A longitudinal analysis of immune escapes from HLA-B*13-restricted T-cell responses at early stage of CRF01_AE subtype HIV-1 infection and implications for vaccine design.
Discussion: Some mutations within epitopes have been reported to reduce viral replication capacity, such as R264K within the B*27-restricted KK10 epitope and T242N within the B*57-restricted TW10 epitope.
HIV-1 Gag mutations alone are sufficient to reduce darunavir susceptibility during virological failure to boosted PI therapy.
PMID: 32556165
2020
The Journal of antimicrobial chemotherapy
Table: T242N
A strongly selected mutation in the HIV-1 genome is independent of T cell responses and neutralizing antibodies.
Conclusion: We have previously found that three other reversion mutations (V247I and T242N in Gag as well as I64T in Tat) also did not cause detectable fitness differences.
Changes in HIV-1 Capsid Stability Induced by Common Cytotoxic-T-Lymphocyte-Driven Viral Sequence Mutations.
Abstract: The frequently occurring HLA-B57- and HLA-B27-associated CTL escape mutations T242N and R264K resulted in delayed capsid uncoating, suggesting modulation of capsid stability.
"Frequencies of Gag-restricted T-cell escape ""footprints"" differ across HIV-1 clades A1 and D chronically infected Ugandans irrespective of host HLA B alleles."
Introduction: Reversion of the transmitted T242N to wild-type sequence implies that this mutation affects virus fitness.
Introduction: The TW10 response dominates in acute HIV infection of HLA B*57 and B*5801 subjects yielding T242N mutations that are associated with lower viral loads over time.
Preexisting compensatory amino acids compromise fitness costs of a HIV-1 T cell escape mutation.
Abstract: Analysis of the global circulating HIV-1 sequences in the Los Alamos HIV Sequence Database showed a high prevalence of compensatory amino acids for the T242N mutation and other T cell escape mutations.
Abstract: BACKGROUND: Fitness costs and slower disease progression are associated with a cytolytic T lymphocyte (CTL) escape mutation T242N in Gag in HIV-1-infected individuals carrying HLA-B*57/5801 alleles.
Abstract: However, the impact of different context in diverse HIV-1 strains on the fitness costs due to the T242N mutation has not been well characterized.
Abstract: Moreover, the transmitted T242N escape mutant in subject CH131 was as fit as the revertant N242T mutant and the elimination of the compensat
Reversion and T cell escape mutations compensate the fitness loss of a CD8+ T cell escape mutant in their cognate transmitted/founder virus.
Discussion: However, how it interacted with the T242N mutation and affected the viral fitness with or without the T242N mutation has not been studied.
Discussion: The T242N mutation that alone could cause significant fitness loss was selected by a late potent T cell response targeting the TW10 epitope.
Discussion: The reversion mutation Discussion: We studied the impact of reversion and T cell escape mutations in their unmodified cognate T/F viral genome and found that reversion mutations did not cause measurable fitness gains in the cognate T/F virus but could compensate the fitness loss caused by the CD8+ T cell escape mutation T242N, and, unexpectedly, weak CD8+ T cell escape mutations could also partially compensate the fitness loss caused by the T242N mutation in the same epitope.
Gag sequence variation in a human immunodeficiency virus type 1 transmission cluster influences viral replication fitness.
PMID: 23136365
2013
The Journal of general virology
Abstract: Viral gag sequences from all three patients contained a mutation at position 242, T242N or T242S, which have been associated with lower virus replication in vitro.
HIV-1 replication fitness of HLA-B*57/58:01 CTL escape variants is restored by the accumulation of compensatory mutations in gag.
Abstract: Escape mutations in CTL epitopes restricted by these HLA alleles come at a fitness cost and particularly the T242N mutation in the TW10 CTL epitope in Gag has been demonstrated to decrease the viral replication capacity.
Introduction: Additional mutations within or flanking the TW10 epitope can have a compensatory effect and partially restore the fitness cost associated with the T242N mutation.
Introduction: The T242N escape mutation in the HLA-B*57/58:01 restricted TW10 epitope in Gag impairs viral replication, which can explain the protective effect of this HLA type even after escape from CTL responses has occurred.
Result: Among these HLA-B*57/58:01 specific amino acid mutations were the HLA-B*57/58:01 associated CTL escape mutations T242N and
Impact of immune escape mutations on HIV-1 fitness in the context of the cognate transmitted/founder genome.
Abstract: A principal TW10 escape mutation, T242N, led to a 42% reduction in replication fitness but V247I and G248A mutations in the same epitope restored fitness to wild-type levels.
Method: The gag amplicon was amplified by the primers A1-lower: 5' Acry-AGGGGTCGTTGCCAAAGAGTGA-3' (nt 2260-2281) and A1-upper: 5'-CACAGGAACAAGCAGCCAGGTC-3', and the amplicons were annealed with the sequencing primer C1548A: 5'-AAGGGGAAGTGATATAGCAGGATCTACTAGTA-3' (nt 1482-1513) to detect the T242N mutation or G1562A: 5'-TATAGCAGGATCTACTAGTACCCTTCAGGAACAA-3' (nt 1494-1527) to detect the V247I mutation.
Result: Analysis of the data using this new model showed that T242N was 42% less fit
HIV mutation literature information.
PMID: 
2022
BMC immunology
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