AIDS success ‘unworkable’ for vast majority


Graphic representation of the AIDS virus.

Graphic representation of the AIDS virus. Copyright: Preshkova,

Speed read

  • For the second time, a bone marrow transplant eliminates the AIDS virus from the blood of a patient
  • Given its complexity and cost, this method is not likely to be used on a large scale
  • Pending ongoing research, ARVs remain the recommended treatment
Medical experts hailed the news this week that a second HIV-positive man appears to have eliminated the virus from his body, but warned the treatment used is completely unviable for the vast majority of the 37 million people living with the disease.

AIDS, caused by infection with the human immunodeficiency virus (HIV) virus, is one of the three big diseases affecting people in the developing world along with tuberculosis and malaria. Around a million people died from AIDS-related illnesses in 2017.

Researchers from University College London (UCL) reported 5 March in the journal Nature the case of an HIV-positive man who, after receiving a bone marrow transplant, no longer showed any sign of the AIDS virus, 18 months after he had stopped taking antiretroviral therapy.

Presenting their work on the same day at the annual conference on retroviruses and opportunistic infections in Seattle, USA, the researchers said they used largely the same method which had been used in 2007 in Berlin on Timothy Ray Brown.

“Even reaching a very limited number of people to achieve ‘near-cure’ of HIV infection is a welcome achievement. It still seemed utopian a decade ago.”

Avelin Aghokeng

The so-called “Berlin patient” is considered the first person in the world to have been cured of HIV/AIDS, as the virus has not been detected in his body since then.
The method involves finding a compatible donor who additionally has a mutation in a gene called CCR5.
It is this gene that causes the AIDS virus to penetrate the immune cells and multiply. But the mutation prevents the virus from entering and taking hold.

As a stem cell, the transplanted bone marrow will produce new immune cells containing the mutated CCR5 gene which will gradually replace the old cells, blocking the virus, which can no longer replicate.

“Continuing our research, we need to understand if we could knock out this receptor in people with HIV, which may be possible with gene therapy,” said Ravindra Gupta, lead author of the study in a statement published by UCL.

There are strong reservations about this method, however, among parts of the scientific community.

Eric Delaporte, head of the laboratory for translational research on HIV and infectious diseases at the Institute of Research for Development (IRD), in France, says the rare genetic mutation is only found in one per cent of the population.

“As is often the case with AIDS, we are dealing with an overrepresentation of a result where we speak of ‘healing’, when in practice, for the millions of people living with HIV, this is not the solution,” he tells SciDev.Net.

‘False hope’

Delaporte also finds the process “complicated and dangerous”.

“You have to put the patient in aplasia, that is, destroy the cells with chemotherapy and then transplant the marrow of a compatible donor,” he says.

“During the aplasia phase when cells are destroyed, the slightest infection can kill, because the patient has no defence. It must therefore take place in a specialist unit with a sterile room, so with an advanced, sophisticated and expensive medical infrastructure.”
For Delaporte, the excitement around the story gives “false hope”.
But Michel Sidibé, executive director of UNAIDS, gives a more nuanced view.
“Although this breakthrough is complicated and much more work is needed, it gives us great hope for the future that we could potentially end AIDS with science, through a vaccine or a cure,” he wrote in a press release issued by the organisation.
“However, it also shows how far away we are from that point and of the absolute importance of continuing to focus HIV prevention and treatment efforts.

Sidibé’s optimism is shared by Avelin Aghokeng, researcher at the International Centre for Medical Research in Franceville, Gabon.

“Even reaching a very limited number of people to achieve ‘near-cure’ of HIV infection is a welcome achievement. It still seemed utopian a decade ago,” he says.
“Advances in research are enriched by such proofs of concept and open up new avenues for research and intervention.”

‘Proof of concept’

“Although it is not a viable large-scale strategy. these new findings reaffirm our belief that there exists a proof of concept that HIV is curable,” says Anton Pozniak, president of the International AIDS Society (ISA).

The British infectious disease specialist said he hoped “that this will eventually lead to a safe, cost-effective and easy strategy to achieve these results using gene technology or antibody techniques.

The authors of the work prefer to focus on the potential for the scientific community.

“If it is too early to say for sure that our patient is now cured of HIV, the apparent success of stem cells gives hope that new strategies can be developed to combat the disease,” says research team member Eduardo Olavarria.

Commenting on the findings in relation to the 2007 case, Aghokeng says the question of reproducibility of a procedure, experiment or intervention is “crucial””It is difficult,” he says, “to draw important conclusions from a single case. A second success, realized by another research team and in a different patient, allows scientists to confirm the first result and consider the experiment reproducible,” he tells SciDev.Net.

“It also helps to better control the approach, its benefits and also its limitations and dangers. It should be noted that behind this success are also many failures of this approach.”
Meanwhile, everyone in the scientific community agrees that the only way to treat this disease, which affects 37 million people worldwide, according to UNAIDS, is to take antiretrovirals for life.

