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25 Years of HIV: Don't Give Up

Thu 23 Apr 2009 In: HIV View at Wayback View at NDHA

25 years ago today, on 23rd April 1984, US Health Secretary Margaret Heckler announced the ground-breaking discovery that HIV is the virus that causes AIDS. A computer simulation of what the HIV virus looks like In November 2008, Scientific American ran two articles on the twenty fifth anniversary of the discovery of HIV. Are we any closer to finding a vaccine after all this time? If so, how would it work? As David Watkins notes in his opening article, HIV has proven resistant insofar as vaccine research and clinical trials have gone, and the prospects of eradication or permanently diminished virulence remain as distant as ever. How do vaccines work? Normally, vaccines depend on stimulating bodily immune system responses. For example, flu vaccines operate through using deactivated and dead flu virus components to stimulate immune cells to recognise and produce antibodies to negate any actual future infection. Why doesn't this work with HIV? HIV rapidly reproduces once it enters host cells and goes on doing so, with intensive viral reproduction going on inside one's bloodstream. It especially targets T cells, which assist the immune system to recognise and combat new infections. What's worse still, it even hits 'memory' T cells, which carry genetic data about earlier body responses to prior infections, rendering the body all the more vulnerable to subsidiary opportunistic infections. Moreover, slight mutations occur rapidly while the HIV infection resides in cells, meaning that they can circumvent antibody responses that are geared toward dealing with the initial infection. Because of the above microbiological concerns, it has been difficult to work on anti-HIV vaccines. In some cases, it was hoped that particular cellular protein molecule sequences might be activated or deactivated to stop the insertion of HIV genetic particles into healthy cells. Other projects have attempted to stimulate T cell production early during exposure, thus reducing its virulence, and assisting the survival of memory helper T cells, which would reduce infection virulence as well. HIV diversity is probably the greatest barrier to vaccine production, leading to emphases on specific proteins and/or amino acids. T cell microbiology is still an evolving science however, and much still remains to be understood about how they work. Mario Stevenson then dealt with how it might be done. Current antiretroviral treatments may force HIV down to low levels through suppressing HIV replication within affected cells, and slow its spread. However, notes Stevenson, some 'lurker' dormant HIV cells still exist, able to manufacture new viral particles, but not actually doing so. As Watkins noted earlier, memory helper T cells are especially hard hit by HIV infection, and HIV replication dormancy can 'blind' immune system responses. In other cases, some infected cells churn out new infected HIV carrying viral particles at a lower level. They act as a bodily reservoir, ready to act once an individual stops his or her course of medication. Particular dormancy reservoirs may exist in dormant lymph node and blood memory helper T cells, macrophages and dendritic cells in the lymph nodes, gut and central nervous system tissue, and concentrate in the central nervous system, gastro-intestinal tract, and genital area. Even protease inhibitors have trouble crossing the blood-brain barrier to retard HIV carrying cells or viral particles, which are not so inhibited. To end on a brighter note, however, there are several prospective new drug therapies that may soon become available to combat the progression of the virus. HIV's Viral infectivity factor cellular proteins can inhibit A3G, a protective cellular protein that adversely mutates HIV genes. What if cellular A3G production could be shielded and fight back, retarding HIV reproduction during exposure to the virus? Lens epithelium-derived growth factor helps other cellular proteins to infect cellular genetic material, so inhibiting LEDGF might lead to decreased viral replication. Chromatin remodelers would alter chromatin production in dormant infected T cells, rendering them 'visible' to immune system response. Viral protein U inhibitors might prevent HIV genetic particles through infecting other cells through preventing their dissemination from the cellular surface. All of these options hold promise. However, even if these options thankfully do end up extending the lifespan of HIV+ people, they will continue to carry HIV within their bodies and require a strict regimen of medication for life. As the above information should suggest, we should not engage in safe sex fatigue, given that it is relatively easy to prevent the spread of this debilitating medical condition. Due to the reservoir effect, a vaccine still lies some years - or perhaps decades - in our future. Scientific American's 25 Years Later articles are on the links below. Craig Young - 23rd April 2009    

Credit: Craig Young

First published: Thursday, 23rd April 2009 - 9:28am

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