Twenty-two percent of OBI patients are lack antibodies for anti-HBc and anti-HBs and they have a very low level of HBV DNA. These antibodies appear from the beginning of the infection, in some patients may not still develop specific antibodies to hepatitis B ("OBI primary") or because of the clearance of specific antibody to hepatitis B in the end stage of chronic hepatitis B. The possibility of the non-detection of HBsAg in serum of HBV-infected individuals may be due to surface gene escape mutants or mutation in the polymerase gene. Therefore, anyone can be a carrier of OBI. In addition, there are cases that are called as “False” OBI. They may carry mutants of HBV (in the S gene) that are not detected by conventional diagnostic kits. But the result of DNA is similar to other cases of HBV, because they are usually positive for HBsAg. Overall, a prevalence of occult HBV infection depends on; geographical region, a sensitivity of HBsAg kits, HBV DNA amplification methods and co infections with …show more content…
Anti-HBc tests do not detect pre-seroconversion WP infections and also, they are not practicable in areas with anti-HBc prevalence >5% where too many donor deferrals would negatively impact the blood supply. Anti-HBc positive, HBsAg negative blood samples often have persistent very low HBV DNA levels ranging from a few to 30 copies/mL.
Therefore, the anti-HBc screening strategy is also not defendable in areas of the world where prevalence of anti-HBc is >5%. The number of units that would be rejected in these countries because of anti-HBc reactivity would be prohibitive to maintaining the blood supply For blood detection of occult hepatitis B requires assays of the highest sensitivity and specificity with a lower limit of detection < 10 IU/mL for individual HBV DNA and < 0.1 ng/mL for HBsAg. studies have indicated that the added benefit of nucleic acid testing( NAT) performed in pooled samples is relatively small in areas of low endemicity. HBsAg tests with high sensitivity (<4 IU/ml