How AIDS conquered North America: Researchers restore HIV genomes from serum samples more than 40 years old


HI
HIV particles (yellow) infecting a T cell, viewed under a scanning electron microscope. T-cells perform important functions in our immune system. 

Researchers at the University of Arizona and the University of Cambridge in the U.K. have reconstructed the origins of the AIDS pandemic in unprecedented detail.

The findings were made possible by a molecular technique the team developed for this project, enabling them to recover genetic material from more than 40-year-old serum samples and decipher the gene sequence of the , or HIV, subtype that started the outbreak on the North American continent in the early 1970s. Phylogenetic analyses estimate the jump to the U.S. at about 1970 and place the ancestral U.S. virus in New York City, strongly suggesting this was the crucial hub from which HIV made its way across the continent.

Insights gained from this study may help researchers and health officials better understand how pathogens move through populations and lead to more effective strategies aimed at reining in, or eradicating, dangerous pathogens.

The results will be published in the advance online publication of Nature on Oct. 26. They confirm previous findings retracing the routes by which the virus entered and spread through the U.S. and eliminate any remaining doubt surrounding the Caribbean region as a key steppingstone from which HIV jumped into the U.S. The paper also reports the first recovery of the full HIV-1 genome from an individual known as “Patient Zero” and shows that there is neither biological nor historical evidence for the widely held belief that he was the primary cause of the HIV epidemic in North America.

While it had been established that HIV already was infecting people in the U.S. before 1981, the year AIDS was recognized, the timing and earliest movements of the virus in the U.S. were unknown until now. Leading an interdisciplinary team of scientists, Michael Worobey, an expert on , and Richard McKay, a scholar specializing in the history of public health, set out on a quest to unravel the secrets surrounding the AIDS epidemic as it unfolded. The endeavor called for new molecular techniques that would make it possible to recover and “restore” genetic material from samples whose age and condition made them intractable to existing analytic methods.

The findings were made possible by a molecular technique the team developed for this project, enabling them to recover genetic material from more than 40-year-old serum samples and decipher the gene sequence of the , or HIV, subtype that started the outbreak on the North American continent in the early 1970s. Phylogenetic analyses estimate the jump to the U.S. at about 1970 and place the ancestral U.S. virus in New York City, strongly suggesting this was the crucial hub from which HIV made its way across the continent.

Insights gained from this study may help researchers and health officials better understand how pathogens move through populations and lead to more effective strategies aimed at reining in, or eradicating, dangerous pathogens.

The results will be published in the advance online publication of Nature on Oct. 26. They confirm previous findings retracing the routes by which the virus entered and spread through the U.S. and eliminate any remaining doubt surrounding the Caribbean region as a key steppingstone from which HIV jumped into the U.S. The paper also reports the first recovery of the full HIV-1 genome from an individual known as “Patient Zero” and shows that there is neither biological nor historical evidence for the widely held belief that he was the primary cause of the HIV epidemic in North America.

While it had been established that HIV already was infecting people in the U.S. before 1981, the year AIDS was recognized, the timing and earliest movements of the virus in the U.S. were unknown until now. Leading an interdisciplinary team of scientists, Michael Worobey, an expert on , and Richard McKay, a scholar specializing in the history of public health, set out on a quest to unravel the secrets surrounding the AIDS epidemic as it unfolded. The endeavor called for new molecular techniques that would make it possible to recover and “restore” genetic material from samples whose age and condition made them intractable to existing analytic methods.

“Standard methodology such as antibody-detecting serological blood tests will tell you whether a person had HIV, but you might not be able to get any of the HIV gene sequences out of it, because to do that, you need the RNA from the virus,” says Worobey, a professor and head of the UA’s Department of Ecology and Evolutionary Biology. “The virus’ RNA is an extremely delicate molecule comprising 10,000 nucleotides, and breaks down very quickly.”

Worobey’s lab developed a technique called RNA jackhammering, which breaks down the huge human genome in the samples into tiny overlapping chunks and extracts the RNA of the virus.

“We then very carefully amplify the RNA of the virus without letting the background RNA get in the way,” he explains.

Worobey says the technique may hold potential for other health care applications, such as more sensitive bioassays for screening blood samples for cancer markers or viruses, including Zika.

How AIDS conquered North America
After HIV moved from Africa to the Caribbean, it first spread to New York and subsequently to different locations in the U.S. By constructing evolutionary trees of the various HIV strains as far back as the 1970s, the researchers found evidence that the virus had been circulating under the radar for ten years before the outbreak in the US was recognized. 

By screening more than 2,000 serum samples collected from U.S. men between 1978 and 1979, all of which degraded over time, the technique allowed the researchers to recover eight near full-length viral RNA genome sequences, representing the oldest HIV genomes in North America. This early, full-genome “snapshot” reveals the U.S. HIV-1 epidemic showed surprisingly extensive genetic diversity in the 1970s but also provides strong evidence of its emergence from a pre-exiting Caribbean epidemic.

