Postgraduate Program of Basic and Applied Immunology, Ribeirão Preto Medical School, University of São Paulo, 3900 Bandeirantes Avenue, 14049-900 Ribeirão Preto, Brazil.
Department of Medicine, Division of Clinical Immunology, Ribeirão Preto Medical School, University of São Paulo, 3900 Bandeirantes Avenue, 14049-900 Ribeirão Preto, Brazil; Commissariat à l'Energie Atomique et aux Energies Alternatives, Direction de la Recherche Fondamentale, Institut de Biologie François Jacob, Service de Recherches en Hémato-Immunologie, Hôpital Saint-Louis, 1 Avenue Claude Vellefaux, 75475 Paris, France; Université Paris-Diderot, UMR 976 HIPI, Institut de Recherche Saint-Louis, 1 Avenue Claude Vellefaux, 75475 Paris, France.
Clin Immunol. 2020 Aug;217:108482. doi: 10.1016/j.clim.2020.108482. Epub 2020 May 27.
Chronic hepatitis C virus (HCV) infection induces liver damage and the HCV/Human Immunodeficiency Virus (HIV)-coinfection may further contribute to its progression. The HLA-G molecule inhibits innate and adaptive immunity and may be deleterious for chronically virus-infected cells. Thus we studied 204 HCV-mono-infected patients, 142 HCV/HIV-coinfected patients, 104 HIV-mono-infected patients and 163 healthy subjects. HLA-G liver expression was similarly induced in HCV and HCV/HIV specimens, increasing with advanced fibrosis and necroinflammatory activity, and with increased levels of liver function-related enzymes. Plasma soluble HLA-G (sHLA-G) levels were higher in HCV/HIV patients compared to HCV, HIV and to healthy individuals. sHLA-G continued to be higher in coinfected patients even after stratification of samples according to degree of liver fibrosis and necroinflammatory activity when compared to mono-infected patients. Some HLA-G gene haplotypes differentiated patient groups and presented few associations with liver and plasma HLA-G expression. HLA-G thus may help to distinguish patient groups.
慢性丙型肝炎病毒（HCV）感染可导致肝脏损伤，HCV/人类免疫缺陷病毒（HIV）合并感染可能进一步促进其进展。HLA-G 分子抑制先天和适应性免疫，可能对慢性病毒感染细胞有害。因此，我们研究了 204 例 HCV 单感染患者、142 例 HCV/HIV 合并感染患者、104 例 HIV 单感染患者和 163 例健康对照者。HCV 和 HCV/HIV 标本中均诱导产生相似的 HLA-G 肝表达，随着纤维化和炎症活性的进展而增加，且与肝功能相关酶水平的升高相关。与 HCV、HIV 和健康个体相比，HCV/HIV 患者的血浆可溶性 HLA-G（sHLA-G）水平更高。即使对纤维化和炎症活动程度进行分层，与单感染患者相比，合并感染患者的 sHLA-G 水平仍持续升高。一些 HLA-G 基因单倍型可区分患者群体，与肝和血浆 HLA-G 表达的相关性较少。因此，HLA-G 可能有助于区分患者群体。
