Driving a wedge between viral lipids blocks infection

• Authors: Gregory Melikian, Emory University
• Journal Title: Proceedings of the National Academy of Sciences
• Volume: Volume 107, Number 40
• Publisher: National Academy of Sciences | 2010-10-05, Pages 17069-17070
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1073/pnas.1012748107
• Subjects: Biology, Virology

Abstract

There is a massive push to develop new drugs to treat viral infection. Traditional therapeutic strategies aim at viral proteins responsible for each and every step of viral replication. The main drawbacks of these approaches include an ever-increasing pool of drugs specific for a given virus and selection for drug-resistant viruses. An alternative strategy, which has recently gained popularity, targets cellular factors (not limited to viral receptors) involved in virus entry and replication. Numerous cellular proteins aiding viral replication have recently emerged from genome-wide screens, showing the virus’ reliance on various cellular processes. Targeting less variable host factors is an attractive concept that is less prone to selecting for drug-resistant viruses. The flip side of this approach is the potential for serious side effects and the need to target a large and often nonoverlapping number of cellular factors. A study by St. Vincent et al. in PNAS and the paper published earlier by another group introduce an exciting paradigm that focuses on a universal cellular target, which happens to be an intricate part of all enveloped viruses. The authors show that infection by enveloped viruses can be blocked by altering their membrane composition in a way that disfavors their merger with a target cell membrane.