Having the complete genomic information in front of them allowed the authors to tackle questions that had vexed researchers—for example, how quickly the virus was spreading at different times in different locations. Once HIV had crossed the Atlantic from Africa, it quickly spread through the Caribbean and from there into the U.S. Yet, the epidemic went unnoticed until it hit the U.S. New York City turned out to be the most critical hub for the AIDS epidemic in the U.S., and the newly sequenced genomes showed the virus must have jumped there in, or very near, 1970. From there, HIV spread to San Francisco and presumably to other locations in California, where AIDS patients were first recognized in 1981.

“In New York City, the virus encountered a population that was like dry tinder,” Worobey explains, “causing the epidemic to burn hotter and faster and infecting enough people that it grabs the world’s attention for the first time.

“That information is stamped into the RNA of the virus from 1970,” he says. “Our analysis shows that the outbreaks in California that first caused people to ring the alarm bells and led to the discovery of AIDS were really just offshoots of the earlier outbreak that we see in New York City.”

From the genetic data, the team was able to construct evolutionary trees of the various HIV strains and how they spread through the U.S. They revealed that by the late 1970s HIV had diversified in almost the same genetic diversity we see today.

“Right around 1970, we see the signal of emergence of this virus, which is evidence that it had to have been there at that point in time in at least one person,” Worobey says.

Being able to look back in time and piece together what it took for the HIV pandemic to happen is encouraging, the researchers say.

“Now we can now look forward in time and really see a future in which—even if the virus is not completely eliminated—it could be driven down to no new transmission in large swaths of the world,” Worobey says.

The molecular biology assays developed in this work could lead to more sensitive tests that detect the virus sooner in people who are unaware that they were infected very recently, he says.

“Earlier detection and better alignment of the various options we have to make it harder for the to move from one person to the next,” he says, “are key to driving HIV out of business.”

GENE THERAPY UPDATE: POTENT WEAPONS AGAINST AIDS, CANCER AND MORE


Hard to believe it was once considered little more than theory. Or the stuff of science fiction.

In the past year, leading-edge gene therapy – the process of fighting lethal illnesses by manipulating their mechanisms at the cellular level – has continued to take bold steps out of the laboratory and into the realm of potentially lifesaving treatments. It is no longer beyond imagination, or even far-fetched, to envision a day when, thanks to edited genes, advanced brain tumors disappear, hemophiliacs create their own clotting factor and AIDS patients can stop taking their daily antiviral drugs.
“The field of cell-based therapy is becoming more mature,” says John Zaia, M.D., the Aaron D. Miller and Edith Miller Chair in Gene Therapy, and director of City of Hope’s Center for Gene Therapy.
In typical City of Hope style, theoretical science is getting down to business, with multiple clinical trials underway at City of Hope’s now one-year-old Alpha Clinic. Patients are being recruited to test the safety of gene-based treatments for several cancers, as well as hemophilia and HIV/AIDS.
Leader in HIV/AIDS Research
Zaia, who’s devoted much of his professional life to the AIDS battle, is especially excited about two unique stem cell transplant options that target HIV in different ways. One employs a zinc finger nuclease, or ZFN, to “edit out” the CCR5 receptor on a patient’s harvested stem cells, then reintroduce them. The modified cells deny HIV its normal path to infection.
Another approach uses a lentivirus to add re-engineered, anti-HIV ribonucleic acid (RNA) genes to stem cells, including one that disrupts CCR5.
In targeting CCR5, Zaia and his research colleagues around the world are trying to replicate the case of the so-called “Berlin patient” whose HIV vanished after he received a stem cell transplant for treatment of leukemia. The donor’s CCR5 gene had a mutation that blocked the virus. “There aren’t enough donors with that mutation to replicate the treatment on a large scale,” says Zaia, “so we have to artificially create the mutation.”
In March of 2016 the first patient received Zaia’s RNA/lentivirus-based treatment under an Food and Drug Administration-approved trial, which permits only one participant at a time. Four months later the recipient is tolerating the treatment well, and the accumulated data is providing critical information.
Clinical Trials’ Challenges
Finding the right patients for these trials is a special challenge. However, although the FDA now allows otherwise healthy people with HIV to participate, the risks associated with a stem cell transplant are high, because the patient must first receive an extremely potent course of chemotherapy to “create a space” for the transplanted cells. For this reason, the RNA/lentivirus trial is focused on AIDS patients with lymphoma who’ve completed treatment and are in remission.
“Those patients are just a better population for this trial,” says Zaia. “They’re also more likely to accept the risks.” He praises those willing to come forward, lauding their “wonderful and generous humanitarian gesture.”
As encouraging as the early results may be, they are baby steps. Current therapies modify only a relatively small percentage of a patient’s stem cells. Zaia hopes to one day develop a more efficient mechanism which would fortify a much larger percentage of stem cells, while protecting them from chemo’s toxic effects.
One possibility may emerge from the treatment of brain tumors performed by collaborators at the Fred Hutchinson Cancer Research Center. The usual chemotherapy drug of choice, BCNU, can be seriously toxic to bone marrow. When researchers altered a gene known as MGMT, the BCNU chemo worked more effectively and the marrow was protected.
It remains to be seen whether this approach would provide similar protection in HIV patients. The possibility is intriguing, and it’s one of many reasons Zaia stands by his prediction of a year ago that a “functional cure” for HIV/AIDS (in which the virus is effectively blocked and daily drugs are no longer needed) may be just five years away.
Making Inroads
In the meantime, gene-based technology is making inroads in other Alpha Clinic trials.
For example, the ZFN technique is being adapted for the treatment of hemophilia in which there is a lack of clotting factor. Using the same gene-editing mechanism, researchers have been able to “cut” a normal “housekeeping” gene  and introduce a “corrected” version of the clotting factor into the liver. The process has worked in animal tests, and human trials will begin soon.
Newer gene-editing methods are emerging as well, including the much-talked-about “CRISPR” technology which can find, cut out and replace specific parts of DNA using a specially-programmed enzyme. China is preparing to test CRISPR in the world’s first human trials, and the FDA has approved trials in the U.S., beginning probably next year. Zaia advises caution:
“We do not have clinical trials going for CRISPR-type treatment just ye. It’s much too new and we need to learn more about it. Bear in mind that it took nearly 15 years to get ZFN approved for human patients. But this could eventually be a game-changer, helping us direct our gene-editing efforts with much greater precision.”
The major partner in City of Hope’s gene therapy journey continues to be California’s stem cell agency, the Institute for Regenerative Medicine. CIRM grants helped establish the Alpha Clinic and other facilities across the state, and CIRM funding is fueling many of the ongoing clinical trials, including Zaia’s.
“California is ahead of the curve,” he says, “changing the culture of gene therapy.”

