■爱泼斯坦-巴尔病毒(EBV)感染涉及不同的临床和血清学特征。我们评估了HIV-1感染患者中EBV感染的不同血清学特征中HLAII类DRB1基因座的等位基因频率。
■我们招募了19例原发感染患者,90伴有血清学转变,467伴有EBV过去感染,HIV-1共感染在原发感染中为100%,在其他血清学特征中为约70%。EBV病毒载量通过实时PCR定量,通过流式细胞术进行T淋巴细胞定量和细胞因子水平分析,通过PCR-SSO进行HLA基因座基因分型。
■DRB1*09等位基因与原发感染有关(p:0.0477),和等位基因的携带者显示EBV病毒载量的变化(p:0.0485),CD8(+)T淋巴细胞计数(p:0.0206),双阳性T淋巴细胞计数(p:0.0093),IL-4水平(p:0.0464)和TNF水平(p:0.0161)。该等位基因在HIV共感染的个体中也很常见(p:0.0023),并且与log10HIV病毒载量(p:0.0176)和CD8()T淋巴细胞计数(p:0.0285)有关。在原发感染中,log10HIV病毒载量较高(p:0.0060),与EBV病毒载量成正比(p:0.0412).DRB1*03等位基因与血清学转变相关(p:0.0477),EBV病毒载量(p:0.0015),CD4(+)T淋巴细胞计数(p:0.0112),CD8(+)T淋巴细胞计数(p:0.0260),双阴性T淋巴细胞计数(p:0.0540),IL-4水平(p:0.0478)和IL-6水平(p:0.0175)。在血清学过渡组中,log10HIV病毒载量高(p:0.0060),但与EBV病毒载量无关(p:0.1214).过去的感染与DRB1*16等位基因有关(p:0.0477),携带者显示IgG水平(p:0.0020),CD4(+)T淋巴细胞计数(p:0.0116)和提示CD8(+)T计数改变(p:0.0602)。DRB01*16等位基因在既往EBV感染的HIV-1患者中也很常见(p:0.0192);然而,等位基因与HIV-1感染的临床标志物无关.
■我们的结果表明,HLAII类等位基因可能与合并感染HIV-1的患者对EB病毒感染的免疫反应的血清学特征的调节有关。
UNASSIGNED: Epstein-Barr virus (EBV) infection involves distinct clinical and serological profiles. We evaluated the frequency of alleles of locus DRB1 of HLA class II in different serological profiles of EBV infection among HIV-1 infected patients.
UNASSIGNED: We recruited 19 patients with primary infection, 90 with serological transition and 467 with past infection by EBV, HIV-1 co-infection was 100% in primary infection and approximately 70% in other serological profiles. EBV viral load was quantified by real-time PCR, T lymphocyte quantification and cytokine level analysis were performed by flow cytometry, and HLA locus genotyping was performed by PCR-SSO.
UNASSIGNED: The DRB1*09 allele was associated with primary infection (p: 0.0477), and carriers of the allele showed changes in EBV viral load (p: 0.0485), CD8(+) T lymphocyte counts (p: 0.0206), double-positive T lymphocyte counts (p: 0.0093), IL-4 levels (p: 0.0464) and TNF levels (p: 0.0161). This allele was also frequent in HIV-coinfected individuals (p: 0.0023) and was related to the log10 HIV viral load (p: 0.0176) and CD8(+) T lymphocyte count (p: 0.0285). In primary infection, the log10 HIV viral load was high (p: 0.0060) and directly proportional to the EBV viral load (p: 0.0412). The DRB1*03 allele correlated with serological transition (p: 0.0477), EBV viral load (p: 0.0015), CD4(+) T lymphocyte count (p: 0.0112), CD8(+) T lymphocyte count (p: 0.0260), double-negative T lymphocyte count (p: 0.0540), IL-4 levels (p: 0.0478) and IL-6 levels (p: 0.0175). In the serological transition group, the log10 HIV viral load was high (p: 0.0060), but it was not associated with the EBV viral load (p: 0.1214). Past infection was related to the DRB1*16 allele (p: 0.0477), with carriers displaying IgG levels (p: 0.0020), CD4(+) T lymphocyte counts (p: 0.0116) and suggestive CD8(+) T count alterations (p: 0.0602). The DRB01*16 allele was also common in HIV-1 patients with past EBV infection (p: 0.0192); however, the allele was not associated with clinical markers of HIV-1 infection.
UNASSIGNED: Our results suggest that HLA class II alleles may be associated with the modulation of the serological profiles of the immune response to Epstein-Barr virus infection in patients coinfected with HIV-1.