"I care… Do you?" is the slogan of the World AIDS Day campaign Dec. 1. It marks the second and concluding year of a sustained focus on the role of men in the epidemic.
One principle goal is to engage young men more fully in assuming their share of responsibility for stemming the spread of new infections. A quarter of all HIV disease is concentrated in men under the age of 25, making them the most likely to already be infected and the most exposed to the possibility of new infections. A second goal is to encourage politicians to exercise leadership in the fight against AIDS.
Men's views of women and of sex encourages spread of the epidemic, while the macho stance that "real men don't get sick" translates into a mentality of denial and a disinclination to visit a doctor when problems first arise. Both serve to perpetuate the plague.
"Gay men tend to weight the benefits and drawbacks of revealing that they have HIV," writes Ohio State University researcher Julie Serovich in the journal AIDS Education and Prevention. Her survey found that the men disclose their status to keep friends and family safe, to seek support, and because they feel that others have the right to know.
But the same set of criteria may not apply when it comes to telling their partners. "The consequences with sexual partners are very different than the consequences with family and friends," says Serovich. "They may worry more about whether or not they'll still have a relationship or if they'll be abandoned if they do disclose."
Another piece of the scientific puzzle of HIV fell into place Nov. 19 when NIH scientists announced that once inside a cell, in order to replicate, the virus must attach itself to floating rafts of cholesterol located in the double-walled outer membrane of the cell. Experiments in the lab showed that reducing or removing this cholesterol in cells greatly inhibited viral replication.
Now the trick is to see if the same thing happens in humans. One substantial fear is that the cell uses cholesterol for other basic functions, perhaps exchanging food or waste through the membrane, or maybe chemical signaling to other cells. Simply removing cholesterol also would disrupt these other functions and the cell may die.
The more likely route to therapy will involve developing a drug that can enter the cell and bind to the Gag protein of HIV that the virus uses to attach itself to cholesterol. That would keep the virus bottled up and unable to replicate.
Another team of NIH researchers, this one lead by Michael Polis and published in The Lancet, has found that measuring the decline in viral load just six days after beginning a new therapy is a good predictor of how successful that regimen will be.
Using data from three previous clinical trials where viral load was monitored daily, the team found that a drop of 50-fold or more at day six usually meant long-term success, while a drop of five-fold or less predicted failure. This single measurement predicted the outcome 95 percent of the time. The practical impact of this discovery may be to limit the time a patient spends on drugs that are not working adequately.