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Treatment
with Didanosine/Hydroxyurea Provides Higher Levels of HIV-specific
CD8+ and CD4+ T-cell Responses Than Standard Triple Drug Regimens
The
role of hydroxyurea (HU) in the
treatment of HIV infection remains controversial. HU potentiates
didanosine (Videx; ddI) antiviral activity and might exert immunomodulatory
effects.
Immunologic
parameters were examined in HIV-infected patients enrolled in a
simplification trial in which ddI-HU was provided to subjects who
had been on complete virus suppression under highly active antiretroviral
therapy (HAART) for longer than 6 months.
A total of
84 of these patients showed plasma viremia repeatedly below 5000
HIV-RNA copies/ml, and were the main study population.
A group of
22 patients who continued on HAART and another of 22 drug-naive
HIV-positive individuals were taken as controls.
Results
At 12 months,
the levels of naive and memory T-cell subsets were similar in patients
on ddI-HU and under HAART, whereas immune activation tended to be
lower in the former group.
The frequency
of HIV-specific CD8+ T cells (CTL)
directed against 125 peptides derived from Gag, Pol, Env, Nef and
HIV regulatory proteins was similar among patients on ddI-HU and
untreated controls, and significantly higher than in patients under
HAART.
This higher
CTL response in patients on ddI-HU was seen even when considering
only subjects with undetectable viral load.
HIV-specific
CD4+ T-cell responses were absent
in almost all patients on HAART, whereas they were present in up
to 19% of patients on ddI-HU.
Conclusion
In conclusion,
the authors write, "Treatment with ddI-HU provides higher levels
of HIV-specific CD8+ and CD4+ T-cell responses than standard triple
drug regimens. Thus, hydroxyurea might exert a beneficial immunomodulatory
effect in HIV infection."
Service
of Infectious Diseases, Hospital Carlos III. Madrid, Spain.
09/22/04
Reference
M Lopez and others. Enhanced HIV-specific immune responses in chronically
HIV-infected patients receiving didanosine plus hydroxyurea. AIDS
18(9): 1251-1261. June 18, 2004.
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