Introduction: In an in vitro uncoating assay, the P38A mutation rendered the HIV CA core unstable, but the E45A mutation resulted in a hyperstable core.
Introduction: found that introducing the T216I and R132T suppressor mutations in HIV CA restored infectivity to both the P38A and the E45A mutant viruses.
Result: The P38A and Q63A+Q67A CA-mutant viruses are reported to have unstable cores, while the E45A and E128A+R132A mutations resulted in great
Second-site suppressors of HIV-1 capsid mutations: restoration of intracellular activities without correction of intrinsic capsid stability defects.
Figure: Amide chemical shift differences between the wild type and E45A, E45A/R132T and P38A mutant CA<
Discussion: Alternatively, the E45A mutation might affect the network of water-mediated hydrogen bonds observed at the NTD-NTD interface in the X-ray crystal structure, with R132T mutation partially restoring the H-bonding network.
Discussion: Our observation that R132T rescues the impaired ability of E45A mutant particles to infect arrested cells confirms that the ability of lentiviruses to infect nondividing cells is dependent on a function of the viral capsid, and suggests that this is linked to the mechanism or timing of uncoating.
Direct visualization of HIV-1 with correlative live-cell microscopy and cryo-electron tomography.
Abstract: We further obtained direct evidence to suggest that a hyperstable mutant capsid, E45A, showed delayed capsid disassembly compared to the wild-type capsid.
Introduction: Using a hyperstable capsid mutant, E45A, we further show intact HIV-1 cores released into the cytoplasm after membrane fusion.
Method: Wild-type and E45A HIV-1 particles were produced by transfecting 293T cells with three plasmids: pL-VSV-G (a kind gift from M.
Result: HIV-1 capsid mutation E45A delays capsid disassembly in HeLa cells.
Result: Microtubules were also observed in half of the E45
Rhesus TRIM5alpha disrupts the HIV-1 capsid at the inter-hexamer interfaces.
Result: Several CA mutants, including A92E, which was used in our previous structural study, and the E45A mutant, which produces hyperstable capsids, were analyzed.
Result: The CA tubular assemblies carrying the capsid-stabilizing E45A mutation also experienced structural damage by TRIM5alpharh, but to a lesser degree.
Interplay between HIV entry and transportin-SR2 dependency.
Discussion: Altered requirements of VSV-G pseudotyped HIV-1 Q63A/Q67A, E45A and N74D CA mutants for certain Nups, compared to wild type virus, were indeed demonstrated.
Result: E45A HIV-1 infection was reduced 275-fold relative to dividing cells expressing mCPSF6-358, and Q63A/Q67A HIV-1 infection was decreased nearly 230-fold compared to cycling counterparts (Figure 6G).
Result: E45A or Q63A/Q67A mutation of CA impairs HIV-1 infection of cell-cycle arrested cells.
Result: Consistent with past reports, both E45A and Q63A/Q67A HIV-1 were impaired approximately 30-fold and 15-fold, respectively, in the infection of aphidicolin-treated control HeLa cells (Figure 6G).
Result: In marked contrast to N74D HIV-1, mCPSF6-358 expression in the growth arrested HeLa cells
Investigation of N-terminal domain charged residues on the assembly and stability of HIV-1 CA.
Abstract: Previous in vivo experiments generated two N-terminal domain charge change mutants (E45A and E128A/R132A) that showed an increase in stability of the viral core.
Abstract: We constructed a number of charge mutants in this region (E45A, E45K, E128A, R132A, E128A/R132A, K131A, and K131E) and evaluated their effect on protein stability in addition to their effect on the rate of CA assembly.
HIV mutation literature information.
PMID: 
2013
Virology
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