Wednesday, Aug. 8, 2007
IN a breakthrough that could potentially lead to a cure for HIV infection, scientists have discovered a way to remove the virus from infected cells, a study released today said.
The scientists engineered an enzyme which attacks the DNA of the HIV virus and cuts it out of the infected cell, according to the study published in Science magazine.
The enzyme is still far from being ready to use as a treatment, the authors warned, but it offers a glimmer of hope for the more than 40 million people infected worldwide.
“A customised enzyme that effectively excises integrated HIV-1 from infected cells in vitro might one day help to eradicate (the) virus from AIDS patients,” Alan Engelman, of Harvard University’s Dana-Farber Cancer Institute, wrote in an article accompanying the study.
Current treatments focus on suppressing the HIV virus in order to delay the onset of AIDS and dramatically extend the life of infected patients.
What makes HIV so deadly, however, is its ability to insert itself into the body’s cells and force those cells to produce new infection.
“Consequently the virus becomes inextricably linked to the host, making it virtually impossible to ‘cure’ AIDS patients of their HIV-1 infection,” Mr Engelman explained.
That could change if the enzyme developed by a group of German scientists can be made safe to use on people.
That enzyme was able to eliminate the HIV virus from infected human cells in about three months in the laboratory.
The researchers engineered an enzyme called Tre which removes the virus from the genome of infected cells by recognising and then recombining the structure of the virus’s DNA.
This ability to recognise HIV’s DNA might one day help overcome one of the biggest obstacles to finding a cure: the ability of the HIV virus to avoid detection by reverting to a resting state within infected cells which then cease to produce the virus for months or even years.
“Numerous attempts have been made to activate these cells, with the hope that such strategies would sensitise the accompanying viruses to antiviral drugs, leading to virus eradication,” Mr Engelman wrote.
“Advances with such approaches in patients have been slow to materialise.”
New experiments must be designed to see if the Tre enzyme can be used to recognise these dormant infected cells, he wrote.
“Although favourable results would represent perhaps only a baby step toward eventual use in patients, the discovery of the Tre recombinase proves that enzymatic removal of integrated HIV-1 from human chromosomes is a current-day reality,” he said.
The researchers who developed the enzyme were optimistic about their ability to design additional enzymes which would target other parts of the virus’s DNA.
However they warned that there were significant barriers to overcome before the enzyme could be used to help cure patients.
“The most important, and likely most difficult, among these is that the enzyme would need efficient and safe means of delivery and would have to be able to function without adverse side effects,” wrote lead author Indrani Sarkar of the Max Planck Institute for Molecular Cell Biology and Genetics in Dresden.
“Nevertheless the results we present offer an early proof of principal for this type of approach, which we speculate might form a useful basis for the development of future HIV therapies,” Sarkar concluded.
Friday, Sep. 22, 2006
The scientist who discovered the Aids virus more than 20 years ago said he has developed a potential vaccine against the disease that has killed 25 million people around the globe.
Professor Robert Gallo, in 1984, along with the French scientist, Luc Montagnier, the first to identify that HIV caused Aids, said the latest discovery had made him more optimistic that the disease could be beaten than he had felt for a decade.
Almost 40 million people are living with HIV, most in sub-Saharan Africa, and four million more are infected each year. A vaccine that would halt its spread is the holy grail for researchers, but despite 20 years of effort and the expenditure of millions of dollars, all attempts to do so have so far failed.
Professor Gallo, director of the Institute for Human Virology at the University of Maryland, said his team had created antibodies that worked against different HIV strains, essential if a vaccine is to provide effective protection but which has defied previous attempts. The candidate vaccine had been tested successfully in four monkeys, selected because of their similarity to man, and tests are now being done on a further 12 monkeys. If those are successful, the next stage would be to test the vaccine in humans, he said.
“Yes, we are at a preliminary stage, but if 10 years ago I had known I could make antibodies that would neutralise a wide range of variants of HIV, I would have been celebratory. People thought this was pretty much impossible. It’s a serious clinical advance; we have been quietly doing it. I do not know what the outcome of the latest trial [on the 12 monkeys] will be but my guess is we will move to phase 1 clinical trials [in humans] in a year’s time.”
He added: “Before there was no pathway. Now there is some light.”
