The Spina model (unpublished results; manuscript submitted) is based on early work demonstrating that HIV-1 can establish infection directly in resting primary CD4+ T lymphocytes in vitro[26], [27], and on recent work showing that during acute HIV infection in a heterogeneous population of primary CD4+ T cells, undergoing varying degrees of cell activation, viral latency is established early and preferentially in non-dividing and minimally activated cells. The gene discussed is CD4; the disease is HIV infectious disease.