Division of Adolescent and Transition Medicine Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave, MLC 4000, Cincinnati, OH, 45229, United States; University of Cincinnati College of Medicine, CARE/Crawley Building, Suite E-870, 3230 Eden Avenue, Cincinnati, OH, 45267, United States.
Westat, 1600 Research Boulevard, Rockville, MD, 20850, United States.
J Clin Virol. 2018 May;102:7-11. doi: 10.1016/j.jcv.2018.02.001. Epub 2018 Feb 7.
Human immunodeficiency virus (HIV) infection is associated with chronic immune activation, and concurrent sexually transmitted infections (STIs) may increase immune activation.
Because HIV-infected youth are at high risk of STIs and little is known about the impact of STIs on immune activation in HIV-infected youth, we conducted an exploratory study examining the association between STIs and systemic inflammation and immune activation among HIV-infected adolescents.
Forty-nine behaviorally infected U.S. youth ages 18-24 years with baseline CD4 T-cells >350 who maintained viral suppression on therapy by week 48 were included. Evaluation for STIs (herpes simplex virus [HSV], Chlamydia trachomatis, syphilis, Neisseria gonorrhoeae) was conducted as standard of care and reported on case report forms. Measures of T-cell subsets, systemic immune activation, and soluble factors were examined at week 48 for differences between participants with an STI diagnosis during the 48 weeks compared to those without an STI.
Forty-three participants (88%) were male; 57% had baseline CD4+ T-cell counts >500 cells/mm. Eighteen youth were reported to have ≥1 STI. At week 48, participants with STIs demonstrated lower CD4 T-cell counts (any STI vs. no STI, p = 0.024; HSV vs. no STI, p = 0.022) and evidence of increased systemic immune activation, including higher CD57 intensity, higher HLA-DR intensity, and lower CD28 percentage, when compared to those without STIs. There were no differences in soluble factors between STI groups.
Results indicate novel activation of CD4 T-cells among HIV-infected youth who have STIs other than HSV, which may contribute to disease progression.
人类免疫缺陷病毒(HIV)感染与慢性免疫激活有关,同时发生的性传播感染(STI)可能会增加免疫激活。
由于感染 HIV 的青年面临高风险的 STI,并且对于 STI 在 HIV 感染青年中的免疫激活的影响知之甚少,因此我们进行了一项探索性研究,以检查 STI 与系统性炎症和 HIV 感染青少年中的免疫激活之间的关联。
本研究纳入了 49 名行为感染的美国青年,年龄在 18-24 岁之间,基线 CD4 T 细胞>350,在第 48 周时通过治疗实现病毒抑制。作为标准护理,对 STI(单纯疱疹病毒[HSV]、沙眼衣原体、梅毒、淋病奈瑟菌)进行评估,并在病例报告表上报告。在第 48 周时,检查 T 细胞亚群、全身免疫激活和可溶性因子的指标,以比较在 48 周期间患有 STI 诊断的参与者与没有 STI 的参与者之间的差异。
43 名参与者(88%)为男性;57%的参与者基线 CD4+ T 细胞计数>500 个细胞/mm。有 18 名青年报告患有≥1 种 STI。在第 48 周时,患有 STI 的参与者的 CD4 T 细胞计数较低(任何 STI 与无 STI,p=0.024;HSV 与无 STI,p=0.022),并且存在全身免疫激活的证据,包括 CD57 强度更高、HLA-DR 强度更高和 CD28 百分比更低,与没有 STI 的参与者相比。在 STI 组之间,可溶性因子没有差异。
结果表明,除 HSV 之外,HIV 感染青年中存在新的 CD4 T 细胞激活,这可能导致疾病进展。