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Background and Objective: Occult hepatitis B infection is a form of hepatitis in which despite of absence of detectable HBsAg, HBV-DNA is present in peripheral blood of patients. The mechanisms which are responsible for progression of OBI yet to be clarified but some investigators believed that the genetics and immunological parameters may are different in resistant individuals and patients. Cytokine network system could be leading alteration in viral immune response. The aim of this study was to investigate the relation between polymorphisms +874 region of IFN-Gama with occult hepatitis B infection. Materials and Methods: In this study, the plasma samples of 3700 blood donors were tested for HBsAg and anti-HBs by ELISA. The HBsAg negative and anti-HBc positive samples were selected and screened for HBV-DNA by PCR. HBV-DNA positive samples assigned as occult hepatitis B infection cases and ARMS-PCR technique were performed to examine the present polymorphisms in +874 region of IFN-Gama genes of patients with occult hepatitis B infection. Results: 352 (9.51%) out of 3700 blood samples were negative for HBsAg and positive for anti-HBc antibody. HBV-DNA was detected in 57 (16.1%) of HBsAg negative and anti-HBc positive samples. Our results showed that there was not any significant difference between patients and control group in polymorphisms in +874 region of IFN-Gama genes. Conclusion: This study showed that there is not any significant difference between polymorphisms in +874 region with IFN-Gama occult hepatitis B infection.

© 2014 Pourfathollah et al; licensee Herbert Publications Ltd. This is an Open Access article distributed under the terms of Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0). This permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction Asthma is a complex and chronic disease in which allergeninduced inflammatory processes in the airways contribute to the development of symptoms, such as wheezing, cough, dyspnea and breathlessness [1]. Asthma is considered to be the most common chronic disease and the leading cause of hospitalization in schoolchildren [2,3]. Control of asthma and response to medication is different in patients, and different asthmatics show various levels of asthma severity and progress which would depend on multiple factors especially genetic composition of patients. The need for management of medication and control of asthma make us improve our knowledge about pathogenesis of asthma and role of different elements that contribute to airway inflammation or influence signs and symptoms [4,5]. Asthma is believed to be a complex disorder involving genetic and environmental factors [6]. Many allergens and environmental microorganisms have pattern molecules on their surfaces, and these molecules interact with pattern-recognition receptors, which are part of the innate immune system. Among the known pattern-recognition receptors for microbial products, toll-like receptors (TLRs) are an evolutionarily conserved group of molecules expressed in antigen-presenting cells and epithelial cells [7]. TLRs recognize microbial patterns and play a crucial role in linking innate and adaptive immunity inducing a proinflammatory immune response that may counterbalance allergic diathesis. They initiate intracellular signaling pathways, bind to downstream protein kinases, induce activation of transcription factors, and initiate transcription of inflammatory cytokines and other host response elements [8]. Among TLRs, TLR4 recognizes lipopolysaccharide, a cell wall component of Abstract Introduction: Asthma as chronic inflammatory airway disease is considered to be the most common chronic disease that is involving genetic and environmental factors. Toll like receptors (TLRs) and other inflammatory mediators are important in modulation of inflammation. In this study we evaluated the role of TLR2 Arg753Gln and TLR4 Asp299Gly polymorphisms in the asthma susceptibility, progress, control levels and lung functions in Iranian subjects. Methods: On 99 asthmatic patients and 120 normal subjects, TLR2 Arg753Gln and TLR4 Asp299Gly polymorphism were evaluated by PCR-RFLP method recruiting Msp1 and Nco1 restriction enzymes, respectively. IgE serum levels by ELISA technique were determined and asthma diagnosis, treatment and control levels were considered using standard schemes and criteria. Results: Our results indicated that the genotype and allele frequencies of the TLR2 Arg753Gln and TLR4 Asp299Gly polymorphisms were not significantly different between control subjects and asthmatics (p>0.05) or even in asthma features such as IgE levels, asthma history and pulmonary factors (p>0.05). Conclusions: Meanwhile some previous studies indicated TLRs and their polymorphisms role in asthma incidence and features, our data demonstrated that TLR2 Arg753Gln and TLR4 Asp299Gly gene variants were not risk factor of asthma or its features in Iranian patients. Genetic complexity, ethnicity, influence of other genes or polymorphisms may overcome these polymorphisms in our asthmatics.