All articles tagged with #viral replication
New research reveals that herpes simplex virus type 1 (HSV-1) can alter human DNA within an hour of infection by hijacking the host's cellular machinery, specifically taking control of RNA polymerase II to facilitate rapid viral replication. The study also identifies a potential enzyme, TOP1, that could be targeted to prevent these changes and combat the virus.
Researchers have discovered that herpes simplex virus-1 (HSV-1) hijacks the 3D structure of human DNA to facilitate its replication, but blocking a key enzyme, topoisomerase I, can prevent the virus from replicating, offering a promising new target for antiviral treatments.
UVA scientists have discovered that small variations in the Rev-RRE axis, crucial for HIV RNA export, significantly influence the virus's ability to replicate and reactivate from latency, offering new insights that could improve strategies to cure HIV by enhancing latency reversal approaches.
A study conducted by researchers at the University of Hong Kong found that initiating the antiviral drug Paxlovid within 0 or 1 day of COVID-19 symptom onset significantly reduced the rates of death and hospitalization by half compared to starting the drug 2 or more days later. The study, based on electronic medical record data of over 87,000 high-risk adult patients, highlighted the importance of early suppression of viral replication in reducing the risk of severe disease and death. The researchers also noted that COVID-19 vaccination may help protect against viral rebound after early Paxlovid initiation. They emphasized the need for easy access to rapid antigen tests and continued awareness of Paxlovid to ensure early diagnosis and treatment for high-risk individuals.
A study investigated the mechanisms behind non-suppressible HIV-1 viremia (NSV), a condition where individuals have persistent low-level viremia despite adhering to antiretroviral therapy (ART) and lacking drug resistance. The researchers found that NSV is fueled by clonally expanded HIV-infected cells and identified features of host integration sites that differentiate proviruses contributing to NSV. They also observed potentially permissive host cell and immune environments in patients with NSV. The study provides a comprehensive evaluation of the viral, cellular, and immune mediators of NSV, shedding light on the factors that contribute to this clinical conundrum.
Mutations in the viral genome of avian influenza A viruses have been discovered that can overcome a newly discovered antiviral protein, BTN3A3, in human cells. BTN3A3 inhibits a crucial step needed for viral replication, making it difficult for the viruses to cross the species barrier from birds into humans. This finding provides insights into mechanisms that prevent the spillover of avian influenza viruses and could contribute to the development of strategies to combat potential pandemics.