Ondondo Beatrice O, Rowland-Jones Sarah L, Dorrell Lucy, Peterson Kevin, Cotten Matthew, Whittle Hilton, Jaye Assan
MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK.
Eur J Immunol. 2008 Dec;38(12):3549-60. doi: 10.1002/eji.200838759.
Majority of HIV-2-infected individuals meet the criteria of long-term non-progressors. This has been linked to superior qualitative HIV-2-specific cellular immune responses that correlate with viral control. However, it is unknown whether this is due to frequent targeting of immunodominant Gag epitopes in HIV-2 than HIV-1 infection. We describe a comprehensive comparison of the magnitude, breadth and frequency of Gag responses and the degree of cross-recognition of frequently targeted, immunodominant Gag peptides in a cross-sectional study of asymptomatic HIV-1- and HIV-2-infected individuals. Fresh PBMC from 20 HIV-1- and 20 HIV-2-infected patients with similar CD4(+) T-cell counts (p=0.36) were stimulated with pools of HIV-1 and/or HIV-2 Gag peptides in an IFN-gamma ELISPOT assay. We found no difference in the cumulative magnitude of IFN-gamma responses (p=0.75) despite significantly lower plasma viral loads in HIV-2-infected people (p<0.0001). However, Gag211-290 was targeted with significantly higher magnitude in HIV-2-infected subjects (p=0.03) although this did not correlate with viral control. There was no difference in frequently targeted Gag peptides, the breadth, immunodominance or cross-recognition of Gag peptide pools between the two infections. This suggests that other factors may control viral replication in HIV-2 infection.
大多数感染HIV-2的个体符合长期不进展者的标准。这与卓越的HIV-2特异性细胞免疫反应质量有关,这种反应与病毒控制相关。然而,尚不清楚这是否是由于与HIV-1感染相比,HIV-2中免疫显性Gag表位的靶向频率更高。我们在一项针对无症状HIV-1和HIV-2感染个体的横断面研究中,描述了Gag反应的强度、广度和频率以及常见靶向免疫显性Gag肽的交叉识别程度的全面比较。在IFN-γ ELISPOT试验中,用HIV-1和/或HIV-2 Gag肽池刺激来自20名HIV-1感染患者和20名HIV-2感染患者且CD4(+) T细胞计数相似(p = 0.36)的新鲜外周血单核细胞。我们发现,尽管HIV-2感染者的血浆病毒载量显著更低(p < 0.0001),但IFN-γ反应的累积强度并无差异(p = 0.75)。然而,在HIV-2感染受试者中,Gag211 - 290的靶向强度显著更高(p = 0.03),尽管这与病毒控制无关。两种感染之间在常见靶向Gag肽、Gag肽池的广度、免疫显性或交叉识别方面没有差异。这表明其他因素可能控制HIV-2感染中的病毒复制。