A really clever approach to stopping HIV In simple language.

By ACSH Staff — Feb 19, 2015
Pick up any newspaper today, and it will be on page 1: A potentially game changing advance in inhibiting HIV replication discovered at Scripps Institute. Rather than regurgitate the story, which is tough reading, we thought we'd try to explain the concept in a more understandable way.

Screen Shot 2015-02-19 at 1.25.15 PMPick up any newspaper today, and it will be on page 1: A potentially game changing advance in inhibiting HIV replication discovered at Scripps Institute.

Rather than regurgitate the story, which is tough reading, we thought we'd try to explain the concept in a more understandable way.

ACSH s Dr. Josh Bloom, a former researcher in the antiviral field, gives it a shot: There are numerous discrete steps that all viruses have in common. Two of these are binding to the host cell, and then chemically drilling their way into the cell, after which they take over the cell and cause it to manufacture more virus. The latter process is called fusion. Both of these steps are required to get the virus into the host cell. Disrupting either step prevents this process, which is also called cell entry.

There are two approved HIV entry drugs one for each step. Pfizer s Selzentry inhibits the binding of HIV to the cell, and Roche s Fuzeon inhibits the fusion. Although both drugs are useful, the virus has ways of defeating them, and there are side effects from both of them.

Bloom continues: But, when a single molecule can bind to two sites at the same time, it not only will be a more potent inhibitor, but will also make it much more difficult for the virus to fight it off. This is the beauty of the Scripps discovery.

This is reflected by Anthony S. Fauci, M.D., director of the National Institute of Allergy and Infectious Diseases, and a champion against AIDS since the very beginning: This innovative research holds promise for moving us toward two important goals: achieving long-term protection from HIV infection, and putting HIV into sustained remission in chronically infected people.

Perhaps even more interesting is that the molecule, which is called eCD4-Ig, acts in some ways like a drug and a vaccine. It is blocking specific mechanisms that are targets of AIDS drugs, but does so using a modified antibody, which can be a vaccine component.

The results speak for themselves. The drug wiped out all traces of HIV and SIV the monkey equivalent of HIV in cell cultures, mice with humanized immune systems as well as macaque monkeys. This is unprecedented.

Dr. Bloom says, Thirty four years since the beginning of the AIDS epidemic, one vaccine candidate after another has gone down in flames. Nothing has come even close to working. This is different. Pay attention.