Defective signal transduction--a common pathway for cellular dysfunction in HIV infection?
Qualitative defects in immune responsiveness after human immunodeficiency virus (HIV) infection have been well characterized and may play a key role in the development of HIV disease. However, no clear picture of the underlying mechanism of the functional deficiencies has yet emerged. In this article, Anthony Pinching and Keith Nye suggest that HIV or HIV proteins can sabotage transmembrane signalling and that this is of primary importance to the alterations in immune responsiveness.
Pinching
A J
AJ
Department of Immunology, St Mary's Hospital Medical School, London, UK.
Nye
K E
KE
D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D006678:HIV / Q000502:physiology*; D015699:HIV Envelope Protein gp120 / Q000502:physiology; D015658:HIV Infections / Q000276:immunology / Q000503:physiopathology*; D006801:Humans; D007108:Immune Tolerance; D007295:Inositol Phosphates / Q000378:metabolism; D008213:Lymphocyte Activation; D008264:Macrophages / Q000502:physiology; D008954:Models, Biological; D009474:Neurons / Q000502:physiology; D009928:Organ Specificity; D015398:Signal Transduction
D015699:HIV Envelope Protein gp120; D007295:Inositol Phosphates; D002118:Calcium