Vishwanathan Sundaram Ajay, Aubert Rachael D, Morris Monica R, Zhao Chunxia, Philips Christi, Khalil George M, Deyounks Frank, Kelley Kristen, Ritter Jana M, Chen C Y, Kersh Ellen N, McNicholl Janet M
From the *Division of HIV/AIDS Prevention, Centers for Disease Control and Prevention; †Libra Management Group, ‡Division of Sexually Transmitted Disease Prevention, Centers for Disease Control and Prevention, Atlanta, GA; §The DESA group, Columbia, SC; and ¶Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA.
Sex Transm Dis. 2017 Sep;44(9):551-556. doi: 10.1097/OLQ.0000000000000644.
Sustained genital tract inflammation caused by sexually transmitted infections (STIs) is known to increase risk of vaginal human immunodeficiency virus (HIV) infections but, to our knowledge, there are no nonhuman primate studies that have evaluated its link to rectal HIV acquisition.
Rhesus macaques inoculated with Chlamydia trachomatis (CT) (serovars LGV-L2 and CT-E; n = 7) or saline (n = 7) received up to 20 rectal challenges twice a week of simian/HIV immunodeficiency virus (SHIVSF162p3). SHIV viremia was determined by real-time PCR and Chlamydia infection by APTIMA Combo 2 testing. The rectal cytokine-chemokine levels were evaluated by multiplex bead assays.
Rectal Chlamydia infection was maintained throughout the study. We did not observe significant differences (P = 1.0) in frequency of SHIV acquisition between the STI and control arms. It took fewer SHIV challenges to infect the STI animals although the difference was not significant (P = 0.59). There were no significant differences in peak plasma viremia between STI and control arms (P = 0.63). The association of plasma viremia with rectal shedding was significantly different by arm (P = 0.038).
In the first such study in a macaque model, we did not observe an increased risk of SHIV acquisition due to rectal Chlamydia coinfection. This macaque model can be further developed and expanded to better investigate the impact of different rectal STIs on HIV acquisition.
已知性传播感染（STIs）引起的生殖道持续炎症会增加阴道感染人类免疫缺陷病毒（HIV）的风险，但据我们所知，尚无非人灵长类动物研究评估其与直肠感染HIV的关联。
接种沙眼衣原体（CT）（LGV-L2血清型和CT-E血清型；n = 7）或生理盐水（n = 7）的恒河猴，每周接受两次多达20次的直肠接种猿猴/人类免疫缺陷病毒（SHIVSF162p3）。通过实时PCR测定SHIV病毒血症，通过APTIMA Combo 2检测法测定衣原体感染。通过多重微珠分析评估直肠细胞因子-趋化因子水平。
在整个研究过程中直肠衣原体感染持续存在。我们未观察到STI组和对照组之间在感染SHIV的频率上存在显著差异（P = 1.0）。虽然差异不显著（P = 0.59），但感染STI的动物感染SHIV所需的接种次数较少。STI组和对照组之间的血浆病毒血症峰值无显著差异（P = 0.63）。血浆病毒血症与直肠病毒脱落的关联在两组之间存在显著差异（P = 0.038）。
在猕猴模型的首个此类研究中，我们未观察到直肠衣原体合并感染会增加感染SHIV的风险。该猕猴模型可进一步开发和扩展，以更好地研究不同直肠性传播感染对感染HIV的影响。
