In individuals with ME/CFS, ancestral HLA-II haplotypes, and latent EBV, these immunological alterations can be explained by the EBV-acquired immunodeficiency model, where the impairment of CD4 T-cell function and activation caused by these ancestral HLA-II haplotypes could generate T-cell depletion and thus an increase in EBV-infected ectopic lymphoid structures [8, 171]. The gene discussed is CD4; the disease is myalgic encephalomeyelitis/chronic fatigue syndrome.