Abstract: A105S and N74D capsid mutant viruses did not accumulate capsid in the nucleus, irrespective of C-A1 treatment.
Method: The A105S and the N74D mutation were introduced into pCMV R8.2 using the QuikChange II XL Kit (Stratagene) as previously described.
Discussion: However this hypothesis is not fully convincing because viruses harboring the A105S and N74D mutations are insensitive to C-A1, they do not show accumulation of capsid in the nucleus yet they are capable of integrating.
Discussion: Mutant viruses N74D and A105S proceed through a PMID: 27876849
2016
Scientific reports
Result: 7C), suggesting that the N74D mutant exhibited an advantage over the WT virus around the time of integration.
Result: Apparently, the N74D change in the capsid allows HIV-1 to escape the action of the factor responsible for the early post-entry block in the marmoset B cell lines.
Result: At early times post-infection, the N74D mutant showed a reduced capacity to synthesize late RT products compared to the WT virus in the marmoset B-LCLs (Figs 6B and 7B).
Result: However, at late time points after the infection (6/7 days), when all the remaining viral DNA should be integrated, the amount of proviral DNA in the marmoset cells was higher for the N74D mutant than for the WT virus.
Result: However, the combination of the N74D<
An HIV-1 capsid binding protein TRIM11 accelerates viral uncoating.
Result: E45A mutant has been reported to increase the capsid stability, N74D resides in a conserved hydrophobic binding pocket, while P90A, G89V and G94V reside in the CypA-binding loop.
Result: Similar to wild type HIV-1, the reverse transcription levels of E45A and N74D were restricted in TRIM11-HA expressing cells while enhanced in TRIM11 knockdown cells.
KIF5B and Nup358 Cooperatively Mediate the Nuclear Import of HIV-1 during Infection.
Figure: (A) MDM or HeLa cells were synchronously infected HIV-1 GFP pseudotyped with VSV-g bearing either the wildtype (WT) CA or N74D and P90A CA mutants(MDMs MOI 0.3, HeLa MOI 0.6).Cells fixed at 3h post infection, incubated with primary antibodies to Nup358 and HIV-1 C
Figure: (A,B) Monocyte derived macrophages (MDM) and HeLa cells were synchronously infected with VSVg pseudotyped HIV-1 reporter virus (MOI 0.3 for MDM and MOI 0.6 for HeLa cells) bearing either the wildtype (WT) CA or N74D and P90A CA mutants.
Complex Interplay between HIV-1 Capsid and MX2-Independent Alpha Interferon-Induced Antiviral Factors.
Result: For instance, in MDMs pretreated with 62.5 U of IFN-alpha/ml, N74D or P90A CA mutants were inhibited ~20-fold, whereas wild-type HIV-1 GFP LV was blocked ~4-fold.
Result: HIV-1 CA mutants N74D or P90A display enhanced sensitivity to IFN-alpha-induced blocks.
Result: IFN-alpha induces an enhanced block to reverse transcription and nuclear import of HIV-1 CA N74D.
Result: In both cell types, the N74D or P90A CA mutants were inhibited more effectively by pretreatment with lower doses of IFN-alpha relative to wild-type virus.|
Identification of capsid mutations that alter the rate of HIV-1 uncoating in infected cells.
Abstract: We found that p24(CA) mutations can significantly increase (A92E), delay (E45A and N74D), or have no effect (G94D) on the rate of uncoating and that these alterations are not due to changes in reverse transcription.
Compensatory substitutions in the HIV-1 capsid reduce the fitness cost associated with resistance to a capsid-targeting small-molecule inhibitor.
Discussion: Interestingly, the N74D/A92E double mutant is resistant to CPSF6-358 restriction, suggesting that N74D mutation rescues A92E presumably by preventing CPSF6 binding.
Discussion: The N74D substitution in CA renders the virus resistant to CPSF6-358 by inhibiting binding of CPSF6-358 to the capsid.
A cyclophilin homology domain-independent role for Nup358 in HIV-1 infection.
Abstract: HIV-1, but not N74D capsid-mutant HIV-1, was markedly sensitive to TNPO3 depletion, but they infected 1-1340 segment-complemented Nup358 knockout cells equivalently.
Abstract: Human and mouse CypA both rescued HIV-1 in CypA gene-/- Jurkat cells and TRIM-Nup358Cyp fusions derived from each species were equally antiviral; each also inhibited both WT and N74D virus.
Introduction: Certain HIV-1 viral capsid mutants, such as N74D, were not impaired by Nup358 knockdown in HeLa cells and interact poorly with Nup358Cyp in vitro; however they remained puzzlingly sensitive to TRIM-Nup358Cyp.
Method: Parental and engineered cells were challenged with HIV-1luc, HIV-1luc with the N74D capsid mutation, FIVluc, and NB
HIV mutation literature information.
PMID: 
2017
Journal of virology
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