Microbiota and cancer: current understanding and mechanistic implications

During last few decades, role of microbiota and its importance in several diseases has been a hot topic for research. The microbiota is considered as an accessory organ for maintaining normal physiology of an individual. These microbiota organisms which normally colonize several epithelial surfaces are known to secrete several small molecules leading to local and systemic effects on normal biological processes. The role of microbiota is also established in carcinogenesis as per several recent findings. The effects of microbiota on cancer is not only limited to their contribution in oncogenesis, but the overall susceptibility for oncogenesis and its subsequent progression, development of coinfections, and response to anticancer therapy is also found to be affected by microbiota. The information about microbiota and subsequent contributions of microbes in anticancer response motivated researchers in development of microbes-based anticancer therapeutics. We provided current status of microbiota contribution in oncogenesis with special reference to their mechanistic implications in different aspects of oncogenesis. In addition, the mechanistic implications of bacteria in anticancer therapy are also discussed. We conclude that several mechanisms of microbiota-mediated regulation of oncogenesis is known, but approaches must be focused on understanding contribution of microbiota as a community rather than single organisms-mediated effects.

APOBEC3, TRIM5α, and BST2 polymorphisms in healthy individuals of various populations with special references to its impact on HIV transmission.

AIDS restriction genes (ARGs) like APOBEC3, TRIM5α, and BST2 can act as immunological detectors of the innate protective mechanism of the body. ARGs influence the course of viral pathogenesis and progression of the disease. The infection caused by different viruses including HIV activates the innate immune receptors leading to production of proinflammatory cytokines, interferons and signals that recruit and activate cells involved in the process of inflammation following induction of adaptive immunity. Differential expression of genes involved in viral infection decide the fate and subsequent susceptibility to infection and its clinical outcome. Nevertheless, comprehensive reports on the incidence of genetic polymorphism of APOBEC3s, TRIM5α, and BST-2 in the general population and its association with pathological conditions have not been described well. Therefore, the occurrence of APOBEC3, TRIM5α, and BST2 polymorphism in healthy individuals and its impact on HIV transmission was analyzed. We conducted an extensive search using the several databases including, EMBASE, PubMed (Medline), and Google Scholar. APOBEC3-D, -F, -G, and -H out of the seven human APOBEC3s, help in the control of viral infection. Amongst various restriction factors, TRIM5α and BST-2 also restrict the viral infection followed by the development of the disease. In the current review, a brief account of the polymorphism in the APOBEC3G, TRIM5α, and BST2 genes are explored among different populations along with the interaction of APOBEC3G with Vif protein. Furthermore, this review specifically focus on ARGs polymorphism (APOBEC3G, TRIM5α, and BST2) associated with HIV transmission.