HBV-HDV co-infected people have a higher chance of developing cirrhosis, fulminant hepatitis, and hepatocellular carcinoma (HCC) compared to those infected only with HBV. The present study was conducted to investigate HBV genotypes and phylogeny among HBV mono-infected and HBV-HDV co-infected patients, as well as analyze mutations in the surface gene of HBV in mono-infected and co-infected patients. A total of 100 blood samples (50 co-infected with HBV and HDV, and 50 mono-infected with HBV only) were collected for this study. HBV DNA was extracted from patient sera and partial surface antigen gene was amplified from HBV genome using polymerase chain reaction. HBV S gene was sequenced from 49 mono-infected and 36 co-infected patients and analyzed to identify HBV genotypes and phylogenetic patterns. Subsequently, HBV S amino acid sequences were analyzed for mutational differences between sequences from mono- and co-infected patients. HBV genotype D was predominantly found in both mono-infected as well as co-infected patients. Phylogenetic analysis showed the divergence of HBV sequences, between mono- and co-infected patients, into two distinct clusters. HBV S gene mutation analysis revealed certain mutations in HBV-HDV co-infected subjects to be distinct from those found in mono-infected patients. This might indicate the evolution of HBV S gene under selection pressures generated from HDV coinfection.

Introduction HBV can evolve under selection pressure exerted by drugs and/or host immunity, resulting in accumulation of escape mutations that can affect the drug or the immune activity. Hepatitis delta virus (HDV) coinfection is also known to exert selection pressure on HBV, which leads to selective amplification of certain mutations, especially in genes that are required for HDV pathogenesis, such as HBsAg. However, little is known about the function of these mutations on HBV or HDV life cycle. The purpose of this study is to determine mutations selectively amplified in the backdrop of HDV, and how these mutations affect processing of CD4‐ and CD8‐T cell epitopes. Methods HBsAg was successfully amplified from 49/50 HBV mono‐ and 36/50 coinfected samples. The sequences were used to identify mutations specific to each study group, followed by an in silico analysis to determine the effect of these mutations on (1) proteasomal degradation, (2) MHC‐I and MHC‐II biding, and (3) processing of T‐cell epitopes. Results HBV‐HDV coinfected sequences exhibited certain unique mutations in HBsAg genes. Some of these mutations affected the generation of proteasomal sites, binding of HBsAg epitopes to MHC‐I and ‐II ligands, and subsequent generation of T‐ cell epitopes. Conclusion These observations suggest that HBV selectively amplifies certain mutations in the backdrop of HDV coinfection. Selective amplification of these mutations at certain strategic locations might not only enable HBV to counteract the inhibitory effects of HDV on HBV replication but also facilitate its survival by escaping the immune response.

In many developing countries, typhoid fever is endemic. Early diagnosis is important for appropriate treatment on time. Typhi dot is important diagnostic tool for early diagnosis of typhoid fever. In the current study from February, 2012 to May 2014, samples from 19433 febrile cases referred to Dow Diagnostic Research and Reference lab were screened for serum IgM and IgG for Salmonella typhi by Typhi dot test. Results showed that about 12501 patients had both IgM and IgG antibodies against Salmonella typhi. Male patients were more commonly affected than female patients. Highest frequency of positive cases was seen during the month of October. Age group >15-44 was most likely affected among different age groups. This study suggested that still we are far behind in improving sanitation and elimination of such controllable disease. Therefore prompt measures should be taken to control the disease especially during hot season by vaccination, improved sanitation and education as well.

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