Developing a vaccine against Aids is regarded as one the most difficult challenges facing medicine and some scientists believe it is impossible. The virus mutates rapidly, it integrates itself into the patient’s genetic material and it infects the very cells used by the immune system to defend the body against attack.
Professor Gallo said the approach taken by his team was to modify the protective envelope that surrounds the virus, opening a site and making antibodies to it that prevented entry of the virus into the body’s cells. But the first challenge the researchers face is that the antibodies do not last longer than three months, meaning a booster dose of vaccine would be needed three to four times a year. “If we can [overcome this] we will be happy bordering on excited,” he said.
There are 15 major strains of HIV, but mixing and re-combining has produced a total of about 20. The strain that dominates in Africa is A and in the US and Europe it is B. But among five people infected with the B strain of the virus only one would be protected by a B vaccine, because of variants in the strains.
Professor Gallo said: “I feel personally more optimistic but I don’t want to look Pollyanna-ish. HIV has always dealt surprises. I see an avenue. But I don’t know if there is a bend ahead and a truck round the corner blocking the way.”
Thomas Hanke, a specialist on HIV vaccines at the human immunology unit of Oxford University, said: “There have been lots of claims for vaccines that can neutralise different strains but a vaccine that would be useful hasn’t been constructed yet. Professor Gallo’s success is a good reason to be positive, but it is also a good reason not to be over-excited.”
Tuesday, Sep. 12, 2006
A team of researchers from the Universite de Montreal and the Centre hospitalier de l’Universite de Montreal (CHUM) say they have made a breakthrough in fighting the human immunodeficiency virus (HIV). They have identified a defect in the immune response to HIV and found a way to correct the flaw.
Dr Rafick-Pierre Skaly, a researcher in cell biology, immunology, and virology, has confirmed the identification of a new therapeutic target (the PD-1 protein) that restores the function of the T cells whose role is to eliminate cells infected with the virus. This constitutes a major breakthrough, opening new prospects for the development of therapeutic strategies for controlling HIV infection. The research findings appear in last weeks issue of the journal Nature Medicine.
Dr Skaly explained that “immune system cells made non-functional by HIV can be identified by the presence of a protein that is significantly overexpressed when infected by the virus.” In fact, high levels of the protein are associated with a more serious dysfunction. “The most important discovery made in this study arises from the fact that by stimulating this protein, we succeeded in preventing the virus from making immune system cells dysfunctional,” he added.
The findings were simultaneously reproduced by two other laboratories – the labs headed by Dr Bruce Walker at Harvard and Dr Richard Koup at the NIH. “It’s a rare occurrence for three teams to work together on attacking a major problem. Up until now, the virus has been more or less invincible. By combining our efforts, we found the missing link that may enable us to defeat the virus,” noted Dr Skaly. Discussions with partners are also underway to translate these research findings into clinical trials, which could start during the coming year.
Friday, Aug. 4, 2006
Expanding free access to drug therapies for everyone infected with HIV could eventually stop the spread of the virus, says a leading Vancouver AIDS researcher.
The hypothesis is based on mounting evidence that transmission of the virus drops significantly when people take anti-retroviral drugs, as the amount of virus circulating in their blood goes down.
If viral loads drop to undetectable levels, it’s as if HIV is quarantined and can no longer be transmitted to others.
Dr. Julio Montaner, director of the B.C. Centre for Excellence in HIV/AIDS, proposed the idea in a viewpoint article appearing in Saturday’s special issue of medical journal The Lancet devoted to AIDS research.
“This is a mathematical model, if you want to call it that way, that suggests that if we were to aggressively expand the anti-retroviral therapy use, we could see a very substantial decrease in transmissions,” Montaner said.
“In fact, over a period of three to four decades, we could see an extinguishing of the HIV epidemic.”
The model is theoretical, based on data from Taiwan showing new infections fell 53 per cent after free access to highly active anti-retroviral therapy or HAART was introduced.
Montaner cautioned the idea is a secondary preventive measure, not a licence for careless sexual behaviour.
The simple idea could be cost effective if it reduces the mounting incidence of cases of HIV/AIDS worldwide, Montaner and his co-authors said.
The current approach is not sustainable given the growth of the HIV global pandemic in the face of prevention and treatment strategies that aren’t completely effective and the lack of a preventive vaccine, they said.
