Consistent patterns in the development and immunodominance of human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses following acute HIV-1 infection - PubMed (original) (raw)
Consistent patterns in the development and immunodominance of human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses following acute HIV-1 infection
Xu G Yu et al. J Virol. 2002 Sep.
Abstract
Human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T-cell responses generated during acute infection play a critical role in the initial control of viremia. However, little is known about the viral T-cell epitopes targeted during acute infection or about their hierarchy in appearance and relative immunodominance over time. In this study, HIV-1-specific CD8+ T-cell responses in 18 acutely infected individuals expressing HLA-A3 and/or -B7 were characterized. Detailed analysis of CD8 responses in one such person who underwent treatment of acute infection followed by reexposure to HIV-1 through supervised treatment interruptions (STI) revealed recognition of only two cytotoxic T-lymphocyte (CTL) epitopes during symptomatic acute infection. HIV-1-specific CD8+ T-cell responses broadened significantly during subsequent exposure to the virus, ultimately targeting 27 distinct CTL epitopes, including 15 different CTL epitopes restricted by a single HLA class I allele (HLA-A3). The same few peptides were consistently targeted in an additional 17 persons expressing HLA-A3 and/or -B7 during acute infection. These studies demonstrate a consistent pattern in the development of epitope-specific responses restricted by a single HLA allele during acute HIV-1 infection, as well as persistence of the initial pattern of immunodominance during subsequent STI. In addition, they demonstrate that HIV-1-specific CD8+ T-cell responses can ultimately target a previously unexpected and unprecedented number of epitopes in a single infected individual, even though these are not detectable during the initial exposure to virus. These studies have important implications for vaccine design and evaluation.
Figures
FIG. 1.
Viral loads (HIV-1 RNA copies per ml of plasma) in study subject AC-06 during the 34-month study period are shown on a logarithmic scale. Shading represents periods on HAART. The number of regions targeted by CD8+ T cells in AC-06 is given below the graph.
FIG. 2.
HIV-1-specific CD8+ T-cell responses to overlapping peptides in subject AC-06. The amino acid sequences and locations within HIV-1 proteins of all overlapping peptides targeted by virus-specific CD8+ T lymphocytes in subject AC-06 are shown. A total of 25 different regions within HIV-1 were targeted by CD8+ T cells.
FIG. 3.
Characterization of HLA-A3- and HLA-B7-restricted optimal HIV-1-specific CTL epitopes in subject AC-06. Graphs show the HLA class I restriction (left panels) and optimal amino acid sequences (right panels) of two novel HLA-A3-restricted CTL epitopes (A) and two novel HLA-B7-restricted CTL epitopes (B). HLA restriction was determined using peptides presented by autologous and partially HLA matched BCL in a 51Cr release assay. Solid bars, percent specific lysis of target cells pulsed with peptide; hatched bars, percent specific lysis of control target cells pulsed with no peptide. Fine mapping of the optimal epitope was done using serial dilutions of truncated peptides in an IFN-γ ELISPOT assay, and results are given as SFC per 106 PBMC.
FIG. 4.
Longitudinal evolution of the magnitude and breadth of HIV-1-specific CD8+ T-cell responses on the single-epitope level during treated acute infection and STI in subject AC-06. The magnitudes of CD8+ T-cell responses (given as SFC/106 PBMC) directed against the HIV-1 proteins Gag, Pol, and Env, as well as against the accessory HIV-1 proteins (Vif, Vpr, and Vpu) and the regulatory HIV-1 proteins (Rev and Tat), in subject AC-06 during the 34-month study period are shown. The number of CTL epitopes targeted within each HIV-1 protein or protein group is indicated above each bar. The periods on treatment (HAART) are indicated above the graph; the time after infection and the total number of CTL epitopes targeted at each time point are shown below the graph. Only two CTL epitopes, one in HIV-1 Gag and one in HIV-1 Env, were targeted during acute infection, but virus-specific CD8+ T-cell responses targeted a total of 27 different CTL epitopes at the end of the second STI.
FIG. 5.
Quantification of the contributions of HLA-A3-restricted and HLA-B7- or -Cw7-restricted CD8+ T-cell responses to total HIV-1-specific CD8+ T-cell responses in subject AC-06. PBMC of AC-06 were incubated with autologous BCL pulsed with either the HLA-B7-restricted immunodominant p24 Gag epitope GPGHKARVL (B), all 27 targeted optimal CTL epitopes (C), the 12 HLA-B7- or -Cw7-restricted optimal CTL epitopes (D), or the 15 HLA-A3-restricted optimal CTL epitopes (E) recognized by AC-06. BCL pulsed without peptide were used as negative controls (A). Percentages of peptide-specific IFN-γ-producing CD8+ T cells after subtraction of background activity are given in the individual plots.
FIG. 6.
Frequency of recognition of optimal CTL epitopes during acute HIV-1 infection and after STI. (A) Percentages of individuals expressing HLA-A3 (n = 14) who recognize the individual HLA-A3-restricted optimal CTL epitopes 1 to 15 during acute HIV-1 infection (solid bars) and after 12 months of treatment with HAART (hatched bars). (B) Percentages of individuals expressing HLA-A3 (n = 7) who recognize the individual HLA-A3-restricted optimal CTL epitopes 1 to 15 following STI. (C) Percentages of individuals expressing HLA-B7 (n = 11) who recognize the individual HLA-B7-restricted optimal CTL epitopes 1 to 15 during acute HIV-1 infection (solid bars) and after 12 months of treatment with HAART (hatched bars). (D) Percentages of individuals expressing HLA-B7 (n = 7) who recognize the individual HLA-B7-restricted optimal CTL epitopes 1 to 15 following STI. The amino acid sequences and corresponding HIV-1 proteins for the CTL epitopes tested are given at the bottom of the figure.
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