Immune Response to the 13-Valent Pneumococcal Conjugate Vaccine Is Reduced in Infants Immunized During the Respiratory Viral Season

Background We hypothesized that response to infant pneumococcal conjugate vaccines (PCVs) administered during peak respiratory viral seasons (RVSs) could be blunted, particularly to higher carrier-load PCVs.Methods We conducted a post hoc analysis of a large, double-blind, randomized study comparing 13-valent vs 7-valent PCVs (PCV13, PCV7) administered to infants (at 2, 4, 6, and 12 months). We defined RVS, based on local epidemiology as December through April and non-RVS as June through October. Infants receiving the first dose at 7-9 weeks during the defined seasons were eligible. Serotype-specific immunoglobulin-G geometric mean concentrations (SSIgG-GMCs; mu g/mL) were compared between the 2 seasons at age 7 and 13 months.Results 179 and 225 infants received PCV13 in RVS and non-RVS. The corresponding numbers for PCV7 were 188 and 217. At 7 months, PCV13 recipients during RVS had significantly lower SSIgG-GMCs compared with non-RVS for 10/13 serotypes (GMC ratios: 0.76-0.86). This difference remained significant in 2/13 serotypes after a booster dose. Unlike PCV13 recipients, PCV7 recipients showed no seasonal difference. Results were similar for both vaccine results among children who had received the first dose only or both the first and second dose during the defined seasons. Similarly, no difference was observed if the booster was given in RVS or non-RVS.Conclusions Administration of the first PCV13 dose to young infants during RVS resulted in a significant blunting of the immune response, partially corrected by booster administration. PCV7 recipients were unaffected, suggesting an increased susceptibility to respiratory viral immune blunting with higher carrier-load PCVs. In a randomized study in infants, immune response to PCV13-CRM197 but not PCV7-CRM197 was blunted when first dose was administered during the respiratory viral season, suggesting that response to PCVs is blunted by viral exposure in a carrier-load-dependent manner.