“We have received a lot of encouraging support from our colleagues not only in North America, but in the rest of the world,” said Montaner, who also chairs AIDS research at the University of British Columbia.
But the idea was dismissed by Dr. Philip Berger, a Toronto physician who has been working in Lesotho, an African nation where an estimated 23 per cent of adults are HIV positive.
People who are infected with HIV may not be willing to start taking antiretroviral drugs before treatment is needed, given its side effects, Berger said.
In sub-Saharan Africa where people are dying because of lack of treatment, the priority should be on meeting emergency needs now, he said.
Montaner now hopes to test the hypothesis with his own study in B.C.
Monday, May. 29, 2006
Testing for HIV and Hepatitis C (HCV) has come a long way over the years – but there is still a mortally dangerous shortcoming in the technology that detects whether a person is infected.
That’s why the Israeli technology SMARTube, developed by Smart Biotech’s Dr. Tamar Jehuda-Cohen – has such far reaching, life-saving implications.
According to the National HIV Prevention Conference, over a million Americans are living with HIV/AIDS, with 24-27% of that number undiagnosed and unaware of their HIV infection. In 2004, the estimated number of diagnoses of AIDS in the US was 42,514.
In addition, over 4,000,000 Americans are infected with HCV. About 85% of individuals acutely infected with HCV become chronically infected. Hence, HCV is a major cause of chronic (lasting longer than six months) hepatitis. Once chronically infected, the virus is almost never cleared without treatment. In rare cases, HCV infection causes clinically acute disease and even liver failure.
The way to identify HIV and HCV carriers is by detecting the antibodies against the virus in the patient’s blood. However antibodies against HIV and HCV take weeks – or months – after infection to develop in the body. This in essence creates a ‘window period’ in which infected people will be considered non-infected as long as they do not produce antibodies in their body.
According to Jehuda-Cohen, Smart Biotech’s Chief Technical Officer, the implications of this time gap are deadly – infected people are told they are not currently infected, and they should come back and be tested again in six months. These individuals pose a greater risk to their community than those that were not tested at all, because:
A. They have a ‘certified OK’ not to use any precautions against infecting others.
B. They have a ‘certified immunity’ against getting infected, as they engaged in high-risk behavior and did not get infected.
“Almost every person that is misdiagnosed because he or she are in the window period are people that have been leading a high risk life, and what you’re telling them – because until the SMARTube, a better tool didn’t exist – is ‘you’re not infected!’, she told ISRAEL21c.
“The natural response is then… ‘hey, I know what I’ve been doing – and I can continue doing it – because I didn’t get infected.'”
According to Jehuda-Cohen, it has been calculated that infected people in this situation will infect 50 people a year on average.
In addition, blood donated at blood banks during the ‘window period’ – and therefore test negative by current testing – can be transfused into patients, and may infect them. The extent of the problem increases with the rate of spread of the epidemic.
“The only way to curtail the epidemic is to have earlier detection of the virus,” says Jehuda-Cohen.
She has done just that. The SMARTube enables antibody production, in a small blood sample, within days from infection, without having to wait for the body to produce antibodies weeks or months later.
The technology is the culmination of more than 12 years of work by Jehuda-Cohen, an immunologist with a PhD in immunology from the Technion – Israel Institute of Technology. She did her post-doctoral work at Emory University in Atlanta (“just down the street from the Center for Disease Control”, she notes), where she began on working in AIDS research.
Jehuda-Cohen doesn’t fit the usual image of a scientist who has made a discovery of world importance. The religiously observant Israeli mother of seven possesses a refined, sophisticated demeanor. And unlike many scientists, she’s able to explain complicated processes in everyday terms.
“What happens when a person is infected with HIV is that the immune cells in the body see the HIV and want to scream and say ‘we’ve seen it – we know how to make antibodies against it!’ But the HIV puts a masking tape on their mouth so they can’t scream so nobody knows what they saw. So what we do in the SMARTube is unmask the mouths of the antibody producing cells and give them a microphone,” she told ISRAEL21c over lunch in a Jerusalem hotel.
She then patiently provides a general background on immune diseases for the medical novice.
“With most infections, the immune system sees the foreign structure and begins making antibodies within a few days – usually you can detect them within 5-7 days of infections. Antibodies are a good marker to use for detecting any infections because they’re available in a drop of blood, and you don’t have to go into the liver or the lungs to fund a liver or lung infection.”
