(WB) New antiviral appears to block the door

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(WB) New antiviral appears to block the door

The Washington Blade - November 13, 1998
Lisa Keen


While other antiviral drugs against HIV work inside the immune cell to stop some phase of the virus's replication process, a new drug receiving favorable attention in recent weeks is one that works to block the virus from entering the cells.

The new drug is T-20 (the T stands for its manufacturer Trimeris), and it is identified as a "fusion inhibitor." From early reports, a fusion inhibitor seem to work like this: If HIV enters the CD4 cell through a door, then a fusion inhibitor, like T-20, would be like a petroleum jelly on the doorknob that would inhibit HIV's ability to open the door.

A study published by researchers at the University of Alabama in the November issue of Nature Medicine reported trying the drug on 16 patients with HIV over the course of two weeks. The results were "equivalent to the activity of the most potent drugs" now available, according to AIDS researcher Douglas Richman, who commented on the study in the same issue.

Richman cautioned, however, that researchers still must prove that T-20 can remain potent and durable on a long-term basis and that the drug at present requires intravenous administration, making it less practical than the other drugs.

More concerns raised around heart problems

Concerns were reported earlier this year that the use of certain antiviral drugs might be causing some heart problems for people with HIV. But a report in the Oct. 15 issue of the New England Journal of Medicine suggests that HIV disease itself might be causing the problems.

Researchers in Italy studied 952 people with HIV who had not yet developed physical symptoms of illness. They found that 8 percent showed some signs of "dilated cardiomyopathy," a heart disease in which the heart muscle loses some of its ability to pump because the left ventricle has become dilated. The problem was more prevalent in patients with CD4 counts below 400.

Their conclusion: The heart disease seen in people with HIV "may be related either to a direct action of HIV" on heart tissue or to an indirect action. Their recommendation: That a "careful cardiologic evaluation should be made to detect early involvement of the heart in HIV positive patients." Those patients with heart disease, noted the researchers, may then be helped with conventional treatments.

In brief ...

CONFIRMING COMBOS: A study in the Nov. 5 Journal of the American Medical Association confirms earlier research indicating that the combination therapies using protease inhibitors have delayed the progression to full-blown AIDS and, to a lesser degree, prolonged the length of survival to death once full-blown AIDS was diagnosed. In the latest study, at UCLA and other sites studied the progress of 536 men whose approximate time of HIV infection could be documented.

ddI ONCE A DAY: A report from an AIDS Conference in Scotland this week indicates that people with HIV taking ddI may be able to take one 400mg dose per day, instead of the current standard of two 200mg doses. Researchers from Alabama reported to the International Congress on Drug Therapy in HIV Monday that a study of dosing with 87 patients found the drug effective "regardless of [its] dosing frequency."

BACTERIAL BUSTERS: People who are infected with bacteria -- especially bacteria associated with sexually transmitted diseases -- when they are infected with HIV have a more rapid disease progression, according to a study published in the October issue of the Journal of Clinical Investigation. The study was conducted by the National Institute of Allergy and Infectious Diseases and Howard University.

COMBO WON'T BE ENOUGH: A small study from Spain, reported in the Oct. 10 issue of The Lancet, indicates that combination therapy with protease inhibitors will "most likely not be enough" to enable the immune system to mount an adequate defense against HIV infection. The study monitored 159 people with HIV who had CD4 counts above 500, viral loads below 10,000, and no outward symptoms of disease. The group was divided into thirds: one subgroup got no therapy, one third got therapy with a two-nucleoside combination, and the third got d4T-3TC-ritonavir. Neither the treated nor untreated subgroups developed immune cells specific to attacking HIV. A report this summer in the journal Infection identified a new immune modulator called WF10 as having the possibility of enhancing the immune system without triggering HIV replication.
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