Pardy, Ryan D.Gentile, Maria E.Carter, Alexandria M.Condotta, Stephanie A.King, Irah L.Richer, Martin J.2023-12-052023-12-052022Pardy RD, Gentile ME, Carter AM, Condotta SA, King IL, Richer MJ. An Epidemic Zika Virus Isolate Drives Enhanced T Follicular Helper Cell and B Cell-Mediated Immunity. J Immunol. 2022;208(7):1719-1728. doi:10.4049/jimmunol.2100049https://hdl.handle.net/1805/37287Zika virus (ZIKV) is a mosquito-borne pathogen that recently caused a series of increasingly severe outbreaks. We previously demonstrated that, compared with a pre-epidemic isolate (ZIKVCDN), a Brazilian ZIKV isolate (ZIKVBR) possesses a novel capacity to suppress host immunity, resulting in delayed viral clearance. However, whether ZIKVBR modulates CD4 T cell responses remains unknown. In this study, we show that, in comparison with ZIKVCDN infection, CD4 T cells are less polarized to the Th1 subtype following ZIKVBR challenge in mice. In contrast, we observed an enhanced accumulation of T follicular helper cells 10, 14, and 21 d postinfection with ZIKVBR This response correlated with an enhanced germinal center B cell response and robust production of higher avidity-neutralizing Abs following ZIKVBR infection. Taken together, our data suggest that contemporary ZIKV strains have evolved to differentially induce CD4 T cell, B cell, and Ab responses and this could provide a model to further define the signals required for T follicular helper cell development.en-USPublisher PolicyB-LymphocytesT Follicular Helper CellsZika Virus InfectionArticle