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In its November issue, (Nature Medicine, Vol. 7, No. 11) is publishing 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 Fauci, director of the US National Institute of Allergy and Infectious Diseases, and Giuseppe Scala, has 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 Baur 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 US 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 Margolis 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.
Author contact:
Dr. Giuseppe Scala
Department of Biochemistry and Biomedical Technology
Medical School, University "Federico II"
80131 Naples, ITALY
Email: scala@dbbm.unina.it Dr. Andreas Baur
Assistant Professor
Department of Dermatology
University of Erlangen
Hartmannstr.14, D-91052 Erlangen, Germany
Tel: +49 9131 8536335
Fax: +49 9131 8536417
E-mail: Andreas.Baur@derma.med.uni-erlangen.de Dr. Jean-Claude Ameisen
Unite INSERM U415
Institut Pasteur
Lille, France
Tel: +33 1 46 33 80 88
Email: ants@club-internet.fr Dr. Leonid Margolis
Laboratory of Cellular and Molecular Biophysics
National Institute of Child Health and Human Development
NIH Bldg. 10, Rm. 9D58
9000 Rockville Pike
Bethesda, MD 20892
Tel: +1 301 594 2476
Fax: +1 301 480 0857
E-mail: margolis@helix.nih.gov Dr. Paolo Lusso
DIBIT- San Raffaele Scientific Institute
Via Olgettina 58
20132 Milano, Italy
Tel: +1 39 02 2643282
Fax: +1 39 02 26434905
E-mail: paolo.lusso@hsr.it (C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza
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