HIV

HIV vaccine breakthrough in discovery of ‘on-off switch’

Posted by

0


  • Researchers have discovered how to generate an ‘on-off’ switch in a form of HIV
  • HIV needs a specific amino acid to replicate so researchers replaced the code that does this with a ‘nonsense’ version that halts amino acid production
  • When the supply of amino acids stopped, so did the replication
  • This technique gave the team control over the virus’s replication.

A breakthrough has occurred in the fight against HIV, new research reveals.

Scientists say they’ve engineered an ‘on-off switch’ into a weakened form of HIV, enhancing the safety and effectiveness of a potential vaccine for the virus.

They say this could be the final necessary step to eradicate the disease that’s killed 35 million people since the beginning of the epidemic in the 1980s.

Researchers at the University of Nebraska-Lincoln have discovered how to generate an 'on-off switch' into a weakened form of HIV (seen here in the bloodstream)

Researchers at the University of Nebraska-Lincoln have discovered how to generate an ‘on-off switch’ into a weakened form of HIV (seen here in the bloodstream)

Vaccinologists often prefer exposing the body to weakened viruses, rather than deactivated ones, because they grant stronger and longer-lasting immunity.

But weakened viruses retain the ability to replicate, meaning that they still pose a risk of becoming full-blown pathogens.

Researchers at the University of Nebraska-Lincoln began addressing this issue in 2014, when they genetically engineered a version of HIV that needs a synthetic amino acid – one not found in the body – to replicate.

Doing so required the team to replace a codon that codes for the amino acid in the HIV’s genetic code.

NEW COMBINATION OF DRUGS COULD ELIMINATE HIV

HIV could be eliminated using a novel combination of drugs, claims a research team on the brink of an unprecedented experiment.

Scientists at Case Western Reserve University’s medical school have been granted $2.5 million to try pairing two never-before-combined AIDS treatments in a human clinical trial.

The properties – a natural protein that kills disease and a lab-made antibody – have been separately used in HIV-suppressing drugs for years.

Our current line-up of medication is highly effective: roughly 30 percent of America’s 1.2 million people with HIV have reached an undetectable viral load – meaning treatment has suppressed the virus to the point it is untransmittable.

But lead researcher Dr Michael M Lederman believes a combination of these two properties could ‘produce more of a wallop in tandem than when administered individually’.

The team swapped out one of these codons for a ‘nonsense’ version that instead signals a stop in the amino-acid assembly line, halting production of the proteins essential for replication.

When the team supplied the synthetic amino acid, the assembly line began churning out proteins, and the virus began replicating. When the supply of amino acids stopped, so did the replication.

This technique gave the team control over the HIV’s replication. And by delivering a consistent supply of amino acids, the team showed that it can kick-start the multiple cycles of replication necessary for an effective vaccine.

‘Safety is always our biggest concern,’ said Dr Wei Niu, an associate professor of chemical and biomolecular engineering.

‘In this case, [it means] we’re one step closer to generating a vaccine.’

Other research teams have managed to generate HIV immunity in organisms, with one vaccine protecting 95 percent of rhesus monkeys against the virus.

Many of these vaccines have relied on deleting HIV genes to limit replication, but the virus’ penchant for mutating can help it overcome this defense and replicate unchecked.

Dr Qingsheng Li, a professor of biological sciences, said the team’s combination of a nonsense codon, genetic switch and synthetic amino acid represents an especially rigid set of safeguards against unchecked replication.

‘That’s the big milestone,’ said Dr Li.

‘If that works well, we need to go to the pre-clinical animal model before going to a clinical trial. That’s our goal and road map.’

Watch the video discussion. URL:http://www.dailymail.co.uk/health/article-4365848/HIV-vaccine-breakthrough-discovery-switch.html#v-3889855243001

Source:dailymail.co.uk

Lurking HIV detected by scientists in a major biomarker discovery.

Posted by

0


Scientists have discovered a unique protein that gives away the presence of inactive HIV in the body.

Sniffing out these hidden caches of the virus is something researchers have been trying to do for decades. Now that we have a lead, the finding could speed up research on a cure.

 Thanks to modern antiretroviral therapies, for many people, HIV is not the death sentence it once was. But we still don’t have a reliable way of permanently flushing it out of someone’s system.

Drugs can keep the virus in check, but unfortunately HIV has a major weapon – it stows away in secret reservoirs in the immune system. There it lies dormant until conditions are more suitable to re-emerge.

