In addition, occult HBV infection increases the risk of HBV transmission through blood transfusion. Significant advances have been achieved in understanding the molecular basis for occult HBV infection, and several factors have been implicated in the pathogenesis of occult HBV infection[9,10]. immunoassay (CLEIA) with the clone containing T120 mutation, compared with the wild type or the clone with S143L mutation despite the similar levels of extracellular and intracellular HBsAg detected by Western blot. Southern blot experiments showed that the levels of intracellular HBV DNA were not different Nucleozin between these clones. CONCLUSION Occult HBV infection is common in patients with hematological malignancies and associated with P120T and S143L mutations. 120T mutation impairs the detection of HBsAg by CLEIA. study of clones inserted with 120T and 143L, it was found that the 120T mutation could impair HBsAg detection by changing its conformation. Patients with hematological malignancies should be screened and closely monitored for anti-HBc and Rac1 HBV DNA. INTRODUCTION Occult hepatitis B virus (HBV) infection is defined by the presence of HBV DNA in the liver (with or without HBV DNA in the serum) in hepatitis B surface antigen (HBsAg) negative individuals. Apart from posing diagnostic challenges, several studies indicated that occult HBV infection also associates with flares of liver disease in hepatitis C virus (HCV) infected patients who do not exhibit changes in HCV RNA levels and reduces the response rate to interferon therapy. Furthermore, occult HBV infection is frequently detected in cryptogenic liver diseases and autoimmune hepatitis[3-5]. HBV reactivation is a well-known complication in patients with occult infection under immune suppression, such as anticancer therapy, and human immunodeficiency virus (HIV) infection[6,7]. Nucleozin In addition, occult HBV infection increases the risk of HBV transmission through blood transfusion. Significant advances have been achieved in understanding the molecular basis for occult HBV infection, and several factors have been implicated in the pathogenesis of occult HBV infection[9,10]. A variety of mutations in HBsAg have been reported to affect antigen detection, immune recognition, HBV infectivity, cell tropism and virion morphology[11-14]. The aim of this study was to determine the prevalence of occult HBV infection in patients with hematological malignancies in South Egypt. An study was performed to assess the virological characteristics of prevalent HBsAg mutations detected in patients with occult HBV infection. MATERIALS AND METHODS Patients Serum samples were collected consecutively from 165 patients with hematological malignancies hospitalized in the Oncology Department of the Sohag Faculty of Medicine and South Egypt Cancer Institution from November 2010 to October 2011. All patients started their treatment regimen at the time of conduction of the study. The serum samples were stored at -80 C for future examination of HBsAg, antibodies to HBsAg (anti-HBs), antibodies to HBV core (anti-HBc), and HBV DNA. Serological markers of HBV infection HBsAg was measured by enzyme immunoassay (AxSYM; Abbott Japan, Tokyo, Japan) and chemiluminescence enzyme immunoassay (CLEIA) (Fujirebio, Tokyo, Japan). The IgG class of anti-HBc was determined by radioimmunoassay (Abbott Japan). Anti-HBs was tested by enzyme immunoassay (AxSYM; Abbott Japan, Tokyo Japan). Anti-HCV was tested by CLEIA (Fujirebio, Tokyo, Japan). All serologic assays were performed according to the manufacturer’s instructions. DNA extraction DNA was extracted from serum samples (200 L) using a QIAamp DNA extraction kit (Qiagen, Hilden, Germany) and re-suspended in 100 Nucleozin L of the storage buffer provided by the kit manufacturer. Quantitation of serum HBV DNA HBV DNA sequences spanning the entire S gene were amplified by real-time polymerase chain reaction (PCR) according to a previously described protocol with a slight modification. The detection limit of the assay was 100 copies/mL (equivalent to 20 IU/mL). HBV genomic amplification, sequencing and molecular evolutionary analysis of HBV Extracted DNA was subjected to PCR for amplifying the complete genome of HBV as previously described. Amplicons were sequenced directly using the ABI Prism Big Dye ver. 3.1 kit on the AMI 3100 DNA automated sequencer (Applied Biosystems, Foster City, CA, United States). All sequences were analyzed in both forward and reverse directions. HBV genotypes were determined by molecular evolution analysis. Target sequences were aligned by CLUSTALX with reference.