AIDS: 21st century’s biggest fraud.


http://www.pravdareport.com/health/16-05-2012/121133-aids_fraud-0/

AIDS: 21st Century’s biggest fraud. 47117.jpeg

Prince ‘diagnosed with AIDS weeks before his death and was preparing to die’ – shock US claims


Music icon Prince was “preparing to die for a little while” after being diagnosed with AIDS, according to reports in the US.

A music industry source interviewed by The National Enquirer messaged friends on April 19 to say the singer was suffering from the disease.

“He was in bad shape,” the source claimed to the newspaper, as reported by Radar Online.

“Doctors told Prince his blood count was unusually low and that his body temperature had dropped dangerously below the normal 98.6 degrees to 94 degrees.

“He was totally iron-deficient, very weak and often disoriented.

Musician Prince performs onstage at the 36th Annual NAACP Image Awards
Prince died last week

“He rarely ate and when he did, it all came right back up.”

The magazine claims the Purple Rain star was diagnosed with AIDS six months ago after contracting the HIV positive virus “in the 1990s”.

However due to his Jehovah’s Witness faith he refused medical treatment instead believing he could be cured by pray.

National Enquirer front page
Shock National Enquirer front page this week

“God can and will cure me,” he is alleged to have told friends.

Members of his faith are also claimed to have told him to ignore it, saying to the singer he had “everlasting life”.

According to the Enquirer the disease saw him lose more than five stone in weight with the source telling them: “His face was yellowish, the skin on his neck was hanging off and the tips of fingers were a brownish-yellow.”

Prince pictured in 2010

Days before he was dead in a lift at his Paisley Park home in Chanhassen, Minneapolis, he had been seen making runs to a local pharmacy to pick up bags of prescriptions.

An employee at the Walgreens that served Prince said: “We were all just shocked that he came in last night looking so beat. We said, ‘We are praying for you.’”

Prince leaving a Walgreens near his home in Minnesota Wednesday night (20th April) at around 7 PM
Prince leaving a Walgreens near his home

 

A day after his death Prince, 57, was cremated in a private ceremony attended by only three family members including his sister Tyka Nelson, 55.

The claims of Prince suffering from AIDS came as the Mirror learnt he was forced to return to touring in order to boost his finances after it was discovered his spending outstripped his income.

Despite his work being valued at more than £150 million he is said to have suffered “chronic money problems” for years before his death.

The star’s refusal to allow the rights to music and back catalogue to be sold placed an immense strain on his finances, sources close the singer have claimed.

Prince’s final words to his lawyer before he died at home in Minnesota
Tributes have been pouring in

Before his death the singer “consistently shut down” opportunities to fuel his finances, such as licensing his songs to be used in movies, TV shows and commercials.

A source said: “He refused to part with his art.

“He always remained true to his beliefs that his work was his own and despite lucrative offers his music was not for sale.

“To get much needed cash Prince braved the pain barrier to tour Australia earlier this year.

Prince has been remembered all over the world

“You can imagine the toll a 36 hour flight would take on his body.

“Although a genius of music, he was not a genius when it came to business.”

Sources close to the star point to how his frequent impulsive shows were poorly planned and involved little promotion, meaning that while some were successful, a lot were staged at a loss.