That’s why people infected with HIV have to spend a lifetime on expensive drugs, because the virus can take only weeks to come back from its latent state if drug treatment is stopped.

Those nasty secret reservoirs HIV creates are located in long-lived immune cells known as resting T cells. Because the virus hijacks these cells and integrates its genetic material into the DNA of the patient, it makes reservoir T cells extremely hard to track down.

Now a team of French scientists has managed to achieve this important milestone in HIV research by discovering a biomarker that exists only on the surface of T cells that harbour the latent virus.

“Since 1996, the dream has been to kill these nasty cells in hiding, but we had no way to do it because we had no way to recognise them,” says virologist Monsef Benkirane from University of Montpellier in France.

 Benkirane’s team discovered that a specific protein, called CD32a, hangs out on the surface of T cells with a latent HIV infection, but is not found on uninfected T cells, or even T cells with active HIV.

This is huge. Having CD32a as a biomarker for HIV reservoirs means scientists have a better chance to track them down in a patient’s blood. This paves the way for more research into the mechanisms that allow HIV to create such reservoirs in the first place.

Armed with such knowledge, scientists could then find ways to actually get rid of these HIV nests for good.

The team first detected the protein in a lab-made model of HIV infection, before moving on to test it as a biomarker in actual blood samples from 12 people who live with HIV and are receiving treatment.

They separated T cells with CD32a from other T cells in the blood samples, and found that the cells with this particular protein indeed had latent HIV harboured inside them.

Unfortunately, it’s not a smoking gun in every case, since the protein was found only on about half of all latently infected T cells.

Douglas Richman from University of California San Diego, who wasn’t involved in the research, writes that “the eradication of latent HIV would require a much greater reduction in the number of latently infected cells in the body.”

But it’s an extremely encouraging first step in the long search for a marker that could help us track down the nasty virus once it goes into hiding.

Tony Fauci, director of the US National Institute of Allergies and Infectious Disease, told Nature that a good next step would be to replicate the findings in more blood samples from a larger variety of patients who have the virus.

It’s still way too soon to say that we’re on the path to an actual HIV cure, but the news is super-exciting to researchers who have been hammering away at this problem for decades.

“I really hope this is correct,” says Fauci. “The fact that this work has been done by such competent investigators, and the data looks good, makes me optimistic.”

In a world where HIV continues to be a major health issue, this discovery indeed gives cause for optimism.

About 36.7 million people around the world live with HIV, but only 17 million have access to antiretroviral therapy, according to data from the US CDC.

The scientists have already filed a patent for the diagnostic and therapeutic use of the new biomarker.

Soource:Nature.

Lurking HIV Detected by Scientists in a Major Biomarker Discovery

Posted by

1


Scientists have discovered a unique protein that gives away the presence of inactive HIV in the body.

Sniffing out these hidden caches of the virus is something researchers have been trying to do for decades. Now that we have a lead, the finding could speed up research on a cure.

 

Thanks to modern antiretroviral therapies, for many people, HIV is not the death sentence it once was. But we still don’t have a reliable way of permanently flushing it out of someone’s system.

Drugs can keep the virus in check, but unfortunately HIV has a major weapon – it stows away in secret reservoirs in the immune system. There it lies dormant until conditions are more suitable to re-emerge.

That’s why people infected with HIV have to spend a lifetime on expensive drugs, because the virus can take only weeks to come back from its latent state if drug treatment is stopped.

Those nasty secret reservoirs HIV creates are located in long-lived immune cells known as resting T cells. Because the virus hijacks these cells and integrates its genetic material into the DNA of the patient, it makes reservoir T cells extremely hard to track down.

Now a team of French scientists has managed to achieve this important milestone in HIV research by discovering a biomarker that exists only on the surface of T cells that harbour the latent virus.

“Since 1996, the dream has been to kill these nasty cells in hiding, but we had no way to do it because we had no way to recognise them,” says virologist Monsef Benkirane from University of Montpellier in France.

 Benkirane’s team discovered that a specific protein, called CD32a, hangs out on the surface of T cells with a latent HIV infection, but is not found on uninfected T cells, or even T cells with active HIV.

This is huge. Having CD32a as a biomarker for HIV reservoirs means scientists have a better chance to track them down in a patient’s blood. This paves the way for more research into the mechanisms that allow HIV to create such reservoirs in the first place.

Armed with such knowledge, scientists could then find ways to actually get rid of these HIV nests for good.

The team first detected the protein in a lab-made model of HIV infection, before moving on to test it as a biomarker in actual blood samples from 12 people who live with HIV and are receiving treatment.

