Mechanisms of immune suppression in AIDS: possibilities of prevention.
AIDS is primarily a disease of the CD4-expressing helper-inducer T lymphocytes and is caused by human immunodeficiency virus (HIV), a retrovirus of the lentivirus subgroup. The interaction of HIV envelope glycoprotein (gp 110) with the CD4 molecule itself accounts for the virus selective tropism and for its pathogenicity, which result in the ultimate destruction of immunocompetent cells. Viral replication occurs preferentially in case of activation of the infected target cells, which explains why multiple infections, frequent in at-risk subjects, might play the role of cofactors and enhance HIV dissemination. There is yet no proof that an effective immune response might be mounted against this virus. Based on the pathophysiological model that can be drawn from HIV biological properties, many therapeutic schemes can be proposed to interfere with the complex pathway of interaction between host and virus. Nevertheless, the use of retroviral agents appears to be central to all these new strategies, since disease progression seems indeed directly related to the extent of viral replication.
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology; D006678:HIV / Q000502:physiology; D006801:Humans; D014779:Virus Replication
D000945:Antigens, Differentiation, T-Lymphocyte