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HIV-1 capsid stability enables inositol phosphate-independent infection of target cells and promotes integration into genes

Fig 1

Identification of IP6-dependent HIV-1 CA mutants.

(A, B, and C) Effect of CA mutations on HIV-1GFP infection of IPMK KOVector CEM CD4+ T target cells. (D) Quantification of HIV-1GFP early RTN products (first strand transfer (FST)) at 8 hours for the indicated IP6-dependent HIV-1 CA mutants. (E and F) Positions of altered residues that were tested for IP6 dependence mapped onto the HIV-1 CA hexamer (PDB 4XFX) (E) or the capsid three-fold interface (CA NMR structure (PDB 6WAP) aligned to the cryo-electron microscopic structure of the HIV-1 capsid (PDB 5MDG)) (F). Black asterisk(s) signify significance between IPMK KOVector and WTVector cells. A significant difference between IPMK KOVector and IPMK KOIPMK-Flag cell lines is shown with a green asterisk(s). All data points represent the average of 3 or more independent experiments. p value levels: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Fig 1

doi: https://doi.org/10.1371/journal.ppat.1011423.g001