They separated T cells with CD32a from other T cells in the blood samples, and found that the cells with this particular protein indeed had latent HIV harboured inside them.

Unfortunately, it’s not a smoking gun in every case, since the protein was found only on about half of all latently infected T cells.

Douglas Richman from University of California San Diego, who wasn’t involved in the research, writes that “the eradication of latent HIV would require a much greater reduction in the number of latently infected cells in the body.”

But it’s an extremely encouraging first step in the long search for a marker that could help us track down the nasty virus once it goes into hiding.

Tony Fauci, director of the US National Institute of Allergies and Infectious Disease, told Nature that a good next step would be to replicate the findings in more blood samples from a larger variety of patients who have the virus.

It’s still way too soon to say that we’re on the path to an actual HIV cure, but the news is super-exciting to researchers who have been hammering away at this problem for decades.

“I really hope this is correct,” says Fauci. “The fact that this work has been done by such competent investigators, and the data looks good, makes me optimistic.”

In a world where HIV continues to be a major health issue, this discovery indeed gives cause for optimism.

About 36.7 million people around the world live with HIV, but only 17 million have access to antiretroviral therapy, according to data from the US CDC.

The scientists have already filed a patent for the diagnostic and therapeutic use of the new biomarker.

Source:http://www.sciencealert.com

Antibiotics resistance could kill 10 million a year by 2050

Posted by

1


A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050

A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050

London (AFP) – A British government-commissioned review has found that resistance to antibiotics could account for 10 million deaths a year and hit global gross domestic product by 2.0 to 3.5 percent by 2050.

The Review on Antimicrobial Resistance said surgeries that have become widespread and low-risk thanks to antibiotics, such as caesarean sections, could become more dangerous without urgent action.

The review announced by British Prime Minister David Cameron was led by Jim O’Neill, former chief economist at US investment bank Goldman Sachs, and included British senior public health experts.

It found the region with the highest number of deaths attributable to antimicrobial resistance would be Asia with 4.7 million, followed by Africa with 4.1 million, while there would be 390,000 in Europe and 317,000 in the United States.

For comparison, the review estimated that the second-biggest killer, cancer, would account for 8.2 million deaths a year by 2050.

“The damaging effects of antimicrobial resistance are already manifesting themselves across the world,” the report said.

“Antimicrobial-resistant infections currently claim at least 50,000 lives each year across Europe and the US alone,” it added.

The calculations were based on existing studies by the think tank Rand Europe and the consultancy KPMG.

It warned drug resistance was not “a distant and abstract risk” and called for “a major intervention to avert what threatens to be a devastating burden on the world’s healthcare systems”.

The review emphasised the economic advantage of investment in tackling the problem early.

It said that three types of bacteria — the Klebsiella pneumonia, Escherichia coli (E. coli) and Staphylococcus aureus — were already showing signs of resistance to medicine.

Treatment of HIV, malaria and tuberculosis were broader public health issues in which resistance “is a concern”, the report said.

In the United States, antibiotic-resistant infections are associated with 23,000 deaths and two million illnesses each year.

The economic costs annually are as high as $20 billion (16 billion euros) in excess direct health care costs and $35 billion (28 billion euros) in lost productivity.

WHY IT’S TOO SOON TO SAY HIV HAS BEEN CURED

Posted by

0


HIV

HIV is good at hiding inside CD4 T cells in the immune system

A 44-year-old British man was seemingly “cured” of HIV last week. Scientists working on the therapy say that the virus is now completely undetectable in his blood, leading to headlines announcing an “HIV breakthrough” that could “spell the end of the virus”.

But here’s the thing: It’s very difficult to determine whether HIV has been truly eliminated from the body, and even conventional antiretroviral therapy — which the patient was also taking — reduces HIV to undetectable levels. So pinning hopes on a single trial to prove a “cure” is a bit too premature, if optimistic.

The hallmark of an HIV infection is that it targets very specific cells in a patient’s immune system, called CD4 T cells. These are white blood cells that usually detect intruders and corral a larger immune response to get rid of the invading bacteria or viruses. But HIV tricks these frontline soldiers and quickly inserts its own genetic material into the CD4 cells so that it can replicate inside them and use the cells to churn out more copies of virus.

Once infected, cells can’t get rid of HIV the way they can most other viruses. Taking combination antiretroviral therapy, however, stops HIV from reproducing and infecting new CD4 cells. Viral levels start declining and after two to three months of treatment, the levels of virus are so low that HIV is “undetectable” in a patient’s blood, says Janet Siliciano, an infectious disease researcher at Johns Hopkins University.

