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Host factors exploited by retroviruses
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Journal Article
Host factors exploited by retroviruses
2007
Overview
Key Points
Retroviruses exploit a vast array of host cellular proteins during their replication. Every step in the viral life cycle requires a distinct set of these host factors.
Host factors provide attractive targets for therapeutic intervention. The cellular genes encoding these factors would not rapidly mutate to produce drug-resistant variants. Nonspecific inhibition of host machinery, however, could prove toxic.
Retroviruses often use transport systems that are involved in the movement of cellular cargoes using cytoskeletal motors, or in vesicle trafficking.
Different retroviruses use different sets of host factors.
Viruses often use redundant pathways, or use alternative pathways present in particular cell types.
Sometimes the viruses disrupt a host process or molecular machine for the purposes of virus replication. For example, the ESCRT machinery, which is normally involved in protein sorting to the endosome, is relocated to the plasma membrane by enveloped viruses and exploited for their budding and release.
Genomic screens indicate that the total number of host factors needed by viruses is enormous and that current information about these factors and their roles in virus replication is still incomplete.
Retroviruses, which encode fewer than ten genes, need to interact with cellular proteins for virtually all aspects of their replication cycle. In this Review, Stephen Goff describes how host factors and cellular pathways are exploited at each stage of the retrovirus lifecycle. Throughout, comparisons are drawn between HIV and other retroviruses.
Retroviruses make a long and complex journey from outside the cell to the nucleus in the early stages of infection, and then an equally long journey back out again in the late stages of infection. Ongoing efforts are identifying an enormous array of cellular proteins that are used by the viruses in the course of their travels. These host factors are potential new targets for therapeutic intervention.
Publisher
Nature Publishing Group UK,Nature Publishing Group
