Abstract
The priority in elucidation of the problems associated with HIV infection has been mainly determined by experimental feasibility rather than by its importance. Molecular biologists have rapidly produced an impressive body of knowledge about the structure of HIV, but this understanding is not sufficient to explain complex biological effects accompanying viral pathogenesis. Physicians, fourteen years into the epidemic have been left with a confused mixture of AZT, CD4 counts, false promises of vaccines, morbidity charts and nothing else. Immunologists, in their turn, disappointed by the results of their own narrow scope of inquiries for a direct explanation of the pathological effect of the virus, started to look for alternative concepts such as self-inflicted immunopathology mediated through the capacity of HIV to mimic host antigens and to trigger autoimmune responses. Although this idea was proposed even before HIV was implicated as a cause of AIDS, mainstream research has been oriented toward goals that were easier to grasp. As a result, little progress has been made to adopt the viral ‘kamikaze’ phenomenon to the development of a meaningful therapeutic strategy.
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Bourinbaiar, A.S., Lee-Huang, S. (1995). Rational Problems Associated with the Development of Cellular Approaches in Controlling HIV Spread. In: Andrieu, JM., Lu, W. (eds) Cell Activation and Apoptosis in HIV Infection. Advances in Experimental Medicine and Biology, vol 374. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1995-9_7
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