Since the Vpr-specific activities have been linked to such clinical manifestation of AIDS as activation of viral replication [57], suppression of host immune responses [19] and depletion of CD4+ T-lymphocytes [12,58], this finding could potentially provide a new approach to reducing Vpr-mediated detrimental effects in HIV-infected patients by stimulating expression of sHsps. The gene discussed is CD4; the disease is AIDS.