Regulation of T cell recruitment and inflammation in the human immunodeficiency virus/hepatitis C virus coinfected liver

Background and Aim Patients coinfected with both hepatitis C virus (HCV) and human immunodeficiency virus (HIV) have accelerated liver disease compared with HCV mono‐infected patients. In chronic HCV infection, it is known that chemokines play a key role in T cell recruitment and in determining the extent of hepatic injury. Methods In this study, we determined by quantitative real‐time reverse transcriptase polymerase chain reaction and immunohistochemistry the intrahepatic phenotype of the cellular infiltrate and its associated chemokine profile and localization in a cohort of relatively immune competent coinfected HIV/HCV subjects. Results Increased lobular expression of CD8+ cytotoxic T cells was found in the coinfected liver in conjunction with increased expression of the T cell chemoattractant, chemokine (C‐C motif) ligand (CCL)5, compared with the HCV mono‐infected liver. Furthermore, the number of lobular‐infiltrating CD8+ T cells was positively correlated with the expression of CCL5. Immunohistochemical staining of CCL5 showed it to primarily localize to the hepatocytes. Within the inflammatory infiltrate, proliferating (Ki‐67+) and apoptotic terminal deoxynucleotidyl transferase 2′‐deoxyuridine 5′‐triphosphate nick end labeling + (TUNEL)+ cells were sparse. Conclusions Collectively, the data suggest that even in the setting of relatively immune competent coinfected subjects, a pro‐inflammatory milieu exists ,which can potentially drive the increased T cell recruitment found in the HIV/HCV coinfected liver. This profile is likely to contribute to the accelerated progression of liver disease observed in HIV/HCV coinfection.