The defect was not only due to impairment of the proliferative capacity of CD4+ T cells, but also the attenuated propensity to differentiate into the Tfh lineage, as evidenced by severely decreased proportions of Tfh cells and GC Tfh cells, along with defective transcription of Tfh signature genes such as Bcl-6, Cxcr5, Pdcd-1 and Il-21 in RACK1-deficient CD4+ T cells early after infection (Fig 3). This evidence concerns the gene CXCR5 and infection.