Autophagy-related genes polymorphism in hepatitis B virus-associated hepatocellular carcinoma: A systematic review.

BACKGROUND: Chronic hepatitis B (CHB) virus is the most common risk factor for developing liver malignancy. Autophagy is an essential element in human cell maintenance. Several studies have demonstrated that autophagy plays a vital role in liver cancer at different stages. In this systematic review, we intend to investigate the role of polymorphism and mutations of autophagy-related genes (ATGs) in the pathogenesis and carcinogenesis of the hepatitis B virus (HBV). MATERIALS AND METHODS: The search was conducted in online databases (Web of Science, PubMed, and Scopus) using Viruses, Infections, Polymorphism, Autophagy, and ATG. The study was conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria. RESULTS: The primary search results led to 422 studies. By screening and eligibility evaluation, only four studies were relevant. The most important polymorphisms in hepatocellular carcinoma were rs2241880 in ATG16L1, rs77859116, rs510432, and rs548234 in ATG5. Furthermore, some polymorphisms are associated with an increased risk of HBV infection including, rs2241880 in ATG16L1 and rs6568431 in ATG5. CONCLUSION: The current study highlights the importance of rs2241880 in ATG16L1 and rs77859116, rs510432, and rs548234 in ATG5 for HBV-induced HCC. Additionally, some mutations in ATG16L1 and ATG5 were important in risk of HBV infection. The study highlights the gap of knowledge in the field of ATG polymorphisms in HBV infection and HBV-induced HCC.

The role of cholesterol 25-hydroxylase in viral infections: Mechanisms and implications.

Viral infections pose significant threats to human health, causing various diseases with varying severity. The intricate interactions between viruses and host cells determine the outcome of infection, including viral replication, immune responses, and disease progression. Cholesterol 25-hydroxylase (CH25H) is an enzyme that catalyzes the conversion of cholesterol to 25-hydroxycholesterol (25HC), a potent antiviral molecule. In recent years, increasing evidence has highlighted the critical involvement of CH25H in modulating immune responses and influencing viral infections. Notably, the review discusses the implications of CH25H in viral pathogenesis and the development of therapeutic strategies. It examines the interplay between CH25H and viral immune evasion mechanisms, highlighting the potential of viral antagonism of CH25H to enhance viral replication and pathogenesis. Furthermore, it explores the therapeutic potential of targeting CH25H or modulating its downstream signaling pathways as a strategy to control viral infections and enhance antiviral immune responses. This comprehensive review demonstrates the crucial role of CH25H in viral infections, shedding light on its mechanisms of action in viral entry, replication, and immune modulation. Understanding the complex interplay between CH25H and viral infections may pave the way for novel therapeutic approaches and the development of antiviral strategies aimed at exploiting the antiviral properties of CH25H and enhancing host immune responses against viral pathogens. In the current review, we tried to provide an overview of the antiviral activity and importance of CH25H in viral pathogenesis.