|
HIV replicates in human cells by disabling an innate protection mechanism, according to two reports in the November issue of Nature Medicine.
A human protein called APOBEC3G interferes with HIV replication by incorporating itself into virus particles and damaging the virus' genetic material. But the viral protein Vif can stop this process in two ways, as the groups of David Kabat and Michael Malim independently found. Vif binds APOBEC3G and prevents it from incorporating into virus particles. The viral protein also targets APOBEC3G for destruction, almost completely eliminating APOBEC3G from the cell. Because HIV exploits the cellular degradation machinery in other ways, Malim and colleagues suggest the proteins involved might be good drug targets. Another promising target might be Vif itself, say Kabat and colleagues. The protein has two important sites—one for binding APOBEC3G and another that helps destroy it. Blocking one or both of these sites could free APOBEC3G to do its job in HIV-infected cells. Author contacts: David Kabat
Oregon Health and Sciences University
Portland, OR
USA
Tel: +1 503 494 8442
E-mail: kabat@ohsu.edu Michael H. Malim
Guy's, King's and St Thomas' School of Medicine
London, UK
Tel: +44 20 7955 4472
E-mail: michael.malim@kcl.ac.uk (C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza
|