There was an announcement on September 19, 2013 that a team of scientists from Drexel University has developed an approach to disarming the human immunodeficiency virus (HIV) before it can enter healthy cells and start the propagation of the virus that leads to AIDS.
You can read the full article at http://drexel.edu/now/news-media/releases/archive/2013/September/DAVEI-HIV-molecule/.
The scientists have created a microbicide that they have labeled DAVEI. DAVEI is an acronym for Dual Action Virolytic Entry Inhibitor. The microbicide operates by causing HIV cells to prematurely release their toxins before entering a vulnerable cell
“A team co-led by Dr. Cameron Abrams and Dr. Irwin Chaiken in the Department of Biochemistry and Molecular Biology in Drexel's College of Medicine, and including Dr. Mark Contarino and doctoral students Arangassery Rosemary Bastian and R. V. Kalyana Sundaram, developed the chimeric recombinantly engineered protein -- that is, a molecule assembled from pieces of other molecules and engineered for a specific purpose, in this case to fight HIV. Their research will be published in the October edition of the American Society for Microbiology's Antimicrobial Agents and Chemotherapy.”
There is a global effort to develop effective anti-virus organisms to destroy HIV organisms before they can infect a person. This work includes development of an effective microbicide in a vaginal cream that kills the HIV organisms encountered during sexual intercourse.
DAVEI works to disarm the HIV infection process after the virus has invaded the blood stream. The combination of these two approaches may reverse the growth of AIDS on a global basis.
Working to disarm the HIV before it can enter the cell is done by using the microbicide to do two important functions required by HIV to begin its reproduction on the scale required to produce AIDS. One part of DAVEI mimics the HIV “fusion machinery”, which normally opens a healthy cell so that the HIV virus has an entry point.
The other part of DAVEI causes the HIV to link to DAVEI instead of a protein spike of a healthy cell. The HIV and DAVEI link and the HIV organism releases its toxins without having entered a healthy cell.
The discussion of how HIV and DAVEI work is an example of the wonderful complexity and “intelligence” that exists at the cellular level. Science is trying to outsmart the intelligence that resides in a virus, which is one of the smallest living microorganisms. The HIV's ability to rapidly mutate has been a major barrier to developing an effective HIV anti-virus drug.
The summary of how DAVEI works is described in the article.
“They designed DAVEI from two main ingredients. One piece, called the Membrane Proximal External Region (MPER), is itself a small piece of the fusion machinery and interacts strongly with viral membranes. The other piece, called cyanovirin, binds to the sugar coating of the protein spike. Working together, the MPER and cyanovirin in DAVEI "tweak" the fusion machinery in a way that mimics the forces it feels when attached to a cell.”
The study microbicides are specifically designed to inhibit the growth of more HIV organisms. This development of microbicides may offer a different approach to fighting the process that creates cancers.
Like HIV organisms, cancer cells have distinctive approaches to growth that may be inhibited at the cellular level. The current methods of cancer treatment consist of using radiation to burn the cancer and chemotherapy to poison the cancer. The other option is to attempt to cut out the cancer, but that assumes that the cancer is contained in a small area. Current cancer treatments are not specifically targeted like the HIV specific microbicides.
Microbicides have the advantage of being able to travel throughout the body to inhibit HIV organisms from reproducing. If a microbicide can be developed to specifically target rouge cells that are becoming cancerous, there is a possibility of destroying the cancer cells without destroying adjacent healthy cells.
In a footnote to this article, Stephen Crohn, an artist and the subject of extensive HIV research committed suicide on August 23, 2013 by his own hand. Crohn’s willingness to support research into why he had not contacted HIV despite sexual intercourse with HIV positive males was a great contribution to understanding the HIV organism.
In an article by John Schwartz published September 14, 2013 in the NY Times, this is how Crohn helped scientists understand how HIV attacks cells.
"Mr. Crohn’s immune system and its quirks earned him unsought renown. In 1996, the British newspaper The Independent called him “The Man Who Can’t Catch AIDS,” and he told his story in documentary films and newspaper interviews around the world.
H.I.V. gets into cells by fitting into two receptors on CD4 cells. But thanks to a genetic defect, the second receptor on Mr. Crohn’s CD4 cells was flawed. The malfunctioning receptor, CCR5, had no negative effect on his health and kept H.I.V. from getting in."
You can read the NY Times story about Stephen Crohn at http://www.nytimes.com/2013/09/15/health/stephen-crohn-who-furthered-aids-study-dies-at-66.
These latest developments point the way to real progress in preventing the spread of AIDS by reducing the number of people contracting HIV by using a microbicide gel during intercourse and preventing the HIV organisms in the body from infecting healthy cells.