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HIV the worst possible STD

Sept 23rd 2017

Scientists have designed a drug to attack nearly all HIV strains and prevent the infection in monkeys.

The International Aids Society has called it an 'exciting breakthrough'. Human trials will start in 2018 to see if it can offer the same protection in people.

What makes it so difficult for our bodies to fight HIV is the virus's incredible ability to mutate and become a different strain.

But after years of infection, a tiny number of patients develop powerful weapons (called broadly neutralising antibodies) that attack the majority of HIV strains. Scientists have been trying to engineer these antibodies to both treat HIV and prevent infection in the first place.

The newly engineered vaccine combines three of these antibodies into an even more powerful defense against HIV. The work is a collaboration between the US National Institutes of Health and the pharmaceutical company Sanofi.

Dr Gary Nabel, the chief scientific officer at Sanofi and one of the report authors, told BBC News: "They are more potent and have greater breadth than any single naturally occurring antibody that's been discovered."

Researchers tested the antibody on 24 monkeys. None of them developed HIV when they were later injected with the virus.

The study is published in the journal Science.

Related: Hunt wants NHS to treat a million more by 2021 (provided by ITN News)

June 3rd 2017

Despite extensive efforts, there’s still no cure for HIV. Since the virus often lives dormant in cells, it’s difficult for doctors to deem a person is cured. But, a newly developed test may be sensitive enough to identify “hidden” HIV, according to research published in Nature Medicine.

The scientists at the University of Pittsburgh who developed the test, also found that the amount of people who are thought to be nearly cured of HIV, is much larger than previous estimates.

"Globally there are substantial efforts to cure people of HIV by finding ways to eradicate this latent reservoir of virus that stubbornly persists in patients, despite our best therapies," said senior author Phalguni Gupta, in a statement. "But those efforts aren't going to progress if we don't have tests that are sensitive and practical enough to tell doctors if someone is truly cured."

Thanks to the development of antiretroviral therapies, or ART, people with the virus have been able to live significantly longer and healthier lives. Despite the therapy being successful, it’s key to know if the present HIV infected cells have the ability to replicate. Currently, the best available test to detect this is called Q-VOA, which stands for quantitative viral outgrowth assay.

Disadvantages of Q-VOA is that it’s costly, requires a large amount of blood, and is time-consuming. Typical costs can be around $1,200 (‎£931.80), according to Johns Hopkins University.

Gupta and his colleagues have developed TZA - a test that’s quicker, cheaper, requires less blood, and is less labour-extensive than Q-VOA. TZA works by detecting a gene that is activated only when replicating HIV is present.

"Using this test, we demonstrated that asymptomatic patients on antiretroviral therapy carry a much larger HIV reservoir than previous estimates—as much as 70 times what the Q-VOA test was detecting," Gupta said. "Because these tests have different ways to measure HIV that is capable of replicating, it is likely beneficial to have both available as scientists strive toward a cure."

In the United States, about 1.2 million people are living with HIV, according to the Centers for Disease Control and Prevention. It’s estimated about 1 in 8 of them don’t know it. People who are most affected include young African American gay and bisexual men.

May 20th

HIV cure a step closer after scientists remove virus's DNA from living tissue

Scientists have managed to remove DNA of the HIV virus from living tissue for the first time in a breakthrough that could lead to an outright cure.

At the moment, treating the disease involves the use of drugs that suppress levels of the virus so the body’s immune system can cope.

Now researchers in the US have revealed they used gene-editing technology to remove DNA of the commonest HIV-1 strain from several organs of infected mice and rats.

In April, the same team reported that they had successfully eliminated the virus from human cells in the laboratory, but a paper in the journal Nature Gene Editing revealed they had managed to do the same thing in live animals for the first time.

The researchers’ team leader, Professor Kamel Khalili, of Temple University, said: “In a proof-of-concept study, we show[ed] that our gene-editing technology can be effectively delivered to many organs of two small animal models and excise large fragments of viral DNAfrom the host cell genome.”

The current antiretroviral drugs for HIV are not able to eliminate HIV-1 from the infected cells.

And if treatment is interrupted, the virus can start replicating quickly, putting patients of risk of getting full-blow AIDS.

This is because it is able to persist in immune system T-cells and other places where it is not actually active and is unaffected by the current treatments.

The researchers used a specially adapted virus to deliver the gene-editing system into the cells.