However, with HIV and HCV, the most devastating and chronic infections, the antibodies don’t show up after five or seven days. It could take weeks or up to many months to see any antibodies in the blood of HIV or HCV-infected patients.
“As long as there are no antibodies, these patients are diagnoses as non-infected. This is called the window period – the time between infection and the detection of antibodies, and that’s where my research comes in,” she said.
It’s a phenomenon that came to prominence in the mid ’90s when people who had been tested and were diagnosed as ‘sero-negative’ went out and infected others.
“Obviously you can’t infect somebody if you’re not infected. And that’s when the realization came that a test was being used that does not diagnose everybody,” she said.
Since then, the medical community has been trying to solve the ‘window period’ problem with modest success. Diagnostic companies and kits have made strides to detect lower and lower levels of antibodies that enable diagnosis several days earlier.
Other methods of looking for proteins or antigens in the virus have likewise been able to shorten the window period by only a few days. This test – called p24 antigen test – is of minimal value. “It has proved to be very non-cost effective and inefficient,” she said.
The greatest stride has been in the testing of the viral genome – the nucleic acid of the virus, which has shortened the window by an additional 12 days or so, she said. But this very expensive test is only positive when there is enough virus in the blood, and this too can take weeks or even months before it happens. Here again, an infected person might test negative
“The fact is that there are no antibodies in the blood because the production of antibodies is suppressed. So there’s a period where no matter how sensitive you make your kit, you will not detect antibodies – because they’re not there,” said Jehuda-Cohen.
“The core of the technology is overcoming the specific immune suppressants of the body. A few drops of blood are placed into the SMARTube and a solution inside helps the cells of the immune system overcome the suppression, and pushes them into an extremely fast process of antibody production.”
The end result? “We can detect those individuals already infected when nobody else can – because they’re still at the very early stages of the window – where there’s no other technology today that can detect them.”
According to clinical studies on high risk populations conducted in Israel and other countries, the SMARTube successfully enables the detection of all the patients who are diagnosed in the conventional testing – but also detects the virus in additional patients that are infected, but otherwise would have gone undetected at that testing time.
“How much earlier can we detect them? We don’t know the point of infections, so nobody can know how long it takes. But in our studies, we’ve seen that it can take weeks or months before the antibodies on their own will reach detectable levels.”
Sensitive to claims that a test also needs to be conducted in the real world – outside of a shiny lab in a scientific paradise like Israel, Smart Biotech has also conducted trials in other countries, under less than optimal conditions.
“It’s very important – not for the sake of proving that it works, because we’re beyond that – but to show to ourselves first and then to potential end users that this is something that can be used anywhere in the world. It’s very nice to do it in nice modern Israel, but can you take this device and give it to somebody in Africa to use with instructions on how to use it? The answer is yes.”
Jehuda-Cohen’s partner in the vision of the SMARTube is Smart Biotech’s founder and CEO Yisrael Serok, a retired government official who has been interested in this technology since learning about it five years ago.
“At some point we were talking and we said, ‘you know what, let’s start the company. We’re very close to having a product ready so… let’s go, it’s time,” he told ISRAEL21c. “So two years ago, we officially started the company, and now we’re starting to sell the SMARTube.”
Having received the CE Mark (the regulatory requirement in Europe for its registration and marketing) as a blood collection and pre-treatment device, the SMARTube is available for use in hospitals, diagnostic labs, blood banks for health or life insurance uses, “basically anywhere blood samples are taken for HIV ttesting,” said Jehuda-Cohen.
US approval by the FDA is in the plans for later this year, accordin to Serok.
While the top-secret SMART-solution in the SMARTube is produced at the company’s Rehovot facility, the actual device can be manufactured by partners in whichever the country is being targeted.
“Filling it into tubes or vacuum tubes is the process that can be done by outsourcing, where our partners in China can do it in China, where our partners in Europe can do it for the rest of the world. We are not planning on having large-scale production. We want to stay small, smart,” said Serok.
For Jehuda-Cohen and Serok, the SMARTube has been an obsession with an altruistic goal, of detecting the HIV virus as early as possible. But even they realize that it’s far from a cure for AIDS.
