Rana Urvi, Driedger Matt, Sereda Paul, Pan Shenyi, Ding Erin, Wong Alex, Walmsley Sharon, Klein Marina, Kelly Deborah, Loutfy Mona, Thomas Rejean, Sanche Stephen, Kroch Abigail, Machouf Nima, Roy-Gagnon Marie-Héléne, Hogg Robert, Cooper Curtis L
School of Epidemiology and Public Health, University of Ottawa, Ottawa, Ontario, Canada.
College of Osteopathic Medicine, Michigan State University, East Lansing, Michigan, United States.
J Assoc Med Microbiol Infect Dis Can. 2021 Jul 20;6(2):137-148. doi: 10.3138/jammi-2020-0011. eCollection 2021 Jun.
The clinical and demographic characteristics that predict antiretroviral efficacy among patients co-infected with HIV and hepatitis B virus (HBV) remain poorly defined. We evaluated HIV virological suppression and rebound in a cohort of HIV-HBV co-infected patients initiated on antiretroviral therapy.
A retrospective cohort analysis was performed with Canadian Observation Cohort Collaboration data. Cox proportional hazards models were used to determine the factors associated with time to virological suppression and time to virological rebound.
HBV status was available for 2,419 participants. A total of 8% were HBV co-infected, of whom 95% achieved virological suppression. After virological suppression, 29% of HIV-HBV co-infected participants experienced HIV virological rebound. HBV co-infection itself did not predict virological suppression or rebound risk. The rate of virological suppression was lower among patients with a history of injection drug use or baseline CD4 cell counts of <199 cells per cubic millimetre. Low baseline HIV RNA and men-who-have-sex-with-men status were significantly associated with a higher rate of virological suppression. Injection drug use and non-White race predicted viral rebound.
HBV co-infected HIV patients achieve similar antiretroviral outcomes as those living with HIV mono-infection. Equitable treatment outcomes may be approached by targeting resources to key subpopulations living with HIV-HBV co-infection.
在人类免疫缺陷病毒(HIV)和乙型肝炎病毒(HBV)合并感染患者中,预测抗逆转录病毒疗效的临床和人口统计学特征仍未明确界定。我们评估了开始接受抗逆转录病毒治疗的HIV-HBV合并感染患者队列中的HIV病毒学抑制和反弹情况。
利用加拿大观察性队列协作数据进行回顾性队列分析。采用Cox比例风险模型来确定与病毒学抑制时间和病毒学反弹时间相关的因素。
有2419名参与者的HBV状态数据可用。共有8%的参与者合并感染HBV,其中95%实现了病毒学抑制。在病毒学抑制后,29%的HIV-HBV合并感染参与者出现了HIV病毒学反弹。HBV合并感染本身并不能预测病毒学抑制或反弹风险。有注射吸毒史或基线CD4细胞计数低于每立方毫米199个细胞的患者中,病毒学抑制率较低。低基线HIV RNA水平和男男性行为者状态与较高的病毒学抑制率显著相关。注射吸毒和非白人种族可预测病毒反弹。
合并感染HBV的HIV患者与单纯感染HIV的患者在抗逆转录病毒治疗方面取得了相似的结果。通过将资源靶向HIV-HBV合并感染的关键亚人群,可能实现公平的治疗结果。