Editorial

What we still don't know about AIDS

Miranda Robertson

• Correspondence: Miranda Robertson editorial@jbiol.com

Journal of Biology 2009, 8:87 doi:10.1186/jbiol200

Published: 27 November 2009

First paragraph (this article has no abstract)

A great deal is known about the human immunodeficiency virus (HIV) that causes acquired immune deficiency syndrome (AIDS) [1], one of whose cardinal features is its exquisite adaptation to its human host. It enters the body through damaged epithelia, or more insidiously, through specialized cells (M cells) in the intestinal epithelium whose function is to deliver viruses and bacteria to waiting immune cells in the tissue below. There, the virus binds to a specialized receptor on the surface of one of these cells - the dendritic cells, which play a central part in activating the CD4⁺ T lymphocytes whose destruction by the virus ultimately and lethally disables the immune system. Recognition of the bound virus causes the dendritic cell to migrate to the lymphoid tissues where it engages with the CD4⁺ T lymphocytes that it activates. This enables the virus to bind to molecules on the surface of the T cell - a highly specific interaction involving the CD4 molecules that give CD4⁺ T cells their name and that enables the virus to enter the cell. Once the virus is inside the cell, it produces DNA copies of its genome that integrate into the host DNA where cellular transcriptional regulators specifically induced by activation of CD4⁺ T cells are instrumental in activating transcription of the viral genome to produce more viruses.