Fibrosis is worse in HIV-HCV patients with low-level immunodepression referred for HCV treatment than in HCV-matched patients.
Hepatitis C virus (HCV) infection is frequent in human immunodeficiency virus (HIV)-infected patients. It is known to have an aggressive course in significantly immunosuppressed patients, and cirrhosis C has become one of the main causes of mortality in HIV-HCV coinfected patients since the improvement of antiretroviral therapy. The reasons for this severe fibrotic evolution are unclear. This prospective study compared chronic HCV lesions, liver immunocompetent cells, fibrosis and liver HCV loads in 2 cohorts of naive patients referred for HCV treatment: 33 HIV-HCV coinfected patients with CD4 >250/microL and 33 HCV-infected patients matched for the main risk factors of fibrosis. Fibrosis, particularly perisinusoidal fibrosis, was more marked in the coinfected patients. This occurred in the absence of a significant difference in disease activity. The number of CD3+ cells in the liver was higher in the HIV-HCV patients than in the HCV patients. Conversely, the number of liver CD4+ cells was lower in HIV-HCV patients than in HCV patients. The numbers of CD8+ and CD68+ cells were similar in the 2 groups. Finally, liver HCV load, assessed by immunostaining and reverse-transcription polymerase chain reaction, was similar in the 2 groups. We conclude that in the population of HIV-HCV coinfected patients with low-level immunosuppression referred for HCV treatment, fibrosis is worse than in HCV patients and the proportion of CD4+ lymphocytes among CD3+ cells is markedly decreased in the liver, whereas intrahepatic viral load is similar. Our data confirm the need to treat such patients against HCV, and suggest that HIV infection could favor fibrosis via the modulation of the intrahepatic immune response.
Rullier
Anne
A
Department of Pathology, Bordeaux Hospital, Bordeaux, France.
Trimoulet
Pascale
P
Neau
Didier
D
Bernard
Pierre-Henri
PH
Foucher
Juliette
J
Lacoste
Denis
D
Winnock
Maria
M
Urbaniak
Rosa
R
Ballardini
Giorgio
G
Balabaud
Charles
C
Bioulac-Sage
Paulette
P
Le Bail
Brigitte
B
D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology / Q000378:metabolism; D017252:CD3 Complex / Q000276:immunology / Q000378:metabolism; D015704:CD4 Antigens / Q000276:immunology / Q000378:metabolism; D016827:CD8 Antigens / Q000276:immunology / Q000378:metabolism; D016022:Case-Control Studies; D005355:Fibrosis / Q000473:pathology*; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy / Q000473:pathology*; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008099:Liver / Q000166:cytology / Q000276:immunology / Q000473:pathology*; D008103:Liver Cirrhosis / Q000209:etiology; D011446:Prospective Studies; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D019562:Viral Load; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D015704:CD4 Antigens; D016827:CD8 Antigens; D007166:Immunosuppressive Agents; C067980:CD68 antigen, human; D000097382:CD68 Molecule