It had been reported that Prince’s estate was worth in the region of £200 but the figure is said to have been grossly exaggerated.

The rights to his music however have been estimated to be worth upwards of £150 million in the future.

Days before Prince’s death, two American websites posted a story about “a VERY popular African American celebrity” suffering from AIDS who they refused to name.

A skywritting tribute to Prince at the 2016 New Orleans Jazz & Heritage Festival
A tribute to Prince

On April 18 Blind Gossip posted: “We just received word that a VERY popular African American celebrity – who has recently been in the news – now has what is being described as AIDS.

“Obviously since we are not able to 100% confirm the story – we’re going to leave it as a Blind Item. We want to make it clear we are NOT talking about Magic Johnson.

“This report really hurt our heart.

“According to a person extremely close to the situation, the celebrity, who is known for having a very extreme sexual past reportedly contracted the illness sometime in the 1990s.

“He kept the illness quiet but began taking his medication religiously up until about 2 years ago.”

They finished the article saying: “We’re told that the celebrity is expected to get sicker and sicker, and eventually pass. It can happen as soon as the summer.

“Very sad news.”

HIV particles do not cause AIDS, our own immune cells do


Researchers from the Gladstone Institutes have revealed that HIV does not cause AIDS by the virus’s direct effect on the host’s immune cells, but rather through the cells’ lethal influence on one another.

HIV can either be spread through free-floating virus that directly infect the host immune cells or an infected cell can pass the virus to an uninfected cell. The second method, cell to cell transmission, is 100 to 1000 times more efficient, and the new study shows that it is only this method that sets off a cellular chain reaction that ends in the newly infected cells committing suicide.

“The fundamental ‘killing units’ of CD4 T cells in lymphoid tissues are other infected cells, not the free virus,” says co-first author Gilad Doitsh, PhD, a staff research investigator at the Gladstone Institute of Virology and Immunology. “And cell-to-cell transmission of HIV is required for activation of the main HIV death pathway.”

In a previous investigation, the scientists discovered that 95% of cell death from HIV is caused by immune cells committing suicide in self-defense after an unsuccessful infection. When the virus tries to invade a cell that is “at rest,” the infection is aborted. However, fragments of viral DNA remain and are detected by the resting host cell. This triggers a domino effect in the cell’s defense system, resulting in the activation of the enzyme caspase-1, which ultimately causes the induction of pyroptosis, a fiery form of cell suicide.

In the new study, published in Cell Reports, it was revealed that this death pathway is only activated through cell-to-cell transmission of HIV, not from infection by free-floating viral particles. Using lymphoid tissue infected with HIV, the scientists compared cell death rates between cell-to-cell and cell-free virus transfer. They discovered that while overall rates of infection remained the same, there was significantly more CD4 T cell death if HIV was spread by infection from other cells than by free-floating virus.

“Although free-floating viruses establish the initial infection, it is the subsequent cell-to-cell spread of HIV that causes massive CD4 T cell death,” says co-first author Nicole Galloway, PhD, a post-doctoral fellow at the Gladstone Institute of Virology and Immunology. “Cell-to-cell transmission of HIV is absolutely required for activation of the pathogenic HIV cell-death pathway.”

To confirm this finding, the researchers perturbed viral transfer through a number of means: genetically modifying the virus, applying chemical HIV inhibitors, blocking inter-cellular synapses, and increasing the physical distance between the cells so they could not come into contact with one another. Notably, disruption of cell-to-cell contact effectively stopped the death of CD4 T cells. What’s more, only during cell-to-cell transmission was caspase-1 activated within the target cells, thereby initiating pyroptosis, the pro-inflammatory cell-suicide response.

The scientists speculate that the difference in cell death rates between the two methods of infection is due to the increased efficiency of cell-to-cell transmission. Aborted viral DNA fragments are quickly removed during infection by cell-free HIV particles, so they are not detected by the cell’s defensive system. However, in cell-to-cell transmission, the viral DNA fragments overwhelm cell maintenance, building up until they surpass a threshold and are detected. This then triggers caspase-1 activation and pyroptosis.

“This study fundamentally changes our mindset about how HIV causes massive cell death, and puts the spotlight squarely on the infected cells in lymphoid tissues rather than the free virus,” says senior author Warner C. Greene, MD, PhD, director of the Gladstone Institute of Virology and Immunology. “By preventing cell-to-cell transmission, we may able to block the death pathway and stop the progression from HIV infection to AIDS.”

Other investigators on the study include Kathryn Monroe, Zhiyuan Yang, and Isa Muñoz-Arias from the Gladstone Institutes, and David Levy from New York University College of Dentistry. Funding was provided by the National Institutes of Health, National Institute of Allergy and Infectious Diseases, the UCSF/Robert John Sabo Trust Award, and the Giannini Foundation Postdoctoral Research Fellowship.


Story Source:

The above post is reprinted from materials provided by Gladstone Institutes. Note: Materials may be edited for content and length.


