Viral Hepatitis Reference and Research Laboratory, National Center of Microbiology, Institute of Health Carlos III, Madrid, Majadahonda, Spain.
Internal Medicine Service, La Paz University Hospital (IdiPAZ), Madrid, Spain.
J Med Virol. 2023 Jul;95(7):e28955. doi: 10.1002/jmv.28955.
Coinfection with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) increases immune activation, inflammation, and oxidative stress that could lead to premature senescence. Different HCV infections, either acute or chronic infection, could lead to distinct premature cellular senescence in people living with HIV (PLWHIV). Observational study in 116 PLWHIV under antiretroviral treatment with different HCV status: (i) n = 45 chronically infected with HCV (CHC); (ii) n = 36 individuals who spontaneously clarify HCV (SC); (iii) n = 35 HIV controls. Oxidative stress biomarkers were analyzed at lipid, DNA, protein, and nitrates levels, as well as antioxidant capacity and glutathione reductase enzyme. Replicative senescence was evaluated by relative telomere length (RTL) measurement. Additionally, 26 markers of Senescence-Associated Secretory Phenotype (SASP) were analyzed by multiplex immunoassays (Luminex xMAP technology). Differences were evaluated by generalized linear model (GLMs) adjusted by most significant covariates. The SC group had a senescence signature similar to the HIV control group and slightly lower SASP levels. However, significant differences were observed with respect to the CHC group, where an increase in the nitrate concentration [adjusted arithmetic mean ratio, aAMR = 1.73 (1.27-2.35), p < 0.001, q = 0.009] and the secretion of 13 SASP-associated factors [granulocyte macrophage colony-stimulating factor (GM-CSF), interferon-β, interleukin (IL)-1β, IL-2, IL-8, IL-13, tumor necrosis factor (TNF)-α, IL-1α, IL-1RA, IL-7, IL-15, C-X-C motif chemokine ligand 10 (IP-10), stem cell factor (SCF); q < 0.1)] was detected. The CHC group also showed higher values of IL-1α, IP-10, and placental growth factor 1 (PIGF-1) than HIV controls. The SC group showed a slightly lower senescence profile than the HIV group, which could indicate a more efficient control of viral-induced senescence due to their immune strengths. Chronic HCV infection in PLWHIV led to an increase in nitrate and elevated SASP biomarkers favoring the establishment of viral persistence.
丙型肝炎病毒(HCV)和人类免疫缺陷病毒(HIV)的合并感染会增加免疫激活、炎症和氧化应激,从而导致过早衰老。不同的 HCV 感染,无论是急性感染还是慢性感染,都可能导致 HIV 感染者(PLWHIV)出现不同的过早细胞衰老。对 116 名接受抗逆转录病毒治疗的 PLWHIV 进行了观察性研究,他们的 HCV 状态不同:(i)n=45 例慢性 HCV 感染者(CHC);(ii)n=36 例自发清除 HCV 者(SC);(iii)n=35 例 HIV 对照组。分析了脂质、DNA、蛋白质和硝酸盐水平的氧化应激生物标志物,以及抗氧化能力和谷胱甘肽还原酶。通过相对端粒长度(RTL)测量评估复制性衰老。此外,通过多重免疫分析(Luminex xMAP 技术)分析了 26 种衰老相关分泌表型(SASP)标志物。通过广义线性模型(GLMs)调整最显著的协变量来评估差异。SC 组的衰老特征与 HIV 对照组相似,SASP 水平略低。然而,与 CHC 组相比,差异显著,硝酸盐浓度升高[调整后的算术平均值比,aAMR=1.73(1.27-2.35),p<0.001,q=0.009]和 13 种 SASP 相关因子的分泌[粒细胞巨噬细胞集落刺激因子(GM-CSF)、干扰素-β、白细胞介素(IL)-1β、IL-2、IL-8、IL-13、肿瘤坏死因子(TNF)-α、IL-1α、IL-1RA、IL-7、IL-15、C-X-C 基序趋化因子配体 10(IP-10)、干细胞因子(SCF);q<0.1)]被检测到。CHC 组也显示出比 HIV 对照组更高的 IL-1α、IP-10 和胎盘生长因子 1(PIGF-1)值。SC 组的衰老特征略低于 HIV 组,这可能表明由于免疫能力更强,他们对病毒诱导的衰老的控制更有效。PLWHIV 中的慢性 HCV 感染导致硝酸盐增加和升高的 SASP 生物标志物,有利于病毒持续存在。