Interestingly, Lucas et al. showed that CD4+ T cells interact with B-cells in an IFNγ-dependent manner, leading to the production of neutralizing IgG2a antibodies that protected mice from lethal infection with ZIKV, whereas the depletion of CD4+ T cells significantly impaired these responses [142], suggesting that critical CD4+ T cell helper responses were essential for the generation of ZIKV-specific antibody-mediated control of infection. The gene discussed is CD4; the disease is infection.