High hepatitis C viraemia and impaired antibody response in patients coinfected with HIV.
OBJECTIVE
To compare hepatitis C virus (HCV) load in patients infected with HCV alone and those coinfected with HIV, and to evaluate the antibody response to HCV in the case of HIV infection.


METHODS
Patients coinfected with both HCV and HIV have been shown to develop hepatic changes more rapidly, which may be due to an interaction between HCV and HIV. In a prospective study, serum samples were taken from 150 patients.


METHODS
Using reverse transcription followed by polymerase chain reaction and the branched DNA assay, we detected HCV RNA in 75 patients coinfected with HIV and HCV and in 75 patients infected with HCV alone. The HIV RNA was also quantified by the branched DNA assay and the p24 antigenaemia was determined by enzyme-linked immunosorbent assay. The immune response to HCV was studied in the 150 patients by the use of third generation recombinant immunoblot assay (RIBA).


RESULTS
Although a comparable number of patients had detectable HCV viraemia in both groups, HCV RNA was quantifiable in 79% of HIV-positive patients and in only 43% of HIV-negative patients (P < 10(-5)), and the mean HCV RNA level was much higher in the HIV-positive group than in the HIV-negative group (P < 10(-7)). The quantity of HCV RNA did not correlate with the CD4 count, p24 antigenaemia or HIV RNA level. The analysis of RIBA showed 14.7% indeterminate or negative results in the HIV-positive group and only 4% indeterminate results in the HIV-negative group. HIV-positive patients had reactivity to less antigen bands than HIV-negative patients (P < 10(-3)), and they had a weaker reactivity to c100, c33c and NS5 antigen bands than HIV-negative patients.


CONCLUSIONS
Our results show that in the case of HIV infection, the HCV RNA levels are strongly increased, but HCV load is not linked to the immunosuppression induced by HIV; therefore, the present data do not support the hypothesis of a direct interaction between HIV and HCV.
Cribier
B
B
INSERM U74, Strasbourg, France.
Rey
D
D
Schmitt
C
C
Lang
J M
JM
Kirn
A
A
Stoll-Keller
F
F
D000293:Adolescent; D000328:Adult; D000368:Aged; D001483:Base Sequence; D018791:CD4 Lymphocyte Count; D005260:Female; D006678:HIV / Q000235:genetics; D016655:HIV Core Protein p24 / Q000097:blood; D015658:HIV Infections / Q000150:complications* / Q000276:immunology / Q000821:virology; D016174:Hepacivirus / Q000235:genetics / Q000302:isolation & purification*; D006526:Hepatitis C / Q000150:complications / Q000276:immunology / Q000821:virology*; D018937:Hepatitis C Antibodies / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D011446:Prospective Studies; D012367:RNA, Viral / Q000097:blood; D014766:Viremia / Q000150:complications* / Q000276:immunology
D016655:HIV Core Protein p24; D018937:Hepatitis C Antibodies; D012367:RNA, Viral