“The rule of thumb is the earlier you detect the better you can treat. Treatment and cure are not the same thing. You cannot cure an HIV infection. We can hold it in place,” said Jehuda-Cohen.
“There are parts of the world where you diagnose, but treatment is not an option. So why diagnose? The answer is that we are trying to detect people all over the world as early as possible because it helps us focus education intervention for changing habits. The most important key for curtailing the epidemic is well targeted education, Early detection is the key.”
Sunday, Feb. 12, 2006
A Nanded-based research centre has claimed that it has transformed at least 200 cases of HIV positive to HIV negative in the last three years using a patented drug ‘HIV-SJ’.
Director of Siddharth Research Centre cum Hospital, Dr Siddharth M Jondhale told PTI that the drug made out of three herbs he used was patented in India, Europe and some other countries. [The Cure For HIV / AIDS]
He has been using the drug on HIV positive patients, including almost terminal aids patients, for the last three years.
“The results are very encouraging with several patients showed gradual improvement in their health subjectively as well as clinically,” he said, adding there were around 4,000 patients under treatment in the institute.
Clinically, Jondhale claimed, the HIV-SJ medicine has shown to increase the cd-4 count, regenerate cd-4 cell, destroy the HIV-RNA (ribonucleic acid) and create the new RNA.
Test results of various clinical labs including SRL Ranbaxy clinical reference laboratories, Mumbai and National AIDS Research Institute Pune supported his claim, he said.
The herbal drug also destroys antigens gp-160, gp-120, P-66,P-55, P-51, GP 41, P-31, P-24 And P-17, he said. [The Herbal Medicine Maker’s Handbook: A Home Manual]
SRL Ranbaxy (which is one of the main clinics in which the patients do their testing before, during and after treatment), when contacted for its comments on the tests done by them, its spokesperson Harsha Sajnani said they did comparative tests “only when there is a request from patients’ families which is very rare as they do consultation with their doctors.”
Jondhale said he had made a scientific presentation on the AIDS treatment at the international conference in Brazil organised by the International AIDS Society six months ago.
He has also submitted his paper to British medical journal Lancet which is yet to accept it.
He has also sent the papers to British Journal of Medicine and New England Journal of Medicine.
Asked whether he has communicated to ICMR the findings, he said he wrote a letter to President A P J Abdul Kalam who had acknowledged saying that he had forwarded his letter to ICMR, NACO as well as to World Health Organisation.
Wednesday, Jan. 18, 2006
‘Friendly bacteria’ found in yoghurt has been genetically modified by a team of US researchers headed by an Indian American to produce a drug that blocks HIV infection.
Although the bacteria has only been tested in a lab dish, scientists are optimistic the technique could provide a cheaper and more effective way of delivering drugs to fight the spread of AIDS, by getting the bugs to live right where the drugs are needed most, Nature magazine reported.
The bacterium (Lactococcus lactis) the researchers have modified naturally produces lactic acid, and so is used to produce cheese and yoghurt. It is also found in some parts of the human anatomy, including the gut and the vagina, where the acid it produces damps down the growth of other, harmful bacteria, Nature said.
Some ‘probiotic’ yoghurts are loaded with such beasties with the aim of keeping consumers’ guts healthy. Bharat Ramratnam, an HIV specialist at Brown Medical School, Providence, Rhode Island, and his colleagues have now altered the genetic make-up of L.lactis so that it generates cyanovirin, a drug that has prevented HIV infection in monkeys and human cells, and is on track for human trials in 2007, the magazine reported.
Cyanovirin binds to sugar molecules attached to the HIV virus, blocking a receptor that HIV uses to infect cells.
“It’s basically passive immunization,” says Sean Hanniffy, a molecular biologist at the Institute of Food Research, Norwich, UK, and part of the team.Gels containing cyanovirin could afford some protection for women against the transmission of HIV, but since the drug breaks down quickly these would have to be used just before sex. “In some countries there’s a reluctance to use these gels frequently,” explains Hanniffy.
Because lactic-acid bacteria live naturally in the vagina, one application of a bacterial goop should see the modified bugs thrive there for at least a week, says Hanniffy. “The next step might be to use other bacteria that can survive for even longer,” he adds.
Saturday, Oct. 1, 2005
The virus which causes Aids may be getting less powerful, researchers say.
A team at the Institute of Tropical Medicine, in Antwerp, compared HIV-1 samples from 1986-89 and 2002-03.