Journal Reference:

  1. Nicole L. Galloway, Gilad Doitsh, Kathryn M. Monroe, Zhiyuan Yang, Isa Muñoz-Arias, David N. Levy, Warner C. Greene. Cell-to-Cell Transmission of HIV-1 Is Required to Trigger Pyroptotic Death of Lymphoid-Tissue-Derived CD4 T Cells. Cell Reports, 2015 DOI:10.1016/j.celrep.2015.08.011

 

N Korea says has ‘cure for MERS, AIDS’


North Korea claims it has produced a single miracle drug that can prevent and cure the deadly diseases of MERS, AIDS, Ebola, and SARS.

This undated image shows a website for Kumdang-2, a drug North Korea claims can cure a range of deadly diseases.

The official Korean Central News Agency (KCNA) reported on Friday that scientists have developed the drug, Kumdang-2, from ginseng and rare-earth elements mixed with very small amounts of gold and platinum.

A South Korean health worker sprays antiseptic solution in a village in Sunchang County, south of Seoul, on June 19, 2015 after the village was opened following two weeks of isolation for quarantine in South Korea’s MERS outbreak. (© AFP)

 

MERS stands for the Middle East Respiratory Syndrome.

Back in 2006 and 2013, North Korea claimed the same drug could cure deadly bird flu outbreaks. According to the pro-North Korea website Minjok Tongshin, the drug was originally developed in 1996.

The report comes as South Korea is battling a MERS outbreak, which has killed two dozen people so far.

Meanwhile, South Korean President Park Geun-hye has held a meeting with World Health Organization (WHO) Director-General Margaret Chan on Seoul’s measures aimed at containing MERS and related cooperation between South Korea and the UN health agency.

MERS, a variant of the SARS virus, causes coughing, fever, pneumonia and kidney failure, but it does not appear to be as contagious as SARS, which swept the Far East and killed some 800 people in a 2003 epidemic.

The vast majority of MERS infections and deaths have been reported in Saudi Arabia, where more than 950 people have been infected and 412 have died of the illness.

There is no vaccine for MERS, which has a mortality rate of 35 percent, according to the WHO.

San Francisco woman proves that HIV doesn’t always cause AIDS: no symptoms after 23 years .


In the 23 years since she was diagnosed with HIV, 61-year-old Loreen Willenberg of Sacramento, Calif., has never taken any drugs to restrain the virus. She has never shown symptoms or become ill from HIV or AIDS. She has experienced no drop in her CD4 T-cells, the immune cells targeted by HIV.

“I haven’t had a decline of CD4 cell count at all, and that’s pretty magnificent, and I’m very humbled by that,” Willenberg said.

“In a clinical sense, I’m not progressing towards AIDS,” she said. “I’m not progressing towards the disease stage.”

“Elite controllers”

Many of the 35 million people who are infected with HIV take complex drug cocktails to prevent damage to their immune system. Scientists hope that Willenberg and others like her can help uncover the key to preventing HIV from progressing to AIDS — without drugs.

According to Dr. Richard Pollard, Willenberg is one of approximately 500 known “elite controllers” whose bodies seem naturally immune to the effects of HIV.

“Their body has such an effective way of reacting to the virus that it’s hard to even detect that they’re virus positive,” he said.

HIV naturally attacks CD4 cells, killing them in order to replicate itself. This allows the virus to overpower the CD8 T-cells that the body would normally use to kill them. Scientists believe that elite controllers have unusually strong CD8 cells that are able to keep the virus in check and prevent it from killing too many CD4 cells or multiplying out of control. Thus, elite controllers are able to be HIV-positive without suffering a loss of immune function.

Willenberg has devoted much of her life to helping elite controllers and others with HIV. She is the founder of the Zephyr Foundation, which advocates around elite controllers, long-term nonprogressors and viremic controllers (those whose immune systems control HIV, but less well than elite controllers), and has participated in 13 separate scientific studies in the past 10 years, to try and help scientists better understand how her body controls HIV.

Life without drugs

Willenberg has been publicly critical of a strain within the medical field that seeks to put elite controllers on HIV drugs. In February, scientists announced the results of a study which concluded that elite controllers actually had worse health than non-elite controllers on HIV drugs. This conclusion was based on the finding that elite controllers spent more nights in the hospital than people on HIV drugs, or even non-elite controllers who were not taking drugs.

Willenberg criticized the research for failing to control for other risk factors.

“I’m really interested in how many of the individuals were obese. How many had diabetes? How many had high levels of LDL?” she said, noting that many of the sites used in the research were in areas known to have high rates of hypertension.

The website Aidsmap also criticized the study, noting that researchers reported that elite controllers had a higher risk of pulmonary disease, even though this effect disappeared after one outlying individual was removed.

According to Willenberg, the very traits that protect elite controllers can be misconstrued as signs of poor health.

