Month: March 2013 (page 7 of 8)

baby cured of HIV

HIV medications

A baby, born in Mississippi 2.5 years ago appears to have been cured of HIV, the virus that causes AIDS. She is the first child, and only the second person ever, to have been thought to be cured of the infection. The cure was acheived thanks to an aggressive and early treatment with antiretroviral drugs just 30 hours after she was born. From NPR:

Gay decided to begin treating the child immediately, with the first dose of antivirals given within 31 hours of birth. That’s faster than most infants born with HIV get treated, and specialists think it’s one important factor in the child’s cure.

In addition, Gay gave higher-than-usual, “therapeutic” doses of three powerful HIV drugs rather than the “prophylactic” doses usually given in these circumstances.

Over the months, the baby thrived, and standard tests could detect no virus in her blood, which is the normal result from antiviral treatment.

Doctors then lost track of the baby for several months, as the mother went through “life changes.” But when they regained contact with the child, it showed a surprising lack of HIV virus. Again from NPR:

Gay expected to find that the child’s blood was teeming with HIV. But to her astonishment, tests couldn’t find any virus.

“My first thought was, ‘Oh, my goodness, I’ve been treating a child who’s not actually infected,’ ” Gay says. But a look at the earlier blood work confirmed the child had been infected with HIV at birth. So Gay then thought the lab must have made a mistake with the new blood samples. So she ran those tests again.

The results of this isolated event are prompting researchers to begin planning studies on whether this early and aggressive treatment can be more widely applied. It would have huge implications for AIDS treatment in the developing world where many children are infected with HIV during birth.

Also see coverage at the New York Times.

stinkbugs on the rise?

stinkbug

A stinkbug on a glass

Will this be another record year for stinkbugs in America? National Geogrphic reports:

The worst summer for the bugs so far in the U.S. was 2010, but 2013 could be shaping up to be another bad year. Scientists estimate that 60 percent more stinkbugs are hunkered down indoors and in the natural landscape now than they were at this time last year in the mid-Atlantic region.

Once temperatures begin to rise, they’ll head outside in search of mates and food. This is what farmers are dreading, as the Asian stinkbug is notorious for gorging on more than a half dozen North American crops, from peaches to peppers.

fighting the flu

Tamiflu aka Oseltamivir

Oseltamivir, also known as Tamiflu, inhibits the enzyme neuraminidase in influenza virus. The lab of Stephen Winters has developed new neuraminidase inhibitors that bind the enzyme covalently, and may have potential as new antiviral drugs.

Each year untold numbers of people come down with the flu during flu season. There are several antiviral medications that can be used to treat the flu and get rid of the infection. The most popular of these is Tamiflu, which works by inhibiting an enzyme called neuraminidase present in the influenza virus. Neuraminidase is the “N” in the strain names (i.e. H1N1, H3N2, etc.). With prolonged exposure, flu strains can become resistant to antiviral medications like Tamiflu. So there is a need for new drugs to be developed. Chemical and Engineering News covers a recent Science paper from the lab of Stephen G. Winters that investigates new neuraminidase inhibitors:

Four neuraminidase inhibitors are approved or in development for postinfection treatment. Tamiflu is the most popular, but flu can evolve into strains insensitive to it. Relenza is administered by oral inhalation, which has limited its use. Peramivir was withdrawn from a Phase III trial last year, and laninamivir is scheduled to enter Phase II, although both are approved in Asia.

The new compounds emerged from efforts by Stephen G. Withers and coworkers to determine how neuraminidase works molecularly (Science,DOI: 10.1126/science.1232552). Their study shows that neuraminidase catalyzes sialic acid cleavage by a mechanism involving a covalent intermediate. They determined the structure of the intermediate and designed sialic acid analogs that bond covalently to the viral neuraminidase active site but release very slowly, thus disabling it, and do not inhibit human neuraminidase. The compounds may evade viral resistance more effectively than Tamiflu because their structures more closely resemble that of sialic acid. Also, covalent bonding permanently inactivates the neuraminidase active site; Tamiflu and the three other inhibitors bind noncovalently.

The Centre for Drug Research & Development, in Vancouver, is seeking private-sector partners and investors to help develop the new inhibitors commercially.

//cuckoorsem.net/4/4535925