Studies of responses to the AS03-adjuvanted influenza

A/09/H1N1 vaccines in HIV-infected patients have generated diverse results. Several studies [13-15] reported low seroprotection rates of 61% [13] to 75% [14] after one dose, increasing to 92% after a second dose [16]. In contrast, seroconversion rates of 88 to 95.3% were observed after a single dose in other studies selleck [17-19]. This may be attributable to differences in the timing of immunization during the pandemic outbreak, reflected by higher baseline or follow-up seroprotection rates. The proportion of H1N1/09-infected adults identified in European sero-epidemiological studies reached 10-to-25% [9], suggesting that the post-immunization seroprotection rate of 85.6% observed in our study was mainly

vaccine-induced. Other potential confounders include vaccine dose [20], use and type of adjuvant [21], and previous seasonal influenza immunization. The severity of HIV disease was not a determinant of antibody responses in our cohort. Given the relatively BMS-777607 cell line small proportion of HAART-treated HIV-infected patients with CD4 counts of <350 cells/μL at baseline, most European studies, including ours, do not have sufficient power to formally exclude an influence of very low CD4 cell counts on antibody responses. However, the superposition of reverse distribution curves comparing HIV-positive patients with CD4 counts Beta adrenergic receptor kinase <350 and >500/cells/μL, as presented in Figure 1b, indicates that their responses were similar. The question of whether CD4 cell counts would have affected responses to a single vaccine dose cannot be answered here because of the design of our study. Bickel et al. [16] identified a lower nadir CD4 cell count in HIV-positive patients who failed to seroconvert, which we did not observe. In our study, the type of antiretroviral agents used as part of the antiretroviral regimen had only a borderline significance: HIV-positive patients on PIs tended to have higher responses than those on an

NNRTI-based regimen without PIs. This treatment effect, however, disappeared after adjustment in the multivariate analysis. Age is also known to affect humoral influenza responses, including those to the AS03-adjuvanted influenza vaccine [22]. Age was indeed a significant titre determinant in healthy subjects, lower responses being observed already between 40 and 60 years. Surprisingly, this was not observed in HIV-infected patients, as patients aged 20–40 years did not respond better than those aged 40–60 years or those aged over 60 years (Fig. 1d). Given that our study design did not include assessment of primary responses, we cannot exclude the possibility that the second vaccine dose provided a greater benefit to patients aged over 40 years, thus masking the impact of age observed in healthy subjects.