title: [Causes of T lymphocyte activation in HIV-infected patients coinfected with hepatitis C virus].
abstract: OBJECTIVE
  To establish the causes of T lymphocyte activation in human immunodeficiency virus (HIV)-infected patients coinfected with hepatitis C (HCV) who are adherent to their antiretroviral therapy regimen and interferon untreated.
  
  
  METHODS
  Examinations were made in 62 people who were HIV+HCV-positive (n=21), HIV+HCV-negative (n=21), and noninfected volunteers (n=20). The activation (CD38+HLA-DR+) and proliferation (Ki-67+) of CD4+ and CD8+ T lymphocytes were estimated. The blood concentration of intestinal fatty acid-binding protein (I-FABP) was determined.
  
  
  RESULTS
  The proportion of activated cells among the CD4+ T lymphocytes was equal in the HIV+HCV-positive and HIV+HCV-negative groups. But these indicators were statistically significantly higher than those in the controls (HIV- HCV-). CD8+ T cell activation was greater in the HIV/HCV-coinfected patients than that in the other groups and that was higher in the HIV monoinfected than in the noninfected. The blood I-FABP concentrations were elevated in the HIV+HCV-positive and HIV+HCV groups compared with those in the HIV-HCV-negative group, but these did not differ among themselves. In the HIV+HCV-negative patients, CD4+ and CD8+ T cell activation directly and statistically significantly correlated with blood I-FABP levels. In the HIV+HCV-positive group, this correlation remained only for CD4+ T lymphocytes. CD8+ T cell activation in HIV/HCV-coinfected patients was unrelated to I-FABP concentrations.
  
  
  CONCLUSIONS
  The increased activation of CD4+ and CD8+ T lymphocytes in HIV monoinfection was found to be associated with intestinal epithelial destruction and unrelated to cell division processes. In HIV/HCV coinfection, the activated state of CD4+ T cells is determined by both the level of proliferative processes and impairment of the intestinal barrier and that of CD8+ T cells is only by proliferation.
authors.affiliation: Perm State National Research University, Perm, Russia; Institute for Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm, Russia.
authors.forename: K V
authors.initials: KV
authors.lastname: Shmagel
authors.affiliation: Perm State National Research University, Perm, Russia; Perm Territorial Centre for Protection and Control of AIDS and Infectious Diseases, Perm, Russia.
authors.forename: N G
authors.initials: NG
authors.lastname: Shmagel
authors.affiliation: Perm State National Research University, Perm, Russia; Institute for Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm, Russia.
authors.forename: L B
authors.initials: LB
authors.lastname: Korolevskaya
authors.affiliation: Perm State National Research University, Perm, Russia; Institute for Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm, Russia.
authors.forename: E V
authors.initials: EV
authors.lastname: Saydakova
authors.affiliation: Perm State National Research University, Perm, Russia; Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences, Perm, Russia.
authors.forename: V A
authors.initials: VA
authors.lastname: Chereshnev
mesh_terms: D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D060085:Coinfection; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D016174:Hepacivirus; D006526:Hepatitis C / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation