Six months after vaccination, fewer than half of the 169 patients had a twofold or greater increase in antibody

titres, suggesting poor immunogenicity of PPV in patients with moderate to severe immunosuppression at HIV diagnosis and at vaccination. The proportions of responders to the three serotypes in the four groups for five consecutive years are shown in Figure 2a, b and c [the proportions of responders are shown in a supplementary table (Supporting Information Table S1) which can be provided upon request]. In each study year, group 1 had a consistently lower proportion of responders to the three serotypes studied compared with the other three groups. For each group, there were decreasing trends of the proportion of responders to all of the three serotypes after vaccination, despite continued increases in CD4 lymphocyte counts for five Cetuximab chemical structure consecutive years of HAART (Table 1). The loss of antibody responses in each follow-up year varied with the serotype selleck studied and it appeared to be faster among patients in group 1 (Fig. 2a, b and c). For example, all of

the subjects in group 1 lost antibody responses to serotype 23F in the first year of follow-up, while none of them lost antibody responses to serotype 19F until year 5; and antibody responses to serotype 14 persisted in two of 22 patients (9.1%) at year 5. At the end of the 5 years of follow-up, approximately one-third of the patients in the other three groups remained responders to serotype 14 while <20% of them were responders to serotype 19F and only 5% of them were responders to serotype 23F. In order to identify risk factors associated with

maintaining significant antibody responses (twofold or greater increase from baseline) from year 1 to year 5, we compared responders and nonresponders with regard to age, sex, risk factor for HIV transmission, nadir CD4 cell count before vaccination, CD4 cell count and plasma HIV RNA load GPX6 at vaccination, proportion of patients with CD4<100 or <200 cells/μL at vaccination, proportion of persons achieving viral suppression and updated absolute CD4 increase at each year of follow-up. The results of univariate analysis for year 5 are shown in Table 2, while those for years 1–4 are shown in supplementary tables (Tables S2–S5, which can be provided upon request). In univariate analysis, we found that patients with CD4<100 cells/μL at vaccination were less likely to achieve twofold or greater antibody responses throughout the 5-year study period. From years 3 to 5, significantly more responders than nonresponders achieved better suppression of HIV replication, as indicated by the proportion of patients with undetectable plasma HIV RNA load (Table 2).