They found the newer samples appeared not to multiply as well, and were more sensitive to drugs – some other studies argue they are becoming more resistant.
The researchers, writing in the journal Aids, stressed their work in no way meant efforts to prevent the spread of HIV should be scaled down.
They were only able to compare 12 samples from each time period, and they were unable fully to tease out any effect that drug therapy may have had on the virus.
Hope for future
Researcher Dr Eric Artz said: “This was a very preliminary study, but we did find a pretty striking observation in that the viruses from the 2000s are much weaker than the viruses from the eighties.
“Obviously this virus is still causing death, although it may be causing death at a slower rate of progression now. Maybe in another 50 to 60 years we might see this virus not causing death.”
Keith Alcorn, senior editor at the HIV information charity NAM, said it had been thought that HIV would increase in virulence as it passed through more and more human hosts.
But the latest study suggested the opposite is actually true.
“What appears to be happening is that by the time HIV passes from one person to another, it has already toned down some of its most pathogenic effects in response to its host’s immune system,” he said.
“So the virus that is passed on is less ‘fit’ each time.
“This would suggest that over several generations, HIV could become less harmful to its human hosts.
“However, we are still far from that point – HIV is still a life-threatening infection.”
Dr Marco Vitoria, an HIV expert at the World Health Organization, said other diseases – such as smallpox, TB and syphilis – had shown the same tendency to weaken over time.
“There is a natural trend to reach an ‘equilibrium’ between the agent and the host interests, in order to guarantee concomitant survival for a longer time,” he said.
However, Dr Vitoria stressed that the latest findings should not lull people into a false sense of security.
“This kind of change cannot be adequately measured in years, but in generations,” he told the BBC News website.
He also questioned whether it was possible to draw firm conclusions from such a small study.
Will Nutland, of the charity Terrence Higgins Trust, said: “This latest study adds to the debate on an apparently confusing and contradictory issue.
“Some studies suggest recent strains of HIV are more sensitive to drugs while others claim strains are becoming more resistant.
“The study adds to the body of evidence but HIV is showing no signs of dying out in the near future.”
Friday, Sep. 9, 2005
The results of an international clinical trial, which included more than 2,000 Australian liver and bowel cancer patients, indicate that a radical new approach to treating the disease has a much higher success rate than conventional therapy.
The experimental treatment works by directly targeting tumours with a dose of internal radiation 40 times higher than conventional radiotherapy.
Now, emboldened by the international success rate, two Australian clinical trials have been launched in Sydney this week, as Jennifer Macey reports
JENNIFER MACEY: Ken Dawson from Queensland was diagnosed with bowel cancer last year. Surgery removed the tumour, but further tests reveal that the cancer had spread to his liver. He was told he had just years to live.
KEN DAWSON: And they knew at the time they did the bowel surgery that there was the possibility of tumours in the liver. And that was confirmed with an ultrasound. That was more or less the diagnosis, that I could have had chemotherapy but they didn’t think it would do any good in the long-term.
JENNIFER MACEY: Ken Dawson travelled to Melbourne for a new treatment called Selective Radiation Therapy, or SIRT, where millions of microscopic radioactive spheres or pellets were directly inserted into the liver.
After three months scans showed that the big tumours in Ken’s liver had shrunk significantly. Further tests this year indicated that Ken had been cured.
KEN DAWSON: Oh, 100 per cent, couldn’t get any better. So at this point in time I’m totally cancer free.
JENNIFER MACEY: So, what was the treatment like?
KEN DAWSON: Oh, it was very non-invasive.
JENNIFER MACEY: And did you feel any side effects?
KEN DAWSON: Oh, slightly fluey, but only a case of a sniffily nose. But I wouldn’t say I was in any discomfort at all.
JENNIFER MACEY: Ken Dawson’s success story is typical of the thousands of cases involved in the international clinical trial led by a team from the University of Pittsburgh in the US.
Dr Peter Gibbs is from the Royal Melbourne Hospital, and is heading two new Australian clinical trials that it’s hoped will advance the results of the international study.
Dr Gibbs says up to 250 patients will be involved in the new targeted radiotherapy treatment.
