Important note: Information in this article was accurate in December 2001. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, December 3, 2001
Staff Medical Writers
NewsRx -- In its November 2001 issue, Nature Medicine published three papers that represent great advances in the fight against HIV.
The first describes a strategy that could be developed to yield an effective vaccine against the disease. The other two papers describe previously unknown molecular mechanisms that explain why HIV is so successful at infecting human cells.
One principle of creating a vaccine is to identify a protein section (epitope) of the pathogen causing disease and to inoculate the body in advance with this epitope so that it raises antibodies to that protein, thus destroying the invading pathogen when it is encountered. However, HIV is a rapidly mutating virus and exists in several different forms, or clades. Thus, efforts to make a vaccine against HIV have floundered because identifying a suitable epitope that can generate antibodies that will attach all forms of the virus has not been possible.
Now, a team lead by Anthony Fauci1, director of the U.S. National Institute of Allergy and Infectious Diseases, and Giuseppe Scala, have identified epitopes that correspond to a range of HIV clades. Fauci's team injected macaque monkeys with these epitopes and found that they were protected from subsequent challenge by the simian counterpart of HIV - SHIV. The next step would be to extend these trials to humans.
In a separate paper, Andreas Baur2 and colleagues at the University of Erlangen, Germany, have discovered that a key protein in HIV called nef, is highly skilled at protecting the cell that the virus has infected from destroying itself. Nef achieves this by inactivating another protein called Bad which would ordinarily trigger apoptosis in the cell.
In an accompanying News & Views article, Jean-Claude Ameisen of INSERM, Paris, eloquently explains that within recent months scientists have found that nef not only protects the cell containing the virus from killing itself, but also prevents destruction of that cell by surrounding cells.
Finally, a joint team of scientists from the U.S. and Italy have discovered that HIV co-infection with the human herpesvirus 6 (HHV-6) virus can alter the course of HIV infection. HIV enters cells using two receptors: CD4 and a co-receptor that is typically the CCR5 or the CXCR4 receptor. CCR5 dominates the early stages of infection and is a route used by the virus throughout the course of the disease. Forms of HIV that use CXCR4 are found later in the course of disease progression.
Leonid Margolis3 and Paolo Lusso tested human tonsillar tissue and found that if this was co-infected with HHV-6, the route of infection deviates away from CCR5 and more toward CXCR4. Understanding precisely how HIV infects cells can lead to improved treatments and hopefully a cure for the disease.
The corresponding author for the first study is Dr. Giuseppe Scala, Department of Biochemistry and Biomedical Technology, Medical School, University Federico II, 80131 Naples, Italy; e-mail: scala@dbbm.unina.it.
This article was prepared by AIDS Weekly editors from staff and other reports.
References
1. Chen X, Scala G, et al., "Protection of rhesus macaques against disease progression from pathogenic SHIV-89.6PD by vaccination with phage-displayed HIV-1 epitopes", Nat Med 2001 Nov;7(11):1225-31
2. Baur AS, et al., "HIV-1 Nef associated PAK and PI3-Kinases stimulate Akt-independent Bad-phosphorylation to induce anti-apoptotic signals", Nat Med 2001 Nov;7(11):1217-24
3. Lusso P, Margolis L, "Suppression of CCR5- but not CXCR4-tropic HIV-1 in lymphoid tissue by human herpesvirus 6", Nat Med 2001 Nov;7(11):1232-5
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