Different Effects of Nonnucleoside Reverse Transcriptase Inhibitor Resistance Mutations on Cytotoxic T Lymphocyte Recognition between HIV-1 Subtype B and Subtype A/E Infections

Kuse, Nozomi; Rahman, Mohammad Arif; Murakoshi, Hayato; Tran, Giang Van; Chikata, Takayuki; Koyanagi, Madoka; Nguyen, Kinh Van; Gatanaga, Hiroyuki; Oka, Shinichi; Takiguchi, Masafumi

doi:10.1128/jvi.00974-15

Cited by 5 publications

(4 citation statements)

References 49 publications

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“…C1R cells expressing HLA-B*52:01 (C1R-B5201) and HLA-C*12:02 (C1R-C1202), and 721.221 cells expressing CD4 and HLA-C*12:02 (721.221-CD4-C1202) were previously generated [ 33 , 54 ]. These cells were cultured in RPMI-1640 medium (Invitrogen) containing with 5–10% fetal bovine serum (R5-R10) and 0.15 mg/ml hygromycin B. RMA-S-C1202 cells, a TAP deficient mouse-derived cell line that expresses HLA-C*12:02, were previously generated and cultured in R10 containing 0.15 mg/ml hygromycin B [ 55 ]. MAGIC-5 cells (CCR5-transfected HeLa-CD4/LTR-β-gal cells) were cultured in R10 as described previously [ 56 ].…”

Section: Methodsmentioning

confidence: 99%

T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics

et al. 2020

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HIV-1 strains harboring immune escape mutations can persist in circulation, but the impact of selection by multiple HLA alleles on population HIV-1 dynamics remains unclear. In Japan, HIV-1 Reverse Transcriptase codon 135 (RT135) is under strong immune pressure by HLA-B*51:01-restricted and HLA-B*52:01-restricted T cells that target a key epitope in this region (TI8; spanning RT codons 128–135). Major population-level shifts have occurred at HIV-1 RT135 during the Japanese epidemic, which first affected hemophiliacs (via imported contaminated blood products) and subsequently non-hemophiliacs (via domestic transmission). Specifically, threonine accumulated at RT135 (RT135T) in hemophiliac and non-hemophiliac HLA-B*51:01+ individuals diagnosed before 1997, but since then RT135T has markedly declined while RT135L has increased among non-hemophiliac individuals. We demonstrated that RT135V selection by HLA-B*52:01-restricted TI8-specific T-cells led to the creation of a new HLA-C*12:02-restricted epitope TN9-8V. We further showed that TN9-8V-specific HLA-C*12:02-restricted T cells selected RT135L while TN9-8T-specific HLA-C*12:02-restricted T cells suppressed replication of the RT135T variant. Thus, population-level accumulation of the RT135L mutation over time in Japan can be explained by initial targeting of the TI8 epitope by HLA-B*52:01-restricted T-cells, followed by targeting of the resulting escape mutant by HLA-C*12:02-restricted T-cells. We further demonstrate that this phenomenon is particular to Japan, where the HLA-B*52:01-C*12:02 haplotype is common: RT135L did not accumulate over a 15-year longitudinal analysis of HIV sequences in British Columbia, Canada, where this haplotype is rare. Together, our observations reveal that T-cell responses to sequentially emerging viral escape mutants can shape long-term HIV-1 population dynamics in a host population-specific manner.

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Section: Methodsmentioning

confidence: 99%

T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics

et al. 2020

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“…These cells express the same level of HLA-C14 on the cell surface. RMA-S-C1202 cells were generated in our lab as previously described (Kuse et al, 2015). RMA-S-C1402 and -C1403 cell lines were generated by the transfection of HLA-C*14:02 and -C*14:03 genes into RMA-S cell lines, respectively.…”

Section: Methodsmentioning

confidence: 99%

HIV-1 Control by NK Cells via Reduced Interaction between KIR2DL2 and HLA-C∗12:02/C∗14:03

et al. 2016

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SUMMARY Natural killer (NK) cells control viral infection in part through the interaction between killer cell immunoglobulin-like receptors (KIRs) and their HLA ligands. We investigated 504 ART-free Japanese patients chronically infected with HIV-1 and identified two KIR/HLA combinations, KIR2DL2/HLA-C*12:02 and KIR2DL2/HLA-C*14:03, that impact suppression of HIV-1 replication. KIR2DL2+ NK cells suppressed viral replication in HLA-C*14:03+ or HLA-C*12:02+ cells to a significantly greater extent than did KIR2DL2− NK cells in vitro. Functional analysis showed that the binding between HIV-1-derived peptide and HLA-C*14:03 or HLA-C*12:02 influenced KIR2DL2+NK cell activity through reduced expression of the peptide-HLA (pHLA) complex on the cell surface (i.e. reduced KIR2DL2 ligand expression), rather than through reduced binding affinity of KIR2DL2 to the respective pHLA complexes. Thus, KIR2DL2/HLA-C*12:02 and KIR2DL2/HLA-C*14:03 compound genotypes have protective effects on control of HIV-1 through a mechanism involving KIR2DL2-mediated NK cell recognition of virus-infected cells, providing additional understanding of NK cells in HIV-1 infection.

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“…The current study definitively demonstrated that PolTY9 is an HLA-B*15:02-restricted epitope in subtype A/E infection. Out of 17 reported best-defined epitopes derived from the subtype A/E virus (Los Alamos HIV-1 database [ https://www.hiv.lanl.gov ]), 5 epitopes only were analyzed to examine their presentation by cells infected with HIV-1 subtype A/E in our previous studies ( 42 – 44 ). In this study, we demonstrated that T cells specific for HLA-B*15:02-restricted epitopes recognized cells infected with an HIV-1 subtype A/E clone established from an individual in our Hanoi cohort.…”

Section: Discussionmentioning

confidence: 99%

Control of HIV-1 Replication by CD8 ⁺ T Cells Specific for Two Novel Pol Protective Epitopes in HIV-1 Subtype A/E Infection

Nguyen

Kuse

Murakoshi

et al. 2022

J Virol

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Different Effects of Nonnucleoside Reverse Transcriptase Inhibitor Resistance Mutations on Cytotoxic T Lymphocyte Recognition between HIV-1 Subtype B and Subtype A/E Infections

Cited by 5 publications

References 49 publications

T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics

T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics

HIV-1 Control by NK Cells via Reduced Interaction between KIR2DL2 and HLA-C∗12:02/C∗14:03

Control of HIV-1 Replication by CD8 ⁺ T Cells Specific for Two Novel Pol Protective Epitopes in HIV-1 Subtype A/E Infection

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Different Effects of Nonnucleoside Reverse Transcriptase Inhibitor Resistance Mutations on Cytotoxic T Lymphocyte Recognition between HIV-1 Subtype B and Subtype A/E Infections

Cited by 5 publications

References 49 publications

T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics

T-cell responses to sequentially emerging viral escape mutants shape long-term HIV-1 population dynamics

HIV-1 Control by NK Cells via Reduced Interaction between KIR2DL2 and HLA-C∗12:02/C∗14:03

Control of HIV-1 Replication by CD8 + T Cells Specific for Two Novel Pol Protective Epitopes in HIV-1 Subtype A/E Infection

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Control of HIV-1 Replication by CD8 ⁺ T Cells Specific for Two Novel Pol Protective Epitopes in HIV-1 Subtype A/E Infection