PETER GIBBS: The way it’s given, a little catheter or a tube is placed into one of the arteries in the groin and then the radiologist feeds that little tube up to the liver artery, and once he’s got that in position then from outside, the small dose of radiotherapy is injected through the catheter and goes directly to the liver.
So we’re getting a high dose of radiation targeting directing to the cancers in the liver. And for several reasons most of the dose ends up in the cancer rather than in the normal liver as well.
JENNIFER MACEY: In most cases, liver cancer is terminal, and spread to the liver from cancer initially found in the bowel or pancreas. Over 12,000 Australians are diagnosed with bowel cancer each year, and half of those will also develop liver cancer.
Dr Gibbs says this new form of radiotherapy will complement surgery and chemotherapy, because it zeroes in on tumours found in the liver only.
PETER GIBBS: And the large clinical trial that we’re about to start is looking at combining the SIRT treatment, the radiotherapy treatment with our best current chemotherapy, and I think that’s got the most promise. We’re optimistic that within the larger trial we’ll be able to demonstrate how good this treatment is.
JENNIFER MACEY: The potentially revolutionary treatment was developed by an Australian company, but without government subsidy. The same treatment, at $7,500 a pop, does get government support in the US.
Patient and beneficiary Ken Dawson hopes the new national trials will get Canberra onboard.
KEN DAWSON: Well, I was surprised to find that it’s available for subsidy in the United States, and this is an Australian company who exports this treatment throughout the world, but it’s not eligible for medical benefits in Australia. It’s not cheap.
JENNIFER MACEY: But it was worth it?
KEN DAWSON: Oh, definitely, I’d do it all again. I’d recommend it for anybody in my situation. Wouldn’t hesitate.
ELEANOR HALL: And that’s cancer survivor Ken Dawson speaking to Jennifer Macey.
A University of Florida researcher has discovered an unexpected link between the viruses that cause feline and human AIDS: Cats vaccinated with an experimental strain of the human AIDS virus appear to be at least as well-protected against the feline version of the disease as those immunized with the vaccine currently used by veterinarians.
The surprise finding may mean cats with feline immunodeficiency virus, also known as FIV or feline AIDS, could eventually be treated even more effectively using some form of the experimental human vaccine.
Researcher Janet Yamamoto, a professor at UF’s College of Veterinary Medicine, also theorizes that these emerging relationships between the two viruses could one day lead to a vaccine for human AIDS.
Results from Yamamoto’s research can be previewed in today’s (Sept. 8) online issue of the journal AIDS.
FIV is a natural infection of domestic cats that results in an immunodeficiency syndrome resembling HIV infection in humans. Since its discovery in 1987, FIV infection of cats has been used in vaccine studies as a small-animal model of human AIDS.
“We were the first to demonstrate that you can make an effective vaccine against a virus in the AIDS family of viruses,” said Yamamoto, a co-discoverer of FIV.
Yamamoto holds the patent on the only approved vaccine available through veterinarians to protect cats against FIV. Her most recent studies have attempted to improve the efficacy of that vaccine by using strains of FIV found in cats in which the disease had not progressed for some reason over several years.
To determine the extent to which the human and feline AIDS viruses react to each other, and any implications that might exist for vaccine efficacy, Yamamoto began experimenting with long-term, nonprogressive strains of FIV that led to the current commercial vaccine. Now she is working on an HIV vaccine consisting of HIV virus from long-term, nonprogressing individuals.
“We purposely made vaccines with strains that weren’t virile,” Yamamoto said. “We found that whenever we tried using less virulent strains of virus, we were able to make a better vaccine.”
Yamamoto’s team was also surprised to discover that a core protein found in HIV also effectively protects cats against FIV.
“So what does this mean to human AIDS research? The viruses HIV and FIV are from the same viral family,” Yamamoto said. “For that reason, the amino acids that make up the proteins in both viruses share some common regions. There appear to be regions of HIV, or variations of the core protein we used in our studies, that may provide protection in vaccine form against HIV.”
Some compounds made from separate virus strains have been successfully used in vaccines against viruses from the same subfamily, such as smallpox in humans, which is made from cowpox virus, and human measles vaccines for canine distemper in puppies.
“Therefore, protective vaccines based on cross-reactive regions of AIDS viruses can provide broad immunity, and may be useful against viruses that are currently evolving in a new host, such as HIV infection of humans,” Yamamoto said.
