Allosteric modulation of the HIV-1 gp120-gp41 association site by adjacent gp120 variable region 1 (V1) N-glycans linked to neutralization sensitivity.
Abstract: To this end, a DSR mutant virus (K601D) with defective gp120-assoc
Result: The phenotype of T138N/K601D was an outlier as gp120-gp41 association was improved by ~2-fold with respect to K601D without a restorative effect on Env fusion function.
Result: The restoration of HIV-1AD8-K601D replication competence was observed with sequential passage of cell-free virus in independent PHA-stimulated PBMC cultures .
Result: We first confirmed that the K601D mutation promoted the shedding of gp120 into the culture supernatant of 293T cells transfected with pcDNA3.1-AD8env, as determined by radioimmunoprecipitation .
Forced virus evolution reveals functional crosstalk between the disulfide bonded region and membrane proximal ectodomain region of HIV-1 gp41.
Result: The WL/KD mutation led to > 95% of total gp120 being sloughed into the culture supernatant (Figure 1B) indicating a shedding phenotype that was more severe than those of the component single K601D and W596L mutants.
Figure: (A) Wild type and W596L/K601D-mutated HIV-1AD8 virus stocks produced by transfected 293T cells were normalized according to RT activity and used to infect U87.CD4.CCR5 cells.
Figure: (B) Infection of U87.CD4.CCR5 cells was initiated with VSV G-pseudotyped WT and W596L/K601D mutant viruses.
HIV mutation literature information.
PMID: 
2013
PLoS pathogens
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