The problem is that most HIV tests measure the amount of viral RNA in free virus particles floating around in the blood and try to extrapolate the amount of virus hiding inside all infected cells. But in 1995, Siliciano’s lab found that some HIV remains invisible deep inside “resting” CD4 T cells. This silent reservoir can’t be measured by normal blood tests, she says. When people go off antiretroviral therapy, the virus rapidly resurges, and that’s when scientists realize that the virus was hidden somewhere inside the patient all along.

“Everyone has a different number of resting infected cells that are acting as a reservoir. They turn back on randomly, so it’s very hard to predict when someone will experience a viral rebound,” says Siliciano.  That is why people with HIV must take antiretrovirals for the rest of their life, she explains.

The only way to know that HIV has left a person’s body is to test many different tissues — not just run a blood test — and keep repeating them over the years. Siliciano’s group is trying to develop one consolidated test.

Shock and Kill Strategy

One popular strategy in searching for a cure aims to obliterate the reservoir of remaining virus using a “shock and kill” approach. The idea behind it is that shocking the resting CD4 cells into waking up will force the virus inside them to become active as well. As HIV starts to rear its ugly head and put its mark on the surface of the infected cells, scientists can then boost a patient’s immune system to recognize and destroy HIV-carrying cells while they are vulnerable.

This is the technique used in the recent “breakthrough” by British researchers. The scientists, who hail from six different hospital centers in the UK, are testing an aggressive shock and kill regimen on 50 HIV patients over a period of about 9 months. The anonymous patient initially quoted in The Sunday Times is simply the first of the participants to have completed the treatment. Official results from the trial are not expected until 2018.

“I’m surprised that they would announce this in the press when they only have one patient and are not expecting all the results to come in until 2018,” says Stephen Morse, an epidemiologist and director of the Center for Public Health Preparedness at Columbia University. “There has been such a history of false optimism and false hope with HIV that you wonder why announcements like that are made.”

 Even if the trial is a complete success, scientists will have to use caution in interpreting the results, according to Morse. Researchers will need to follow up on patients for several years, testing their viral levels regularly to make sure that HIV is truly eradicated from their system. They’ll also have to conduct a more extensive search for the virus to make sure it isn’t hiding in reservoir cells in the immune system or in other inaccessible parts of the body, such as cerebrospinal fluid or semen, Morse says. “We need a lot of good evidence before we can declare victory over HIV.”

To date, only one person has undergone that kind of rigorous testing. Timothy Ray Brown, who is also known as “the Berlin patient”, is the first and only person who can claim the distinction of being cured of HIV. In 2006, after living with the virus for 11 years and controlling his infection with antiretroviral drugs, Brown learned that he had developed an unrelated case of acute myeloid leukemia. He underwent chemotherapy and whole-body radiation that wiped out his immune system — and possibly the virus with it. Then he received a bone marrow transplant from a donor with a natural immunity to HIV. Researchers haven’t been able to find any trace of HIV in his blood or in multiple brain, gut, colon, and lymph-node biopsies since.

But bone marrow transplants have a high fatality rate, and there are just too many people with HIV — 33 million around the world — to make it a feasible therapy. And they may not even work consistently. Other patients who seemed to have been cured of the virus after receiving bone transplants still experienced a rebound of the virus after ditching their antiretroviral therapy — sometimes after nearly five years of being “HIV-free”.

Any new treatment that successfully eradicates the virus needs to be replicated in larger studies, says Siliciano. It also needs to match or surpass current standards of antiretroviral therapy, in terms of safety and accessibility of the drugs. Scientists also need to develop better, more sensitive assays to test for the presence of HIV. Only then will they be able to say accurately if a treatment is an effective cure for the viral infection.

“It’s a really hard, complex problem, and lots of scientists around the world are trying to work toward a cure,” she says. “But right now we have nothing that’s really close.”

UN Classifies Antibiotic Resistance as a Crisis, Putting It on Par With Ebola and HIV

Posted by

0


IN BRIEF

Antibiotic resistance, the ability of bacteria to evolve to combat treatment, has been declared a crisis by the United Nations. The classification will hopefully lead to the funding and research needed to combat, or even fully eradicate, the problem, which is currently responsible for more than 23,000 deaths per year in the U.S. alone.

