INTRODUCTION
In the world, 245 million people are infected with Hepatitis B virus (HBV), 40 million people are infected with human immunodeficiency virus (HIV), and 7.4% of HIV-infected patients are co-infected with HBV. Acute and chronic HBV infection causes approximately 887 thousand deaths annually. However, when compared with HBV monoinfection, the mortality and morbidity of HIV and HBV coexistence is higher (1).
HIV transmission routes (such as sexual intercourse, use of infected blood and blood products, infected stab injuries, unsafe injection, etc.) also increase the risk of developing HBV infection. Individuals with HIV infection should also be screened for HBV. However, in HIV-infected individuals, a situation called occult hepatitis B (OHB) can be encountered in HBsAg negativity, anti HBc IgG +/-, anti HBs +/-, and the HBV DNA level in serum or plasma is generally lower than 200 IU / ml. Two scenarios are mentioned in HBsAg-negative cases with suspected HIV / OHB coinfection. The first is that HBV infection is in the acute period after virus ingestion, when the surface antigen is not yet positive. The second is that although it is HBsAg, anti HBc, anti HBs negative, it is in the chronic period when there is cccDNA in the liver cell nucleus. OHB infection can also be detected by HBV DNA positivity in the patients serum or liver tissue in cases where cccDNA (covalently, closed, circuler DNA) persists in the liver cell nucleus even if HBsAg is found negative in HIV-infected individuals (2,3).
Immunosuppressive conditions such as HIV positivity, hematological malignancies, solid organ transplantations may cause hepatitis B reactivation. Among the mechanisms associated with the emergence of OHB infection, mutations in the PreS / S regions of HBV, the presence of HBV DNA molecules integrated into the HBV genome, HBV infection in mononuclear cells in peripheral blood, presence of HBV particles complexing with immunoglobulin (Ig) in the blood despite the formation of anti HBs, decrease in cellular humoral immune response and co-infection. HBsAg negativity can be associated with analytical sensitivity of laboratory methods and also viral genotypes (4). The border between healing HBV infection and occult HBV infection is not clear. In cases where HBV is eradicated and HBsAg loss occurs, in the presence of mechanisms that cause occult disease, the disease may flare up again. In a study in which 16 patients with occult HBV infection developing secondary to acute HBV infection were examined, anti HBc IgG positivity was found in all of the cases 30 years after the infection, and anti HBs positivity was found in 11 of them. In the same study, while HBV DNA was below the detectable level in the serum of the patients, it was found positive in the liver in two patients (5). Investigating the presence of OHB infection in HIV-infected patients is important in determining treatment options and predicting the survival of patients. It has been reported that the use of highly active antiretroviral therapy (HAART) reduces morbidity and mortality and delays the occurrence of complications in HIV-infected and HIV / HBV co-infected patients (6). In our study, we aimed to research the prevalence, demographic and clinical characteristics of occult HBV coinfection in a multicenter study in naive patients infected with HIV who received antiretroviral therapy and did not receive treatment.