Review of the twelfth West Coast retrovirus meeting

Abstract

Every year the Cancer Research Institute from University of California at Irvine organizes the West Coast Retrovirus Meeting where participants have a chance to discuss the latest progress in understanding the pathology of retroviruses. The 12 th meeting was held at the Hyatt Regency Suites in Palm Springs, California from October 6 th to October 9 th 2005, with the major focus on human immunodeficiency virus (HIV) pathogenesis. Philippe Gallay from The Scripps Research Institute and Thomas J. Hope from Northwestern University organized the meeting, which covered all the steps involved in the lifecycle of retroviruses with an emphasis on virus:host interactions. The trend in research appeared to be on the restriction of viral infection, both by the endogenous, cellular restriction factors, as well as by the potential antimicrobial compounds of known or unknown mechanisms. Additionally, new stories on the inevitable feedback from the host immune system were presented as well. HIV still represents a challenge that an army of motivated people has been working on for over 20 years. And yet, the field has not reached the plateau in knowledge nor enthusiasm, which was proven again in October 2005 in Palm Springs. Review Viral EntryJohn Young of the Salk Institute began this session by describing work his lab has recently completed in understanding cellular requirements for replication of Murine Leukemia Virus (MLV) [1]. Through use of chemically mutagenized CHO cells, they identified five clones that became resistant to MLV infection. Additional studies revealed this restriction was specific to the MLV core. After confirming the virus was blocked prior to integration, the clones were separated into two phenotypes, those which blocked reverse transcription early and those which allowed reverse transcription and nuclear entry, but prevented viral integration. Young and colleagues are currently identifying cellular factors involved in the latter phenotype. While the exact identities of these cellular factors were not revealed, Young shared that they believe one is an enzyme and the other a putative transcription factor. Pankaj Kumar from Lorraine Albritton's lab at the University of Tennessee continued this theme by examining cellular factors involved in Moloney MLV entry. Previous work found that the exposure of MLV to proteases enhanced the viral infectivity and certain cell lines, including XC cells, innately possessed proteases that could facilitate MLV infection. The group decided to focus on cathepsins, since expression of these cellular proteases is induced under these conditions. They found a broad spectrum cathepsin inhibitor as well as a cathepsin B-specific inhibitor reduced Moloney MLV infectivity. Additionally,