SUPER DRUG, SUPER BUG

Since Alexander Fleming’s discovery of penicillin in 1928, antibiotics have come to revolutionize medicine in the 20th century. By systematically killing off microbes that cause infections, antibiotics made it easy to cure bacterial infections from wounds as well as highly communicable diseases such as pneumonia, gonorrhea, and syphilis. Along with vaccines, antibiotics have considerably improved the life expectancy of people all over the world.

Here’s the rub: like humans, microbes can adapt.

When exposed to antibiotics frequently enough, bacteria can evolve to combat the treatments. Also known as antibiotic resistance, this phenomenon results in bacteria that is more resistant (if not fully immune) to the drugs that could treat them before. A report from Quartz showed that the U.S. Centers for Disease Control and Prevention (CDC) has estimated that 23,000 people die each year as a direct consequence of antibiotic resistance, and that’s just in the U.S.

The issue is so serious that the United Nations has now elevated the problem of antibiotic resistance to crisis level.

https://embed.ted.com/talks/ramanan_laxminarayan_the_coming_crisis_in_antibiotics

TAKING COLLECTIVE ACTION

The new categorization puts antibiotic resistance on par with Ebola and HIV as a threat to humanity, and while the declaration alone won’t be enough to completely eradicate the problem of antibiotic resistance, it marks a global commitment to combating the issue and saving lives. With 193 member states of the UN General Assembly signing the document, the world is clearly in agreement that action needs to be taken.

As more companies in those countries, particularly those in the pharmaceutical and food industries, adopt policies aimed to reduce the overuse of antibiotics and more research is conducted on the topic, we should see a decrease in the number of deaths related to antibiotic resistance. Perhaps the next ruling the UN makes on the issue will be one in the other direction, from crisis level to problem of the past.

Preexposure Prophylaxis for HIV: Where Are We Now and How Did We Get Here?

Posted by

0


In July 2012, the US Food and Drug Administration (FDA) approved a once-daily, fixed-dose combination of emtricitabine (FTC) and tenofovir disoproxil fumarate (TDF) for preexposure prophylaxis (PrEP) against human immunodeficiency virus (HIV) infection. FTC/TDF, initially approved in 2004 to treat HIV in combination with other antiretroviral agents, became the first drug to be approved to prevent HIV infection in people who are at high risk for infection.1 In May 2014, the US Public Health Service (USPHS) released a set of clinical practice guidelines for PrEP. 2

image

Take Note

  • PrEP is one of several prevention options for sexually active adults who are at high risk for HIV infection based on their sexual practices.
  • PrEP may be indicated for gay and bisexual men, heterosexual men and women, and partners in serodiscordant relationships, among others.
  • PrEP should be provided in the context of access to appropriate risk-reduction services.

The FDA approved FTC/TDF for PrEP on the basis of 2 large, randomized, double-blind, placebo-controlled trials.1,3,4

One, the iPrEX (Preexposure prophylaxis initiative) study, was conducted among 2499 HIV-negative men and transgender women who have sex with men. Participants received FTC/TDF or placebo once daily along with HIV testing, risk-reduction counseling, condoms, and treatment for sexually transmitted infections (STIs). After a median 1.2 years of follow-up, 100 participants were found to have acquired HIV infection: 36 in the active prophylaxis group and 64 in the placebo group. This result amounted to a significant 44% reduction in the incidence of new HIV infections among the participants receiving PrEP.3 While demonstrating the efficacy of PrEP, the study also showed the importance of adherence to the regimen. That is, study participants in the active arm who became infected were found to have low levels of FTC/DTF in their blood.3

The other study, called Partners PrEP, was conducted among 4758 serodiscordant heterosexual couples (couples in which 1 partner was HIV-positive and the other was HIV-negative) in Kenya and Uganda. The HIV-negative partners in this study received FTC/TDF, TDF alone, or placebo. A total of 82 of the HIV-negative partners became infected with HIV during the study. Compared with placebo, there was a 67% reduction in the incidence of infection among participants who received TDF alone, and a 75% reduction with FTC/TDF. Both of these results were statistically significant.4

The 2014 USPHS guidelines are based on these studies plus a number of others. Among the most important were the TDF2 Study and the Bangkok Tenofovir Study.5

The TDF2 Study evaluated PrEP in heterosexual men and women in Botswana. The 1219 participants (48% women, 52% men) were randomly assigned to FTC/TDF or placebo with monthly follow-up and prevention services including HIV testing, risk-reduction and adherence counseling, and management of STIs, as well as monitoring for potential drug side effects. Compared with placebo, PrEP reduced the risk of HIV infection by 62%. Again, efficacy correlated strongly with adherence as measured by drug levels.6