“The ability of the rAAV delivery system to enter many organs containing the HIV-1 genome and edit the viral DNA is an important indication that this strategy can also overcome viral reactivation from latently infected cells and potentially serve as a curative approach for patients with HIV,” Professor Khalili said.

In a statement, Temple University said the implications of the new study were "far-reaching".

"The gene-editing platform by itself may be able to eradicate HIV-1 DNA from patients, but it is also highly flexible and potentially could be used in combination with existing antiretroviral drugs to further suppress viral RNA. It also could be adapted to target mutated strains of HIV-1," it added.

Professor Khalili said a clinical trial could happen within the next few years, but he first planned to carry out a similar study involving a larger group of animals.

The hottest news in AIDS in the last year was the partial success in a South African clinical trial of a microbicide — a gel women can put in their vaginas to kill the virus before it can infect them with HIV.

The whole field of protection before sex is “red-hot cool right now,” said Sharon L. Hillier, a gynecology professor at the University of Pittsburgh’s medical school and principal investigator of the Microbicide trials network . “People are really energized.”

Although the gel offered only about 40 percent protection against the virus, it was the first form of protection that women could use without men knowing, which is crucial because so many men around the world absolutely refuse — sometimes violently — to wear condoms when having sex with their wives or girlfriends.

Other clinical trials will report their results in 2011 and 2012 and, if all goes well, researchers hope to have a product or two ready to enter the market by 2013.

The first may not be a gel, however.

In the next few months, said Mitchell Warren, executive director of AVAC, an advocacy group for AIDS prevention, “we’re going to see a cascade of results” from trials of what is called “oral pre-exposure prophylaxis,” or “oral prep” for short. In them, men and women who are not infected with the AIDS virus but who regularly engage in high-risk sex, like anal sex without condoms or sex for money with strangers, take a daily dose of one or two of the antiretroviral drugs normally taken by infected people. If many fewer of those subjects become infected than subjects taking a placebo, a second breakthrough will have been achieved.

Should that happen, regulatory authorities may approve pills faster than a gel, because they have already been found safe and effective for treatment.

But that doesn’t mean a gel isn’t still worth pursuing, said Dr. Salim Abdool Karim, a professor of epidemiology at the University of KwaZulu-Natal in South Africa and a leader of the microbicide trial for which results were released in July.

Gels have advantages. The drug in them stays in the vaginal tissue, so it is unlikely that anyone who gets infected anyway would develop a drug-resistant form of the virus. And unlike pills, gels also protect against herpes.

Also, as several experts pointed out, women like having choices in birth control: some prefer a daily pill, some prefer condoms, or IUDs, or shots that last three months, or skin implants that last three years. Presumably, they will also want choices in AIDS prevention.

“The simple truth is: one size does not fit all,” Dr. Karim said.

Because 95 percent of gay American men and 40 percent of heterosexual American women have had anal sex at least once during their lifetimes, according to surveys, rectal versions of the gel are being developed. Tests of new, less viscous formulations that are less likely to draw water into the rectum, making use unpleasant, will begin soon, said Dr. Ian McGowan, another leader of microbicide trials at the University of Pittsburgh’s medical school.

Gay and bisexual black and Hispanic men, who are now the highest AIDS risk groups in the United States, will be recruited soon in Boston, Pittsburgh and Puerto Rico to see if they find the gels acceptable, he said.

But first it is crucial to make sure gels don’t inflame the rectal lining, which is more fragile than the vagina’s. Since H.I.V. zeros in on activated immune cells, inflammation increases infection risk. Brief tests of irritation and acceptability will be done on people advised to remain celibate during the tests, he added. Larger trials, in which thousands of men and women regularly practicing anal sex are given gel or placebo will not begin for two to three more years.

“The rectal microbicide field is about 10 years behind the vaginal one,” Dr. McGowan said.

That is partly due to misconceptions.

“When you mention rectal microbicides, a lot of people say ‘Oh, come on,’ because they think you have to protect the whole colon, and it’s meters long,” Dr. McGowan said. In fact, researchers believe protecting only the last six to eight inches will suffice.

A 2008 British study showed that rectal tenofovir gel was very protective in monkeys that were then given anal doses of the virus that causes simian AIDS.

Farther over the horizon, another method is being tested for possible deployment by 2015 or so. Next year, a trial will begin of a vaginal ring containing a new antiretroviral drug, dapivirine. Dapivirine was never approved as a pill because the body doesn’t absorb it well, but it can build up in vaginal tissue. Also, it is so concentrated that a month’s worth fits in a ring that allows a tiny amount to trickle out each day.

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