“We need to stay mindful that some of the biomarkers that they’re measuring for levels of immune activation and inflammation are those that are closely related to elite controllers’ adaptive immune responses,” she said.

“Do I think that all elite controllers need to be put on meds? No I don’t. I’m not convinced.”

One of Willenberg’s goals — and Pollard’s — is to find a way to free HIV patients from a lifetime of dependency on drugs. Indeed, many of these drugs can have severe side effects that can mimic the symptoms of HIV and AIDS themselves. These side effects include fatigue, cough, diarrhea, fever, headaches, skin rashes, shortness of breath and weight loss. Some drug side effects, such as increased rates of cardiovascular disease, can even be fatal.

Learn more: http://www.naturalnews.com/049726_HIV_AIDS_elite_controllers.html#ixzz3aTPIqYmW

Ability of HIV to cause AIDS is slowing, research suggests.


The rapid evolution of HIV, which has allowed the virus to develop resistance to patients’ natural immunity, is at the same time slowing the virus’s ability to cause AIDS, according to new research. The study also indicates that people infected by HIV are likely to progress to AIDS more slowly — in other words the virus becomes less ‘virulent’ — because of widespread access to antiretroviral therapy (ART).
Dr Mike Turner, Head of Infection and Immunobiology at the Wellcome Trust said: “The widespread use of ART is an important step towards the control of HIV. This research is a good example of how further research into HIV and drug resistance can help scientists to eliminate HIV.”
The rapid evolution of HIV, which has allowed the virus to develop resistance to patients’ natural immunity, is at the same time slowing the virus’s ability to cause AIDS, according to new research funded by the Wellcome Trust.

The study also indicates that people infected by HIV are likely to progress to AIDS more slowly — in other words the virus becomes less ‘virulent’ — because of widespread access to antiretroviral therapy (ART).

Both processes make an important contribution to the overall goal of the control and eradication of the HIV epidemic. In 2013, there were a total of 35 million people living with HIV worldwide according to the World Health Organisation.

The study, published today in the journal Proceedings of the National Academy of Sciences (PNAS), was led by researchers at the University of Oxford, along with scientists from South Africa, Canada, Tokyo, Harvard University and Microsoft Research.

The research was carried out in Botswana and South Africa, two countries that have been worst affected by the HIV epidemic. Across those countries, researchers enrolled over 2000 women with chronic HIV infection to take part in the study.

The first part of the study looked at whether the interaction between the body’s natural immune response and HIV leads to the virus becoming less virulent.

Central to this investigation are proteins in our blood called the human leukocyte antigens (HLA), which enable the immune system to differentiate between the human body’s proteins and the proteins of pathogens. People with a gene that expresses a particular HLA protein called HLA-B*57, are known to benefit from a ‘protective effect’ to HIV. Infected patients with the HLA-B*57 gene progress more slowly than usual to AIDS.

This study showed that in Botswana, where HIV has evolved to adapt to HLA-B*57 more than in South Africa, patients no longer benefit from this gene’s protective effect. However, the team’s data show that the cost of this adaptation to HIV is that its ability to replicate is significantly reduced, therefore making the virus less virulent.

The authors show that viral adaptation to protective gene variants, such as HLA-B*57, is driving down the virulence of transmitted HIV and is thereby contributing to HIV elimination.

In the second part of the study the authors examined the impact of ART on HIV virulence. They developed a mathematical model, which concluded that selective treatment of people with low CD4 counts will accelerate the evolution of HIV variants with a weaker ability to replicate.

Lead scientist, Professor Phillip Goulder from the University of Oxford, said “This research highlights the fact that HIV adaptation to the most effective immune responses we can make against it comes at a significant cost to its ability to replicate. Anything we can do to increase the pressure on HIV in this way may allow scientists to reduce the destructive power of HIV over time.”

Dr Mike Turner, Head of Infection and Immunobiology at the Wellcome Trust said “The widespread use of ART is an important step towards the control of HIV. This research is a good example of how further research into HIV and drug resistance can help scientists to eliminate HIV.”


Story Source:

The above story is based on materials provided by Wellcome Trust. Note: Materials may be edited for content and length.


Journal Reference:

  1. Rebecca Payne, Maximilian Muenchhoff, Jaclyn Mann, Hannah E. Roberts, Philippa Matthews, Emily Adland, Allison Hempenstall, Kuan-Hsiang Huang, Mark Brockman, Zabrina Brumme, Marc Sinclair, Toshiyuki Miura, John Frater, Myron Essex, Roger Shapiro, Bruce D. Walker, Thumbi Ndung’u, Angela R. Mclean, Jonathan M. Carlson, and Philip J. R. Goulder. Impact of HLA-driven HIV adaptation on virulence in populations of high HIV seroprevalence. PNAS, December 2014 DOI: 10.1073/pnas.1413339111

Nelson Mandela: Aids campaigner


Nelson Mandela in October 2003
Like many others, Nelson Mandela did not at first realise the dangers of HIV

Though at first muted in his approach to the issues surrounding HIV/Aids, Nelson Mandela eventually became a dedicated and extremely effective advocate for a more vigorous approach to the disease.

