title: Multiple T-cell responses are associated with better control of acute HIV-1 infection: An observational study.
abstract: Cytotoxic T lymphocyte (CTL) responses play pivotal roles in controlling the replication of human immunodeficiency virus type 1 (HIV-1), but the correlation between CTL responses and the progression of HIV-1 infection are controversial on account of HIV immune escape mutations driven by CTL pressure were reported.The acute HIV-1-infected patients from Beijing were incorporated into our study to investigate the effects of CTL response on the progression of HIV-1 infection.A longitudinal study was performed on acute HIV-1-infected patients to clarify the kinetic of T-cell responses, the dynamic of escape mutations, as well as the correlation between effective T-cell response and the progression of HIV infection.Seven human leukocyte antigen-B51+ (HLA-B51+) individuals were screened from 105 acute HIV-1 infectors. The detailed kinetic of HLA-B51-restricted CTL responses was described through blood sampling time points including seroconversion, 3 and 6 months after HIV-1 infection in the 7 HLA-B51+ individuals, by using 16 known HLA-B51 restricted epitopes. Pol743-751 (LPPVVAKEI, LI9), Pol283-289 (TAFTIPSI, TI8), and Gag327-3459 (NANPDCKTI, NI9) were identified as 3 dominant epitopes, and ranked as starting with LI9, followed by TI8 and NI9 in the ability to induce T-cell responses. The dynamics of escape mutations in the 3 epitopes were also found with the same order as T-cell response, by using sequencing for viral clones on blood sampling at seroconversion, 3 and 6 months after HIV-1 infection.We use solid evidence to demonstrate the correlation between T-cell response and HIV-1 mutation, and postulate that multiple T-cell responses might benefit the control of HIV-1 infection, especially in acute infection phase.
authors.affiliation: Beijing You'An Hospital, Capital Medical University, Beijing, PR China Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford University, Oxford, UK.
authors.forename: Jianping
authors.initials: J
authors.lastname: Sun
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Yanchun
authors.initials: Y
authors.lastname: Peng
authors.forename: Zhen
authors.initials: Z
authors.lastname: Han
authors.forename: Guihai
authors.initials: G
authors.lastname: Liu
authors.forename: Ling
authors.initials: L
authors.lastname: Qin
authors.forename: Sai
authors.initials: S
authors.lastname: Liu
authors.forename: Huanhuan
authors.initials: H
authors.lastname: Sun
authors.forename: Hao
authors.initials: H
authors.lastname: Wu
authors.forename: Tao
authors.initials: T
authors.lastname: Dong
authors.forename: Yonghong
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000208:Acute Disease; D000328:Adult; D018450:Disease Progression; D058501:Enzyme-Linked Immunospot Assay; D015658:HIV Infections / Q000276:immunology* / Q000821:virology; D006679:HIV Seropositivity / Q000235:genetics / Q000276:immunology; D015497:HIV-1 / Q000235:genetics* / Q000276:immunology*; D059949:HLA-B51 Antigen / Q000276:immunology; D018451:Homosexuality, Male; D006801:Humans; D057131:Immune Evasion / Q000235:genetics / Q000276:immunology; D008297:Male; D013601:T-Lymphocytes / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014779:Virus Replication / Q000235:genetics / Q000276:immunology
chemical_list: D059949:HLA-B51 Antigen