The Bangkok Tenofovir Study evaluated PrEP among a group of injection drug users (IDUs) in Thailand, a population that had not previously been studied as candidates for PrEP. The 2413 participants were assigned to receive either TDF or placebo along with monthly HIV testing, risk-reduction and adherence counseling, and safety assessments, and were offered condoms and methadone treatment. Compared with placebo, TDF reduced the risk of HIV infection by 49%. Once again, efficacy was correlated with adherence: among patients with detectable TDF in their blood, the reduction in risk of HIV infection was 74%.7

The USPHS guidelines are based on the premise that daily oral PrEP with FTC/TDF has been proven safe and effective at reducing the risk of becoming infected with HIV through sex with an infected partner. The guidelines recommend PrEP as 1 prevention option for sexually active adults who are at high risk for HIV infection based on their sexual practices. This includes gay and bisexual men, heterosexual men and women, and members of serodiscordant couples. The guidelines note that the safety and efficacy of PrEP for adolescents has not been fully characterized, so clinicians should weigh the risks and benefits of PrEP in counseling adolescent patients.2

Before prescribing PrEP to an eligible patient, clinicians must rule out current HIV infection. PrEP should be prescribed for daily use; the USPHS does not recommend PrEP for so-called coitally-timed or other noncontinuous use. Once a patient has initiated PrEP, the prescribing physician should test for HIV infection at least every 3 months. It is important for patients who acquire HIV infection while on PrEP to discontinue the medication, as the 2-drug FTC/TDF regimen is not sufficient treatment for HIV infection and its continued use may lead to viral resistance to 1 or both drugs.2

Before patients initiate PrEP, clinicians should assess renal function and test for hepatitis B virus (HBV) infection. Impaired renal function and loss of bone mineral density are potential safety concerns with the use of FTC/TDF. It is also important for clinicians to know if a patient is co-infected with HBV as FTC/TDF can be used to combat HBV, and discontinuation of HBV therapy may not be advisable. Clinicians should not prescribe FTC/TDF to any person with an estimated creatinine clearance rate (CrCL) of < 60 mL/min. In patients on PrEP, clinicians should assess renal function at least every 6 months so that patients who develop renal failure do not continue to take PrEP.2

As reflected in the clinical trial data, a high level of adherence is important for the success of PrEP but was not always achieved by participants in trials. Consequently, patients on PrEP should be encouraged to use PrEP in combination with other effective prevention methods (including condoms) and should be provided with access to such methods (directly by the prescribing clinician or via referral to appropriate risk-reduction services).2

Finally, a French study termed Ipergay has shown the success of an approach termed “PrEP on demand,” in which individuals at risk for acquisition of HIV were prescribed FTC/TDF only on the day of anticipated sexual relations and for 2 days thereafter instead of every day. The advantage of the latter approach is that it may lower the side effects associated with FTC/TDF since some patients would be taking fewer pills that once daily. This would also help reduce costs.8 As previously mentioned, however, the USPHS does not sanction this approach.

The complete USPHS Clinical Practice Guidelines for PrEP and A Clinical Provider’s Supplement are available online.The supplement includes a patient checklist to help maximize the benefit of PrEP and informational patient handouts. It also includes a risk measurement tool for MSM, allowing physicians to identify those patients at highest risk for HIV infection for whom PrEP may be indicated. Information about adherence and risk-reduction counseling is also provided, as well as information on administrative and billing codes for PrEP-related services.

Bayer and US Govt. Knowingly Gave HIV to Thousands of Children

Posted by

0


needles

 

 

What if a company that you thought you could trust, knowingly sold you a medicine for your child that they knew had the potential to give your child HIV? How would you react? What if a government agency that claims the responsibility for protecting you from such treachery, not only looked the other way, but was complicit in this exchange?

Everyone has heard of Bayer aspirin, it is a household name. Bayer AG also manufactures numerous other products, from pesticides to medicine for hemophiliacs called Factor 8.

bayer

In 1984 Bayer became aware that several batches of this Factor 8 contained HIV. They knew this because there was an outbreak of HIV among hemophiliac children, and this outbreak was traced back to Bayer.

Unable to sell their Factor 8 in the US, Bayer, with the FDA’s permission, (yes that’s right, the FDA allowed Bayer to potentially kill thousands) sold this HIV infected medicine to Argentina, Indonesia, Japan, Malaysia, and Singapore after February 1984, according to the documents obtained by the NY Times. The documents showed how Cutter Biological, a division of Bayer, shipped more than 100,000 vials of unheated concentrate, worth more than $4 million, after it began selling the safer product.

