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Innate immunity

HIV undercover

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Detection of viral components, including nucleic acids, by pattern recognition receptors of the innate immune system, triggers the production of type 1 interferons that suppress viral replication. A new study shows that HIV-1 can replicate in human macrophages by recruiting host cofactors that help the virus avoid detection by the innate immune system (Nature doi:10.1038/nature12769).

Jane Rasaiyaah et al. show that two HIV-1 capsid mutants, N74D and P90A, which cannot interact upon entry with the host cofactors CPSF6 (cleavage and polyadenylation specificity factor subunit 6) and cyclophilins, respectively, stimulate IFN-b production upon infection and are unable to replicate in macrophages. Because blocking of the IFN receptor with an antibody allows replication to wild-type levels, IFN induction is probably involved in suppressing viral infection. Silencing of CPSF6 or pharmacological inhibition of cyclophilin with cyclosporine or a cyclosporine analogue reduce replication of wild-type virus and induce cell-autonomous IFN-b production in macrophages. These findings suggest that in the early stages of infection, the viral capsid conceals nucleic acids and recruits host cofactors, allowing HIV to escape detection by the innate immune system, preventing IFN production and allowing viral replication.

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Da Silva, K. HIV undercover. Nat Med 19, 1582 (2013). https://doi.org/10.1038/nm.3430

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