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Host Factors that Restrict Retrovirus Replication

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Viral Genome Replication

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Abstract/Primer

Over the past several decades, it has become clear that a variety of cellular proteins actively restrict retrovirus replication. Two families of proteins in particular, the TRIMs and the APOBEC3s, coordinate a robust innate defense to retrovirus infection. The TRIM proteins, led by TRIM5alpha, impose a replication block after entry, such that the invading retrovirus is degraded prior to integration. The APOBEC3 proteins, notably APOBEC3G, inhibit the replication of retroviruses by a mutagenic mechanism that is associated with degradation of viral DNA. Retroviruses have evolved means of avoiding their host’s TRIM and APOBEC3 defenses. Often, however, this leaves the virus susceptible to TRIMs and APOBECs from other species. Thus, these restriction systems limit the cross-species mobility of retroviruses. The prospects of developing new antiviral therapies that exploit these innate host defenses are promising.

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Acknowledgments

We thank N. Somia, L. Mansky, M. Huseby, and several laboratory members for thoughtful comments. Studies in the authors’ laboratory are supported by grants from the National Institutes of Health (AI064046 and GM080437), the Medica Foundation (Minnesota Partnership for Biotechnology and Medical Genomics) and the University of Minnesota (Leukemia Research Fund and Cancer Center Brainstorm Program), and the Cancer Biology Training Grant (CA009138).

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  1. Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, 321 Church Street South East, 6-155 Jackson Hall, Minneapolis, MN 55455, USA

    Mark D. Stenglein, April J. Schumacher, Rebecca S. LaRue & Reuben S. Harris

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    Stenglein, M.D., Schumacher, A.J., LaRue, R.S., Harris, R.S. (2009). Host Factors that Restrict Retrovirus Replication. In: Raney, K., Gotte, M., Cameron, C. (eds) Viral Genome Replication. Springer, Boston, MA. https://doi.org/10.1007/b135974_15

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