Objective: To evaluate whether duration of HIV-1 infection influences the r
esponse to highly active antiretroviral therapy (HAART).
Design: Prospective study of individuals (Italian Seroconversion Study coho
rt) with well-estimated dates of HIV-1 seroconversion.
Methods: This analysis included 277 participants who began HAART (defined a
s three antiretroviral drugs used in combination). Cox regression models we
re used to evaluate the association between duration of infection (as categ
orical variable [less than or equal to3, 3-7.5, >7.5 years from seroconvers
ion] or continuous variable) and an immunologic (rise in CD4 count >100 cel
ls/mm(3)) and a virologic (decline in plasma HIV-RNA to unquantifiable leve
ls) outcome. All analyses were stratified by center of recruitment and adju
stment, when used, was for gender, age at inception of HAART, injection dru
g use. previous antiretroviral therapy, lag-time between positive and negat
ive HIV test result, year of starting HAART, clinical stage, CD4 count, and
HIV-RNA at time of HAART.
Results: HAART was initiated a median of 6.4 years after seroconversion, Th
ere was a median follow-up of 1.6 years after starting HAART to the calenda
r cut-off (November 1999). One-hundred-eighty-one (65.3%) patients experien
ced a decline in viral load to below quantifiable levels and 184 (66.4%) ex
perienced a rise in CD4 >100 cells/mm(3). In the Cox models, by 1-year incr
ease in duration of infection, we estimated a lower crude hazard of achievi
ng a CD4 count increase >100 cells (relative hazard [RH], 0.96: 95% confide
nce interval [CI]. 0.92-1.01; p = .09), and a lower hazard of reaching an u
nquantifiable level of plasma HIV-RNA (RH, 0.97; 95%CI, 0.93-1.02; p = .20)
. After adjustment, these values became 0.99 (95%CI, 0.93-1.04; p = .62) an
d 0.98 (95%CI, 0.93-1.03; p = .48), respectively. When duration of HIV infe
ction was considered as a categorical variable, the results were consistent
with those already described.
Conclusions: These results suggest that the duration of HIV infection does
not seem to play an important independent role in determining the virologic
and immunologic responses to HAART.