HIV was a virus which had medical professionals stumped for many years. How the virus operated was unknown and much research was needed to establish the modus operandi of the virus. It took until 2001 for it to be established that the virus attacked the immune system in a unique manner. This article is going to take a quick look at the research conducted and the conclusions drawn.
Research discovered that the immune system generated HIV specific T cells to combat the viral infection. However, it was found that a high viral load inhibited the ability of these HIV specific cells to react to the infection by proliferation. The cells effectively were deactivated. This inhibited ability to respond to the HIV infection does not only apply to that specific virus. The virus also inhibits the immune system’s ability to respond to other pathogens. It was established that the virus did not just attack the human immune system, it manipulated the immune system in such a way that it enhanced the virus’ ability to survive. For more information on hiv insurance, go to http://www.hivlifecover.co.za
A set of tests were conducted on three groups of individuals. One group consisted of individuals with progressive HIV infections, the second of individuals who were classified as long term non-progressors and the third group consisted of individuals who elected to cease treatment for a sufficient length of time to allow the virus to rebound. It was found that all three groups of individuals had comparative levels of CD4+ T cells in their blood streams. This indicated that the virus did not destroy the T cells. It was found that the T cells did not increase in population when the virus load increased indicating that the virus had managed to render them inactive. When treatment was stopped in those individuals who had active T cells the viral loads increased and the T cells became inactive once again until such time as treatment was resumed and the viral load was brought under control.
The conclusion of this study was that the loss of active CD4+ T cells was not a cause of the increased viral load but rather an effect of the virus itself. Prior to this study it was theorised that interruptions in treatment for HIV might stimulate anti-HIV responses in the immune system. This has led to the conclusion that interrupting therapy is more likely to be detrimental than helpful in the long term treatment of HIV. Some information was also gathered with regards to how the virus disrupts the immune system and causes the deactivation of the CD4+ T cell.
Although the study really opened up a lot of questions with regards to how to treat the condition it also provided a number of answers to questions regarding the actual operation of the virus. It is hoped that further study will provide more answers and lead to more effective treatment for the disease. It will take a great deal of time and many years of study to develop more advanced and more effective treatments.