The HIV-AIDS hypothesis has come under attack by a few dissidents from the main stream scientific community. Peter Deusberg is one who has denounced the idea that HIV infection causes AIDS. He suggests a chemical basis for the acquisition of AIDS that is independent of HIV. As of yet, there is no clear answer to this debate, but there is only evidence that can support one side or the other. One of Deusberg's allegations against the HIV-AIDS hypothesis is that HIV is said to cause AIDS by killing more CD4 T-cells than the body can replace; however others have shown that less than 1 in 500 T-cells that is killed is infected with HIV, even in severe AIDS patients (Duesberg et al., 2003). From this he concludes that HIV must be a latent passenger virus. The data, however, seem to be slightly misleading in that they do not directly suggest that HIV is not causing harm, as he claims, because they do not account for any effects that HIV has on cells that it is not directly infecting. If it can be shown that the course of HIV infection induces greater cell death than merely the cells it is directly associated with, then it would seem that HIV is actively causing damage to the host and is not a passenger virus. This would make Deusberg's claim invalid because HIV would ultimately be responsible for much greater cell death than he has implied. Such immune suppression would also be ideal for the progression of many opportunistic infections that are characteristic in AIDS patients (Deusberg et al., 2003).
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A study by Mohri et al. (2001) compares the proliferation and death of T cells between healthy controls and HIV-positive, untreated patients. Their results showed an overall increase of cell proliferation in CD4 T cells of 6.3 times higher than that in healthy controls and a cell death rate of 3 times greater. Thus in HIV-positive, untreated patients the turnover of CD4 T cells is significantly higher than their healthy controls. These high turnover rates in patients were greatly decreased when put on antiretroviral medication and became almost normal over time (Mohri, et al., 2001). A potential mechanism for this immune hyper activation is described by Ott et al. (1997). They have determined that the HIV protein Tat is responsible for increased release of IL-2, a proliferation and activation signal released by T cells. They have used this in combination with a study by Zack et al. (1990) who have shown that HIV does not infect inactive cells to show that this is a possible mechanism that allows HIV to proliferate into many previously inaccessible cells. It would seem that the hyper activation of immune system should lead to increased numbers of T cells in blood rather than a lower count that is indicative of an HIV infection (Mohri, et al., 2001). However, Correa and Munoz-Fernández (2001) have shown that even though rates of division of T-cells are high, the thymus is shown to have lower than normal levels of naÃ¯ve T-cell output in HIV positive patients. Thus, even though mature T-cells may be dividing rapidly to produce clones, over time they will die off and are not replaced by new cells. This is suggested to lead to the low T-cell count phenotype seen in untreated HIV patients (Correa & Munoz-Fernandez, 2001). In this way, it can be seen how HIV, while present in one cell, can release proteins to increase cell proliferation, and at the same time decrease the generation of new cells. In this situation there would be a large number of shorter lived mature T-cells, but over time the regenerative abilities of the thymus are inadequate at replacing lost cells leading to T-cell depletion and immune suppression. This described mechanism outlines how immune suppression can develop by loss of regenerative ability rather than increased loss of infected cells.
Next, a study by Banda et al. (1992) describes how CD4 T cells stimulated with gp120 show rates of apoptosis four times greater than that of normal cells in vitro. Even though their method involves in vitro testing, they suggest that it is comparable to in vivo situations as it has been found that gp120 is released from infected cells and can be found free in solution around infected cells (Schneider et al. 1986). This mechanism for increased apoptosis in CD4 T cells is expanded upon by Finkel et al. (1995) who have found that cells dying from apoptosis are not cells that are infected with HIV, but are instead cells in near proximity to HIV infected cells. Of the 1000 apoptotic cells and 700 HIV infected cells that they counted using microscopy, none were both apoptotic and HIV infected. This adds additional evidence against the claim made by Deusberg et al. (2003). HIV does not necessarily act by killing the cells that it infects, but instead increases cell death rates in all of the T cells around it. In this way one would expect to find HIV present in only a small percentage of cells that die because it is increasing the cell death rate of uninfected cells, but not infected cells.
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I have described above two methods that suggest that HIV does not act as a passenger virus. HIV is accountable for lower regenerative capacity of the immune system to replace lost T cells and the gp120 glycoprotein from HIV is responsible for apoptosis in cells in proximity to an infected cell, but not the infected cell itself. Thus, HIV kills T cells and leaves the body incapable of replacing them. Not only does this suggest that HIV is not a latent passenger virus, but it also offers a potential mechanism for immune suppression in the host. This could lead to increased susceptibility to opportunistic infections that are indicative of an AIDS diagnosis. Even though HIV infected cells constitute only a small percentage of the total T-cell population, they cause damage that is far more significant.