Hepatitis B Virus Infection: A Mini Review.

Hepatitis B and C viruses (HBV and HCV) are the leading causes of end-stage liver disease worldwide. Although there is a potent vaccine against HBV, many new infections are recorded annually, especially in poorly resourced places which have lax vaccination policies. Again, as HBV has no cure and chronic infection is lifelong, vaccines cannot help those already infected. Studies to thoroughly understand the HBV biology and pathogenesis are limited, leaving much yet to be understood about the genomic features and their role in establishing and maintaining infection. The current knowledge of the impact on disease progression and response to treatment, especially in hyperendemic regions, is inadequate. This calls for in-depth studies on viral biology, mainly for the purposes of coming up with better management strategies for infected people and more effective preventative measures for others. This information could also point us in the direction of a cure. Here, we discuss the progress made in understanding the genomic basis of viral activities leading to the complex interplay of the virus and the host, which determines the outcome of HBV infection as well as the impact of coinfections.

Cytokine gene polymorphisms implicated in the pathogenesis of Plasmodium falciparum infection outcome.

Cytokines play a critical role in the immune mechanisms involved in fighting infections including malaria. Polymorphisms in cytokine genes may affect immune responses during an infection with Plasmodium parasites and immunization outcomes during routine administration of malaria vaccines. These polymorphisms can increase or reduce susceptibility to this deadly infection, and this may affect the physiologically needed balance between anti-inflammatory and pro-inflammatory cytokines. The purpose of this review is to present an overview of the effect of selected cytokine gene polymorphisms on immune responses against malaria.