Greer Amy E, Ou San-San, Wilson Ethan, Piwowar-Manning Estelle, Forman Michael S, McCauley Marybeth, Gamble Theresa, Ruangyuttikarn Cholticha, Hosseinipour Mina C, Kumarasamy Nagalingeswaran, Nyirenda Mulinda, Grinsztejn Beatriz, Pilotto Jose Henrique, Kosashunhanan Natthapol, Gonçalves de Melo Marineide, Makhema Joseph, Akelo Victor, Panchia Ravindre, Badal-Faesen Sharlaa, Chen Ying Q, Cohen Myron S, Eshleman Susan H, Thio Chloe L, Valsamakis Alexandra
*Department of Pathology, Johns Hopkins Hospital, Baltimore, MD;†Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA;‡Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD;§FHI 360, Washington, DC;‖FHI 360, Durham, NC;¶Research Institute for Health Sciences, Chiang Mai University, Chaing Mai, Thailand;#University of North Carolina at Chapel Hill, Chapel Hill, NC;**UNC Project-Malawi, Institute for Global Health and Infectious Diseases, Lilongwe, Malawi;††YRGCARE Medical Centre, VHS, Chennai, India;‡‡College of Medicine-Johns Hopkins Project, Blantyre, Malawi;§§Instituto Nacional de Infectologia Evandro Chagas-INI-Fiocruz, Rio de Janeiro, Brazil;‖‖Hospital Geral de Nova Iguacu and Laboratorio de AIDS e Imunologia Molecular-IOC/Fiocruz, Rio de Janeiro, Brazil;¶¶Hospital Nossa Senhora da Conceição, Porto Alegre RS, Brazil;##Botswana Harvard AIDS Institute, Gaborone, Botswana;***Kenya Medical Research Institute, Kisumu, Kenya;†††Center for Disease Control, Kisumu, Kenya;‡‡‡University of the Witwatersrand, Perinatal HIV Research Unit, Soweto HPTN CRS, Soweto, South Africa;§§§University of Witwatersrand, Johannesburg, South Africa;‖‖‖Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC; and¶¶¶Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
J Acquir Immune Defic Syndr. 2017 Dec 1;76(4):388-393. doi: 10.1097/QAI.0000000000001511.
Data comparing hepatitis B virus (HBV) infection in HIV-infected [HIV(+)], and HIV-uninfected [HIV(-)] individuals recruited into the same study are limited. HBV infection status and chronic hepatitis B (cHB) were characterized in a multinational clinical trial: HIV Prevention Trials Network (HPTN 052).
HBV infection status at enrollment was compared between HIV(+) (N = 1241) and HIV(-) (N = 1232) from 7 HBV-endemic countries. Hepatitis B e antigen and plasma HBV DNA were determined in cHB. Median CD4, median plasma HIV RNA, and prevalence of transaminase elevation were compared in HIV(+) with and without cHB. Significance was assessed with χ, Fisher exact, and median tests.
Among all participants, 33.6% had HBV exposure without cHB (8.9% isolated HBV core antibody, "HBcAb"; 24.7% HBcAb and anti-HB surface antibody positive, "recovered"), 4.3% had cHB, 8.9% were vaccinated, and 53.5% were uninfected. Data were similar among HIV(+) and HIV(-) except for isolated HBcAb, which was more prevalent in HIV(+) than HIV(-) [10.1% vs. 7.7%, P = 0.046]. Median HBV DNA trended higher in HIV(+) than in HIV(-). In HIV(+) with cHB versus those without cHB, transaminase elevations were more prevalent (alanine aminotransferase ≤ grade 2, 12% vs. 5.2%, P = 0.037; aspartate aminotransferase ≤ grade 2, 26% vs. 6.0%, P < 0.001), CD4 trended lower, and HIV RNA was similar.
HBV infection status did not differ by HIV infection status. HIV co-infection was associated with isolated HBcAb and a trend of increased HBV DNA. In HIV, cHB was associated with mild transaminase elevations and a trend toward lower CD4.
在同一研究中,对比人类免疫缺陷病毒(HIV)感染者[HIV(+)]和未感染者[HIV(-)]中乙型肝炎病毒(HBV)感染情况的数据有限。在一项多国临床试验:HIV预防试验网络(HPTN 052)中,对HBV感染状态和慢性乙型肝炎(cHB)进行了特征分析。
比较了来自7个HBV流行国家的HIV(+)(N = 1241)和HIV(-)(N = 1232)参与者入组时的HBV感染状态。对cHB患者检测了乙型肝炎e抗原和血浆HBV DNA。比较了合并cHB和未合并cHB的HIV(+)患者的CD4中位数、血浆HIV RNA中位数以及转氨酶升高的患病率。采用χ²检验、Fisher精确检验和中位数检验评估显著性。
在所有参与者中,33.6%有HBV暴露但无cHB(8.9%为单纯HBV核心抗体阳性,“HBcAb”;24.7%为HBcAb和抗-HB表面抗体阳性,“已康复”),4.3%有cHB,8.9%接种过疫苗,53.5%未感染。除单纯HBcAb外,HIV(+)和HIV(-)的数据相似,单纯HBcAb在HIV(+)中比在HIV(-)中更常见[10.1%对7.7%,P = 0.046]。HIV(+)中的HBV DNA中位数高于HIV(-)。在合并cHB和未合并cHB的HIV(+)患者中,转氨酶升高更常见(丙氨酸转氨酶≤2级,12%对5.2%,P = 0.037;天冬氨酸转氨酶≤2级,26%对6.0%,P < 0.001),CD4中位数呈下降趋势,HIV RNA相似。
HBV感染状态不因HIV感染状态而异。HIV合并感染与单纯HBcAb及HBV DNA升高趋势相关。在HIV感染者中,cHB与轻度转氨酶升高及CD4下降趋势相关。