Discussion: A similar mechanism was reported based on the study of the subtype B virus-infected Japanese individuals having a detrimental allele HLA-B*35:01, which study showed that the Nef Y135F mutation selected by HLA-A*24:02-restricted T cells impaired the TCR recognition and viral suppression ability of YF9-specific T cells restricted by HLA-B*35:01.
[Analysis of HIV-1 (Human immunodeficiency virus-1, Lentivirus, Orthoretrovirinae, Retroviridae) Nef protein polymorphism of variants circulating in the former USSR countries.]
Abstract: RESULTS AND DISCUSSION: The existence of noticeable differences in the prevalence of Nef natural polymorphisms (A32P, E38D, I43V, A54D, Q104K, H116N, Y120F, Y143F, V168M, H192T, V194R, R35Q, D108E, Y135F, E155K, E182M, R184K and F191L), some of which are characteristic mutations for variant A6, was shown.
Impact of a single HLA-A*24:02-associated escape mutation on the detrimental effect of HLA-B*35:01 in HIV-1 control.
Abstract: However, the accumulation of an Y135F mutation in NefYF9 out of the 4 epitopes, which is selected by HLA-A*24:02-restricted T cells, affected the ability of YF9-specific T cells to suppress HIV-1 replication.
Abstract: INTERPRETATION: These findings indicate that the Y135F mutation is a key factor underlying the detrimental effect of HLA-B*35:01 on disease outcomes in HIV-1 clade B-infected individuals.
Abstract: YF9-specific T cells failed to suppress replication of the Y135F mutant in vitro.
Introduction: Only Y135F mutation within NefYF9 out of the 4 epitopes, which selected by HLA-A*24:02-restircted T cells, impaired an ability of YF9-specific T cells to suppress HIV-1 replication in vivo and in vitro.
Result: 3d), indicating that the emergence of the Y135F mutant impairs the ab
Rapid HIV-1 Disease Progression in Individuals Infected with a Virus Adapted to Its Host Population.
Abstract: Here, we combine genetic and immunological analyses to identify A*24:02-positive individuals likely to have been infected with Y135F-containing HIV-1.
Abstract: Japan's population features limited HLA diversity which is driving population-level HIV adaptation: for example, >60% of Japanese express HLA-A*24:02 and its associated Nef-Y135F escape mutation represents the population consensus.
Introduction: Furthermore, the presence of Y135F in the infecting HIV-1 strain may signal the presence of other unknown A*24:02-associated escape mutations in other viral epitopes that might also compromise CTL responses to the incoming HIV strain.
Introduction: If this were the case, infection of A*24:02-expressing persons (representing the majority of Japanese individuals) by Y135F-containing HIV-1 (rep
Switching and emergence of CTL epitopes in HIV-1 infection.
Abstract: An escape mutation from tyrosine to phenylalanine at the 135th amino acid (Y135F) of the HIV-1 nef gene is frequently observed in patients with HLA-A*24:02, an HLA Class I allele expressed in ~70% of Japanese persons.
Abstract: Critically, the selection of Y135F also launched the expression of Nef126-10, indicating that the latter epitope is created as a result of escape within the former.
Abstract: Moreover, experiments utilizing antigen specific CTL clones to recognize endogenously-expressed peptides with or without Y135F indicated that this mutation disrupted the antigen expression of Nef134-10.
Abstract: The robust targeting of Nef126-10 following transmission (or in vivo selection) of HIV-1 containing PMID: 24192765
2013
Scientific reports
Abstract: Y135F has been reported as a processing mutant but CTL carrying structurally adequate TCR can be found in the patients.
Abstract: Y135F was an early-appearing major mutation, while F139L was a late-appearing mutation which was selected in the patients without Y135F.
Abstract: Although Y135F mutation disrupted the hydrogen bond to HLA-A*2402 His70, newly formed hydrogen bond between T138 and His70 kept the conformation of the epitope in the reconstituted pMHC.
Abstract: TCR from Y135F- or dually-specific CTL had unique mode of binding to the mutant epitope.
Introduction: At a very early phase of primary HIV-1 infection, a Tyr-to-Phe mutation at the 2nd position of the Nef
Immune selection in vitro reveals human immunodeficiency virus type 1 Nef sequence motifs important for its immune evasion function in vivo.
Abstract: Functional testing of naturally occurring in vivo polymorphisms at the 7 sites with no previously known functional role revealed 3 mutations (A84D, Y135F, and G140R) that ablated MHC-I downregulation and 3 (N52A, S169I, and V180E) that partially impaired MHC-I downregulation.
HIV mutation literature information.
PMID: 
2021
AIDS (London, England)
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