2 T-cell immune responses against HBV are usually more active in seropositive than in seronegative OBI.3 In epidemiologic studies, the prevalence of OBI differs regionally around the world. It appears that rates selleck chemicals of OBI are generally higher among subjects at high risk for HBV infection and those with liver disease.4-6 These regional variations are thought to result from the fact that the majority of HBV infections in highly endemic countries are contracted perinatally or during early childhood; thus, a higher proportion of infected adults have long-term chronic HBV infection, with a gradual decrease of the HBsAg into the undetectable range. In addition, serological findings in patients with OBI vary significantly; in one review article, approximately
22% of OBI sera were negative, 35% of individuals with OBI were anti-HBs positive, and 42% were anti-HBc positive.7 The detection of HBV DNA in liver tissue is the current gold-standard test for confirming OBI. Several HBV DNA assays exist that target different regions of the HBV genome, including the surface, precore/core, polymerase, and X gene regions or cccDNA, a key DNA replication step of the virus present in the nucleus of infected hepatocytes. DNA amplification, using two consecutive rounds of polymerase chain reaction (PCR) (nested PCR) or real-time PCR with oligonucleotide primers specific for conserved HBV regions, has been used for measuring HBV DNA levels in OBI patients.