Viruses are the intracellular pathogens that reproduce only in the living cell and manipulate the cellular machinery to produce more viruses. Viral replications can affect cellular genes of the host in multiple cancerous ways. Approximately, 20% of all human oncogenesis is caused by cancer-causing viruses known as oncoviruses. Viral infection causes chronic inflammation leading to cell death, uncontrollable proliferation, and modulated expression of some of the regulatory proteins. Oncogenesis is a multistep phenomenon in which normal host cells are transformed into cancerous cells on the basis of host genetic variability. Oncogenic viruses encode genes that cause viral replication and transformation of the host cells to produce viral proteins and protein complexes. The phenomenon from basic viral infection to tumorigenesis is lengthy due to the involvement of factors like immunity complications, cellular mutations, and exposure to other cancerous agents. The viruses that are involved in human cancer development are Hepatitis B virus (HBV), Hepatitis C virus (HCV), Epstein–Barr virus (EBV), Human papilloma virus (HPV), Kaposi's sarcoma herpes virus (KSHV), and Human T lymphotrophic virus 1 (HTLV-1). This review article summarizes advanced knowledge related to human oncogenic viruses and the molecular mechanisms that lead to tumorigenesis in humans.

The current standard of care (SOC) for hepatitis C virus (HCV) infection is the combination of pegylated interferon (PEG-IFN), Ribavirin and protease inhibitor for HCV genotype 1. Nevertheless, this treatment is successful only in 70-80% of the patients. In addition, the treatment is not economical and is of immense physical burden for the subject. It has been established now, that virus-host interactions play a significant role in determining treatment outcomes. Therefore identifying biological markers that may predict the treatment response and hence treatment outcome would be useful. Both IFN and Ribavirin mainly act by modulating the immune system of the patient. Therefore, the treatment response is influenced by genetic variations of the human as well as the HCV genome. The goal of this review article is to summarize the impact of recent scientific advances in this area regarding the understanding of human and HCV genetic variations and their effect on treatment outcomes. Google scholar and PubMed have been used for literature research. Among the host factors, the most prominent associations are polymorphisms within the region of the interleukin 28B (IL28B) gene, but variations in other cytokine genes have also been linked with the treatment outcome. Among the viral factors, HCV genotypes are noteworthy. Moreover, for sustained virological responses (SVR), variations in core, p7, non-structural 2 (NS2), NS3 and NS5A genes are also important. However, all considered single nucleotide polymorphisms (SNPs) of IL28B and viral genotypes are the most important predictors for interferon based therapy of HCV infection.

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Background. Polycystic ovary syndrome (PCOS), also clinically known as Stein-Leventhal syndrome, is an endocrine disorder that affects 5–10% of women. Objective. To evaluate the risk factors for developing early onset of cardiovascular disease (CVD) in young patients with PCOS from our local population. Design. Case-control study. Methods. Fifty women with PCOS selected by history and transvaginal ultrasounds and 30 age-matched healthy women (controls). The case subjects and controls were further divided into two age categories comprising of equal number of subjects, of 20–29 and 30–39 years of age. The subjects underwent a detailed medical history, general physical examination, systolic (SBP) and diastolic blood pressures (DBP). Fasting blood samples were analyzed for glucose, insulin, triacylglycerides (TAG), total cholesterol, high density lipoprotein-C (HDL-C), low density lipoprotein-C (LDL-C), follicle-stimulating hormone (FSH), and luteinizing hormone (LH). Results. Women with the PCOS had significantly higher mean arterial pressure (MAP), serum TAG, LDL-C, insulin, and LH levels when compared with the age-matched control subjects. No significant differences were observed between serum cholesterol, glucose, and FSH levels between cases and controls. However, no marked differences were observed in biochemical parameters between the two age groups of PCOS patients. Conclusions. Younger women with PCOS are equally at risk of developing CVD as older women.