The result of this sale of HIV tainted medication ended up infecting tens of thousands and killing thousands. Thousands of innocent children and adults have died at the hand of this corporation and no punitive action has been taken against them. The health department leaders in Argentina, Indonesia, Japan, Malaysia, and Singapore were all imprisoned, while the US FDA continues down its hellish path.

When asked about the sale of the tainted Factor 8, Bayer responded, ”Decisions made nearly two decades ago were based on the best scientific information of the time and were consistent with the regulations in place.” This can be interpreted as Bayer asking the FDA for permission to murder children for profit and the FDA giving its approval. According to the NY Times, the Food and Drug Administration’s regulator of blood products, Dr. Harry M. Meyer Jr., asked that the issue be ”quietly solved without alerting the Congress, the medical community and the public.”

No one in the government nor Bayer have been charged with anything in regards to this matter. Bayer continues to sell its Factor 8 medication to this day.

Monthly Dosing Drug Raises Hopes and Concerns

Posted by

0


Cabotegravir suppresses HIV but patients, doctors differ on risks

The investigative anti-HIV agent cabotegravir, plus ripivirine – given as a once-monthly intramuscular injection – appears to control viral replication at undetectable levels, but the delivery of the antiretroviral integrase inhibitor has raised some concerns among patients and physicians, researchers reported here.

Remarkably, what most concerns patients – injection site pain and discomfort – is not what worries physicians who express fears that patients won’t return for treatments or there could be long-lasting allergic reactions to a drug that stays on board for weeks, saidDeanna Kerrigan, PhD, associate professor of health, behavior, and society at Johns Hopkins University Bloomberg School of Public Health.

“Long acting injectable antiretroviral therapy was preferable to a daily oral regimen among people living with HIV participating in a phase IIb trial given its practical and emotional benefits,” Kerrigan said. “Further research is needed regarding appropriate candidates for long-acting injectable antiretroviral therapy, including among women and ‘non-adherent’ populations.”
In her oral presentation at the International AIDS Conference, Kerrigan reported on how 27 patients and 12 clinicians described use of the long-lasting agent after 32 week of treatment in a phase II trial. In some patients injections were delivered monthly; in others it was injected every other month. In phase III trials expected to begin last this year, the monthly dosing will be tested, said David Margolis, MD, MPH, director of HIV drug development at ViiV Healthcare, Chapel Hill, N.C.
The patients were from Spain and the U.S., and all but two were men, mostly men who have sex with men. One of the patients was a heterosexual man; both women were heterosexual.
About 82% of the patients reported injection site pain as their major concern about receiving the injections, although most thought the pain was a minor inconvenience. About 17% of the patients found the pain was moderate. But Kerrigan quoted one participant from Spain as saying: “One day (of pain) is nothing … it’s as if you have a day with a headache. You take ibuprofen and that’s it. You put up with it. It’s temporary.”
Kerrigan said that overall, the patients endorsed the treatment because they perceived it was more convenient than taking daily pills; it provided greater confidentiality and privacy and provided some relief from the unwanted daily reminder of their HIV status. They said they perceived that the monthly injections were less stigmatizing and created less pressure on them personally to remember to take their medication.

“Patients felt very comfortable coming to the clinics; they expressed feeling well-treated, respected and support,” she said. However, some patients said they were questioned by friend and co-workers about their numerous doctors’ visit so some made up excuses such as having to meet a roofer or a plumber.
Kerrigan said the patients said that the injections would benefit “everyone” living with HIV who were tolerant of needles. The treatment might also especially benefit younger people or those with adherence issues.
While the clinicians surveyed through the structured interviews were supportive of the injections they did express some concerns:
The therapy needed to be considered on a case by case basis.
Many patients can take pills just fine.
That even with injections, patients still need to come to the clinic as scheduled.
They also had concerns about development of resistance and clinical management.
She quoted one provider from Spain: “The fear is that the patient does not reappear … [and] after the injection if there is an allergy or intolerance, the medication cannot be removed. It may be many months without really knowing its secondary effects.”
Margolis, who reported on the 48-month results in a second presentation at the oral session, said that there have not been patients who failed to show up for their scheduled treatment.