When Mr Mandela was released from prison in February 1990, HIV/Aids had yet to make its full impact on South Africa.

“Start Quote

We are facing a silent and invisible enemy that is threatening the very fabric of our society”

Nelson Mandela

Following his election as president four years later, Mr Mandela faced huge challenges and – like so many other world leaders at the time – failed to fully understand the depth of the problem and did little to help those with Aids.

At the time, the African National Congress (ANC) was gripped by an ongoing debate about both the causes of, and treatment for, Aids.

Some figures, like Thabo Mbeki, Mr Mandela’s successor as president, openly questioned whether Aids was caused by HIV.

After Mr Mandela left office in 1999, he campaigned for more research into HIV/Aids, for education about safe sex and for better treatment for those affected. However, most South Africans still did not mention the disease in public.

Controversy within ANC

According to UN figures, the rate of HIV infection among adult South Africans rose from less than 1% in 1990 to about 17.9% by 2012.

Aids activists demonstrate outside the US consulate in Johannesburg - 17 June 2010South Africa has one of the highest HIV rates in the world

South Africa is currently home to more people with the virus than any other country – 6.1 million of its citizens were infected with HIV in 2012, including 410,000 children (aged 0-14), out of a population of just over 51 million.

The causes of an epidemic on this scale have been many – primarily poverty, but also economic migration, the poor status of women, and unsafe sexual practices, have all contributed to the rapid spread of the disease.

Apart from the human misery caused by Aids, its economic impact has been huge, with South African economic growth rates badly affected.

Having put the issue of Aids on the back burner when in office, Mr Mandela began to make strong pronouncements on the subject after he stepped down in 1999.

HIV/Aids in South Africa

  • People living with HIV: 6.1 million
  • Rate of infection in adults aged 15-49: 17.9%
  • Children aged 0-14 living with HIV: 410,000
  • Deaths due to Aids in 2012: 240,000
  • Orphans due to Aids aged 0-17: 2.5 million

Source: UNAids 2012

On World Aids Day in 2000, he sent out a hard-hitting message, saying: “Our country is facing a disaster of immeasurable proportions from HIV/Aids.

“We are facing a silent and invisible enemy that is threatening the very fabric of our society.

“Be faithful to one partner and use a condom… Give a child love, laughter and peace, not Aids.”

Mr Mandela said his country should promote abstinence, the use of condoms, early treatment, counselling and drugs to reduce mother-to-child transmission.

Urgency

At the time, there was a marked reluctance on the part of the South African government to fund anti-retroviral drugs for those with HIV.

Nelson Mandela with Makgatho (R) in 2003
Mr Mandela’s son, Makgatho (R) died from Aids-related illness in 2005

The then President Mbeki outraged many people when he told a US journalist that “personally, I don’t know anybody who has died of Aids” and that he did not know if he had ever met anyone infected with HIV.

One of his ministers suggested that people with HIV eat garlic and beetroot to combat the infection.

In November 2003, Mr Mandela – and his Nelson Mandela Foundation – stepped up the campaign, launching an HIV/Aids fundraising campaign called 46664, after his prison number on Robben Island.


Nelson Mandela

1918 Born in the Eastern Cape

1943 Joined African National Congress

1956 Charged with high treason, but charges dropped after a four-year trial

1962 Arrested, convicted of incitement and leaving country without a passport, sentenced to five years in prison

1964 Charged with sabotage, sentenced to life

1990 Freed from prison

1993 Wins Nobel Peace Prize

1994 Elected first black president

1999 Steps down as leader

2001 Diagnosed with prostate cancer

2004 Retires from public life

2010 Last major public appearance at football World Cup in Johannesburg

He compared the urgency and drama of his country’s struggle against HIV/Aids to the fight against apartheid.

Pop stars like Beyonce, Youssou N’Dour and Dave Stewart supported the campaign, and a star-studded concert, held in Cape Town in 2003, was seen by a worldwide television audience of two billion.

The money raised by Mr Mandela’s initiatives has been used to fund research projects and provide practical support for South Africans with HIV/Aids.

The campaign received a further boost in 2005, when Mr Mandela shocked the nation by announcing that his son, Makgatho, had died of Aids.

He urged people to talk about HIV/Aids “to make it appear like a normal illness”.

It was a significant move, which had a huge impact, said Michel Sidibe, head of the UN’s Aids agency Unaids.

“The country has become a leader in the Aids response because of Mr Mandela, and is moving towards an Aids-free generation thanks to his campaigning,” he said.

Mr Mandela also became a central figure in the African and global Aids movement, Mr Sidibe said.

“He was instrumental in laying the foundations of the modern Aids response and his influence helped save millions of lives and transformed health in Africa,” he said.

“He was a statesman who had Aids at the top of his agenda and he used his stature and presence on the global stage to persuade world leaders to act decisively on Aids. His legacy will be felt by generations.”

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