HSV infection in humans is largely controlled by the T cell response (Ouwendijk et al., 2013), and CD4+ T cells persisting in anogenital HSV-2 lesion sites possess characteristics that render them highly susceptible to HIV infection, such as an activated (e.g., CD69+) CCR5+ or α4β7high phenotype (Zhu et al., 2009; Martinelli et al., 2011; Goode et al., 2014; Shannon et al., 2014). The gene discussed is CCR5; the disease is HIV infectious disease.