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In the past decade, studies of innate immune activity against HIV-1 and other retroviruses have revealed a powerful array of host factors that can attack the virus at various stages of its life cycle in human and primate cells, raising the prospect that these antiviral factors could be manipulated in immunotherapeutic strategies for HIV infection. This has not proved straightforward: while HIV accessory genes encode proteins that subvert or destroy many of these restriction factors, others, such as human TRIM5α show limited potency against HIV-1. However, HIV-1 is much more susceptible to simian versions of TRIM5α: could this information be translated into the development of an effective gene therapy for HIV infection? Reigniting research into the restriction factor TRIM5α in the era of superior gene editing technology such as CRISPR-Cas9 presents an exciting opportunity to revisit this prospect.

Original publication




Journal article


Front Immunol

Publication Date





CRISPR-Cas9, HIV-1, HIV-2, PRYSPRY/B30.2, TRIM5α, adeno-associated virus, gene editing