Role of hepatitis C virus (HCV) viremia and HCV genotype in the immune recovery from highly active antiretroviral therapy in a cohort of antiretroviral-naive HIV-infected individuals.
BACKGROUND
The roles of hepatitis C virus (HCV) viremia and HCV genotype in the immune response to highly active antiretroviral therapy (HAART) are poorly understood. Our aim was to assess the CD4+ cell count recovery after HAART in human immunodeficiency virus (HIV)-infected patients with HCV viremia and HIV-infected patients who tested negative for HCV antibody (HCV-Ab). We also aimed to assess whether the response to HAART in these patients varied according to HCV genotype.


METHODS
The analysis focused on 1219 HCV-Ab-negative patients and 284 HCV-viremic patients from a cohort of HIV-infected subjects that includes persons who were antiretroviral naive before initiating HAART after cohort enrollment. HCV RNA load and HCV genotype were determined in plasma specimens obtained and stored during the 6-month period preceding the initiation of HAART.


RESULTS
The chance of achieving a CD4+ cell count increase of > or = 100 cells/microL from the pre-HAART level tended to be poorer in HCV-viremic patients than in patients who tested negative for HCV-Ab (adjusted relative hazard [RH], 0.82; 95% confidence interval [CI], 0.66-1.01; P = .06). In contrast, a comparison of patients who had a HCV RNA load >1 x 10(6) IU/mL with patients who had a HCV RNA load of 5-1 x 10(6) IU/mL revealed no significant association between HCV RNA load and achievement of an increased CD4+ cell count (adjusted RH, 0.97; 95% CI, 0.75-1.27; P = .83). There was no clear association between HCV genotype and the probability of achieving a CD4+ cell count increase.


CONCLUSIONS
An association between the presence of HCV-Ab and immune reconstitution after HAART has been shown elsewhere. Results of our large, prospective study support a direct role of HCV viremia in the CD4+ cell count response to HAART. Moreover, our results underline the fact that, in individuals coinfected with HIV and HCV, the goal of treating HCV infection is to eradicate HCV, to both slow the rate of HCV progression and limit potential interference with the response to HAART.
Antonucci
Giorgio
G
National Institute of Infectious Diseases, L. Spallanzani, Rome, Italy. antonucci@inmi.it
Girardi
Enrico
E
Cozzi-Lepri
Alessandro
A
Capobianchi
Maria Rosaria
MR
De Luca
Andrea
A
Puoti
Massimo
M
Petrelli
Enzo
E
Carnevale
Giuseppe
G
Rizzardini
Giuliano
G
Grossi
Paolo Antonio
PA
Viganò
Paolo
P
Moioli
Maria Cristina
MC
Carletti
Fabrizio
F
Solmone
Mariacarmela
M
Ippolito
Giuseppe
G
Monforte
Antonella D'Arminio
AD
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D000914:Antibodies, Viral / Q000097:blood; D023241:Antiretroviral Therapy, Highly Active; D018791:CD4 Lymphocyte Count; D015331:Cohort Studies; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology; D016174:Hepacivirus / Q000235:genetics*; D006526:Hepatitis C / Q000097:blood* / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D013997:Time Factors; D019562:Viral Load; D014766:Viremia
D019380:Anti-HIV Agents; D000914:Antibodies, Viral; D012367:RNA, Viral