Humoral and cellular response to influenza vaccine in HIV-infected children with full viroimmunologic response to antiretroviral therapy

Objective: It is unclear whether the ability to respond to vaccines is restored by antiretroviral therapy. We evaluated the influenza-specific immune responses elicited by a virosomal vaccine in HIV-infected children on long-term successful highly active antiretroviral therapy (HA,ART). Methods: This was an observational, prospective, open-label study enrolling 24 HIV-infected, HAART-treated (85 months' mean exposure), vaccine-naive children (median age = 11.9 years) and 14 age- and gender-matched healthy controls. Mean CD4 T-cell counts (>900 cells/mu L) and percentages (>37%) were comparable. The HIV RNA level was <50 copies/mL in all patients. Children received a single dose of trivalent virosome-adjuvanted influenza vaccine. A/H3N2-, A/H1N1-, and B-antigen-specific antibody (Ab) titers and subclasses and vaccine-specific interferon-gamma (IFN gamma)- and interleukin (IL)-2-producing T lymphocytes were analyzed at baseline and I and 6 months after immunization. Results: Seroconversion ( >= 4-fold Ab titer raise in >40% of patients) and seroprotection (Ab titer >= 1:40 in >70% of patients) was achieved at I month in both groups; however, fewer HIV-infected children fulfilled these criteria. The A/H3N2- and A/H1N1-specific Ab geometric mean titers were lower in HIV-infected children compared with healthy controls at 1 and 6 months; interestingly, a boost in vaccine-specific IgG3 T helper I type Ab was seen in healthy controls alone. Finally, vaccine specific-IFN gamma- and IL-2-producing T lymphocytes were reduced at both time points in HIV-infected children compared with healthy controls. Conclusions: One injection of virosomal-adjuvanted influenza vaccine stimulates good immune responses, although the humoral and cellular immune responses are reduced in HIV-infected children compared to healthy children. This indicates that immunologic function impairments may persist upon HIV infection even if HIV-positive viremia is suppressed and immune recovery seems to be achieved.