Entry of HIV begins with the envelope protein gp120 binding with high affinity to CD4. A G protein coupled coreceptor of the chemokine family, typically CCR5, must also bind to allow HIV entry. Recent research in the field of cytokines has revealed several major ligands for CCR5. These coreceptor ligands are members of the beta-chemokine family and include RANTES, MIP-1 alpha, and MIP-1beta (Janeway et al., 1999) Subsequently, gp41 will fuse the viral envelope and cell membrane to allow the viral RNA to enter the host cell (Schwartz and Nair, 1999).
The image on the left shows gp120 binding to CD4 and the chemokine coreceptor ligand binding to CCR5. The animation on the right shows the overall process of viral fusion and entry into a health cell. Used with permission of Cells Alive.

The provirus produces mRNA upon activation by using the host cells' transcription factors (Schwartz et al., 1999). Transcription is controlled and activated by the HIV tat gene as well as tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) which are secreted in elevated levels of HIV infected cells (www.aegis.com). The mRNA of the HIV virion is then transported from the nucleus of the host cell to the cytoplasm where structural HIV proteins are made (www.aegis.coml).

The structural proteins synthesized from translation begin to take form the of the HIV virus. After the envelope of the virus aggregates the virion "pinches off" from the host cell. In this process of budding, the host cell membrane is taken up by the virus as part of the fatty envelope. It is important to note that immediately after budding the HIV viral core is immature and not infectious. After budding the HIV protease cleaves the long viral core polypeptide chains to form a functional and infectious molecule
(www.aegis.com).

A scanning electron microscope image of HIV daughter cells budding from an infected host cell. Used withe permission of http://www.cmsp.com/datav1/cg010001.htm.