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Varicella is a common, benign and self-limiting disease. It is related to hepatitis and malfunction/failure of the liver. This study was designed to assess Varicella-Zoster Virus/ Hepatitis C Virus (VZV/HCV) co-infection on the levels of liver enzymes. A total of 88 blood samples regardless of Hepatitis C Virus positivity were collected. The age and sex of the sample population are included in the demographic statistics. HCV-RNA was detected by RTnested PCR and VZV-DNA was identified by nested PCR in all the sera. Approximately 27 patients were positive for HCV and VZV co-infection. Liver function was also tested on the basis of parameters such as Aspartate Amino Transferase (AST) and Alanine Amino Transferase (ALT). Infection with HCV and VZV is more prevalent in the 34-55 age group tested by nested-PCR and liver function tests based on Alt and AST levels using qualitative test kits. The ALT and AST levels were high 102 and 99.6 IU/L in co-infected cases as compared to 35 and 32 IU/L in normal cases without HCV, HIV and VZV. The study results indicate the impact of VZV in the abnormality of liver function. This study concludes that coinfection with HCV/VZV can be seen as a highrisk category for the development of liver disease where long-term outcomes of the disease should be controlled.

The Coronavirus Diseases 2019 (COVID-19) seriously affecting human health all over the world. More than 107 M people are reported positive for SARS-CoV-2, the virus causing COVID-19 pneumonia, from which +2.3 M died. Nucleotide Inhibitors (NI) have promising results in terms of its efficacy against different viral polymerases, including the Hepatitis C Virus (HCV) Non-Structural Protein 5 B (NS5B) RNA dependent RNA polymerase (RdRp) 1. Thus, the non-structural protein 12 (nsp12) RdRp of the human coronavirus represents an attractive target to develop a possible therapeutic agent. Sofosbuvir proved itself as a potential anti-SARS-CoV-2 RdRp and could inhibit viral replication and infection propagation.

Background and Aim Epigenetics involved in multiple normal cellular processes. Previous research have revealed the role of hepatitis C virus infection in accelerating methylation process and affecting response to treatment in chronic hepatitis patients. This work aimed to elucidate the role of promoter methylation (PM) in response to antiviral therapy, and its contribution to the development of fibrosis through hepatocarcinogenesis-related genes. Methods A total of 159 chronic hepatitis Egyptian patients versus 100 healthy control group were included. The methylation profile of a panel 9 genes (SFRP1, p14, p73, APC, DAPK, RASSF1A, LINE1, O6MGMT, and p16) was detected in patients’ plasma using methylation-specific polymerase chain reaction (MSP). Results Clinical and laboratory findings were gathered for patients with combined pegylated interferon and ribavirin antiviral therapy. Regarding the patients’ response to antiviral therapy, the percentage of non-responders for APC, O6MGMT, RASSF1A, SFRP1, and p16 methylated genes were significantly higher versus responders (P