In the LATTE-2 extension trial, researchers examined the use of cabotegravir plus rilpivirine as maintenance therapy. Patients were first enrolled in a run-in period in which they were treated with once daily cabotegravir plus abacavir and lamivudine for 20 weeks to determine tolerability to cabotegravir. During the last 4 weeks rilpivirine was added to the regimen to ensure patients tolerated that drug as well. They patients were randomized to continue on the oral regimen or receive once-monthly dosing or dosing every 8 weeks.
At 48 weeks, 89% of the 56 patients on the oral regimen had suppressed HIV to undetectable levels, assessed using the 50 copies/mm3 assay; 91% of the 115 patients assigned to every 4 weeks achieved undetectable viral loads; 92% of the 115 patients assigned to every 8 week dosing achieved undetectable virus, Margolis said.
In commenting on the study, session co-moderator Paula Munderi, MD, head of the HIV Care program of the MRC/UVRI Uganda Research Unit on AIDS, in Entebbe, Uganda, told MedPage Today that the concerns of clinicians about whether patients would return for their scheduled injections might be dependent upon the population. “In my clinic, patients believe we are helping them with their disease. I have a lot more women in my clinic and women, in general, have much better health-seeking behavior than men.”
She said that most of the complaints about injection paid was from men, but women have been getting injections for depot shot for birth control for many years and handle those injections well. “Most of the concerns are the providers projecting onto patients,” she said, “which is something we tend to do. Sadly.”
Munderi said, “a certain type of patient who wants a break from pills would be a candidate for the monthly injection.” The real question, however, is whether the company would make the injection affordable, especially for low or middle income nations.

Stop stalling and make PrEP for HIV available now

Posted by

0


Further delay to pre-exposure prophylaxis risks the NHS appearing discriminatory of populations at risk

Compelling evidence of the effectiveness of pre-exposure prophylaxis (PrEP) for HIV has been available for over five years. But we are still waiting for the NHS to embrace this potentially revolutionary intervention.

Truvada, a combination of emtricitabine and tenofovir usually used to treat HIV, can also prevent HIV infection. PrEP could at last mean real headway in reducing the transmission of HIV, with the number of newly diagnosed people unchanged in the UK for the past decade.1

In November 2010, the iPrEX (pre-exposure prophylaxis initiative) trial found efficacy of 92% among those who took PrEP as prescribed.2 Subsequent studies have confirmed its efficacy and its effectiveness. One of the most recent is the UK’s PROUD (pre-exposure prophylaxis to prevent the acquisition of HIV-1 infection) study, which looked at the real world effect among men who have sex with men.3 The reduction in incidence among men in the PrEP arm was 86%. Additionally, those who did get HIV while participating in the study were not likely to be taking PrEP when infected.

The US Food and Drug Administration licensed Truvada for use as PrEP in 2012, and in 2014 the Centers for Disease Control and Prevention recommended PrEP for those at high risk of acquiring HIV. Other countries such as France are now following suit. In England, however, progress is painfully slow.

Strong equalities argument

Men who have sex with men and people from black African communities are at highest risk of HIV infection.1 So there is a strong equalities argument for PrEP to be made available now. And, conversely, any further delay may appear to reflect a lack of value placed on the health of these most affected communities. The stigma that still surrounds HIV and its sexual route of transmission cannot be allowed to trump evidence.

We know that PrEP works and that it is cost effective when provided to people at high risk of HIV infection. Yet NHS England’s vacillating has thrown into stark relief a health system that is not designed to come to timely and confident decisions about nationally important preventive interventions, for all the talk we hear of prevention being the new health priority.

PrEP highlights the lack of system-wide accountability. Even if the drug were commissioned by NHS England, the sexual health clinic service to prescribe and monitor PrEP would have to be separately commissioned by each local authority. So even if we eventually get a positive decision from NHS England on the drug, that won’t be the end of the story. Does it make sense for the prevention of infectious disease to be delegated to 150 local bodies, without any national strategic direction?

In September 2014 NHS England began the process to decide whether to commission the drug used in PrEP. In March 2016, after 18 months of work and just before its final decision was due, NHS England announced that this specialised commissioning process was inappropriate because PrEP is a preventive intervention.

Despite a legal argument by the National AIDS Trust (NAT), NHS England reconfirmed this decision in late May 2016. Faced with this impasse, NAT has no choice but to take the matter before a court for judicial review. The public interest in resolving this is too great to ignore it.

Fractured decision making

This is a health system failing to look at the bigger picture, with decision making dangerously fractured and with no one providing clear direction and leadership. The provision of PrEP for those at high risk, who need it and want it, could reduce the human and financial costs of this preventable condition. While we delay, 17 people a day are being diagnosed with HIV.1