Virologie最新文献

Long COVID has emerged as a debilitating condition, severely impacting the daily functioning and quality of life of affected individuals. The pathogenesis of Long COVID is complex and multifactorial, involving immune dysregulation, persistent inflammation, and potential reactivation of other pathogens. A key driver of Long COVID is the potential persistence of SARS-CoV-2 in various tissues beyond the respiratory tract, leading to the formation of viral reservoirs that contribute to ongoing symptoms, several months after initial infection. These reservoirs have been suggested in the gastrointestinal tract, central nervous system, cardiovascular system, and other tissues, often persisting months after the initial infection. Additionally, viral RNA and proteins in these tissues are associated with chronic inflammation and immune system disruptions, which are primary contributors to Long COVID symptoms. This article explores the mechanisms and consequences of SARS-CoV-2 persistence in respiratory and non-respiratory tissues, highlighting its impact on the immune system and underscoring critical areas for future research to improve outcomes for individuals suffering from Long COVID.

Long COVID has emerged as a debilitating condition, severely impacting the daily functioning and quality of life of affected individuals. The pathogenesis of Long COVID is complex and multifactorial, involving immune dysregulation, persistent inflammation, and potential reactivation of other pathogens. A key driver of Long COVID is the potential persistence of SARS-CoV-2 in various tissues beyond the respiratory tract, leading to the formation of viral reservoirs that contribute to ongoing symptoms, several months after initial infection. These reservoirs have been suggested in the gastrointestinal tract, central nervous system, cardiovascular system, and other tissues, often persisting months after the initial infection. Additionally, viral RNA and proteins in these tissues are associated with chronic inflammation and immune system disruptions, which are primary contributors to Long COVID symptoms. This article explores the mechanisms and consequences of SARS-CoV-2 persistence in respiratory and non-respiratory tissues, highlighting its impact on the immune system and underscoring critical areas for future research to improve outcomes for individuals suffering from Long COVID.

Interferons (IFNs) are cytokines that play a key role in the innate immune response, possessing antiviral, antiproliferative, and immunomodulatory properties. Currently, IFNs are used clinically as treatments for lymphomas, multiple sclerosis, and chronic viral infections such as hepatitis B, C, D, and E virus infections. HEV infection can lead to fulminant hepatitis, while chronic infections with HBV, HCV, and HDV are the leading global causes of hepatocellular carcinoma. Despite their limited efficacy and numerous side effects, IFNs remain essential in the treatment of these infections. In this review, we summarize the current knowledge on the interactions between hepatic viruses and the IFN pathway to understand the virus-dependent molecular mechanisms involved in IFN induction and its antiviral effects.

The reverse transcriptase of Moloney Murine Leukemia Virus (MMLV) is an enzyme that synthesizes DNA from an RNA template. Among reverse transcriptases, this enzyme is currently the most commonly used in molecular biology and diagnostics. Since its discovery, this viral protein has been extensively studied, shedding light on its structural and functional characteristics, and offering opportunities to optimize the catalytic performances for biotechnological applications. The review describes the structural motifs of the reverse transcriptase of MMLV, the key amino acids in enzymatic catalysis and the enzyme's properties such as processivity, fidelity and thermal stability. This review reports the optimizations made to improve these parameters, which enabled the modified enzymes to be integrated in the molecular biology tests used in the laboratory on a daily basis.