LAUSR

The pathogenesis of AIDS comorbidities are the result of a number of mechanisms that can ultimately lead to cell death. One such mechanism for which there is accumulating evidence is chronic oxidative stress (COS). The impact of COS is not limited only to HIV infected cells. Uninfected cells have been shown to experience COS in patients and models of AIDS. Affected cells can have altered physiology and can die early. This makes the impact of COS far reaching, because the HIV reservoir cells are not the only cell types which are dying or displaying altered functions. This mechanism is believed to be dependent on the HIV proteins (for example: GP-120, Tat) that the infected cells release. These viral products have been demonstrated to cause oxidative stress in experimental cell cultures. Importantly, the process of COS has given insight to the comorbidities that are becoming more evident as the patients age. Currently, antiviral treatment is very effective and has improved and extended life. But even with the elimination of most opportunistic infections and keeping the HIV viral load very low, various tissues still display evidence of pathology. It is believed that the low levels of the viral proteins produced by the reservoirs, (which are not eliminated by the antivirals), produce the pathology slowly over time. This is why the magnitude of the comorbidities develop as the patient ages. It also explains why some non-infected cell types display pathology.