Alan L. Landay, a professor of immunology and microbiology and associate department chairman at Rush University Medical Center in Chicago called Yamamoto’s findings “very exciting.”
“This raises a potential whole new area for research in the field of vaccines that with the current approaches haven’t yielded any success to date,” said Landay, whose research team is working to develop novel immune strategies to treat HIV infection. “We need to explore all the potential options available to us for developing an HIV vaccine.”
Saturday, Aug. 27, 2005
Scientists have found that a simple, harmless virus might hold the key to the more effective and efficient development of HIV and anti-viral drugs, claims a study published in the online version of the Journal of the American Chemical Society.
UCI chemical biologists, Weiss and Allison Olszewski employed the virus, called bacteriophage, to learn how a HIV protein could respond to a new class of anti-viral molecules they have discovered. They found that the virus can model millions of different mutational variants of an HIV protein called Nef.
Knowing how the entire population of Nef variants responds to new drugs gives researchers greater ability to identify broad-spectrum, anti-HIV compounds.
“Viruses are clever about mutating to defeat the best efforts of chemists and biologists. By recruiting a harmless virus, we’re learning how HIV will respond to new classes of anti-viral drugs before these compounds are tested in the clinic, which is currently an expensive and time-consuming process,” said Weiss.
The researchers first created one such library by attaching the Nef protein onto the bacteriophage, which was then coaxed into synthesizing the millions of mutational variants of Nef. They then targeted this library, which they call an allelome, with a second library of small-molecule compounds in order to identify the specific compounds that could target the entire population of Nef mutational variants.
The results suggested that chemically simpler, more flexible compounds could better accommodate viral mutations.
Wednesday, Aug. 17, 2005
Scientists in Australia’s tropical north are collecting blood from crocodiles in the hope of developing a powerful antibiotic for humans, after tests showed that the reptile’s immune system kills the HIV virus.
The crocodile’s immune system is much more powerful than that of humans, preventing life-threatening infections after savage territorial fights which often leave the animals with gaping wounds and missing limbs.
“They tear limbs off each other and despite the fact that they live in this environment with all these microbes, they heal up very rapidly and normally almost always without infection,” said U.S. scientist Mark Merchant, who has been taking crocodile blood samples in the Northern Territory.
Initial studies of the crocodile immune system in 1998 found that several proteins (antibodies) in the reptile’s blood killed bacteria that were resistant to penicillin, such as Staphylococcus aureus or golden staph, Australian scientist Adam Britton told CNN. It was also a more powerful killer of the HIV virus than the human immune system.
“If you take a test tube of HIV and add crocodile serum it will have a greater effect than human serum. It can kill a much greater number of HIV viral organisms,” Britton said from Darwin’s Crocodylus Park, a tourism park and research centre.
Britton said the crocodile immune system worked differently from the human system by directly attacking bacteria immediately an infection occurred in the body.
“The crocodile has an immune system which attaches to bacteria and tears it apart and it explodes. It’s like putting a gun to the head of the bacteria and pulling the trigger,” he said.
For the past 10 days Britton and Merchant have been carefully collecting blood from wild and captive crocodiles, both saltwater and freshwater species. After capturing a crocodile and strapping its powerful jaws closed the scientists extract blood from a large vein behind the head.
“It’s called a sinus, right behind the head, and it’s very easy just to put a needle in the back of the neck and hit this sinus and then you can take a large volume of blood very simply,” said Britton.
The scientists hope to collect enough crocodile blood to isolate the powerful antibodies and eventually develop an antibiotic for use by humans.
“We may be able to have antibiotics that you take orally, potentially also antibiotics that you could run topically on wounds, say diabetic ulcer wounds; burn patients often have their skin infected and things like that,” said Merchant.
However, the crocodile’s immune system may be too powerful for humans and may need to be synthesised for human consumption.
“There is a lot of work to be done. It may take years before we can get to the stage where we have something to market,” said Britton.
Friday, Aug. 12, 2005
U.S. scientists have tested a new approach to AIDS therapy that raises hope of an eventual cure of the disease. Doctors have found an old drug used for another condition can dramatically decrease the levels of the AIDS virus in the body.
HIV is a tenacious virus. Current drugs can suppress it to almost immeasurable levels to keep patients alive. But this is not a cure, since the organism continues to exist within some of the body’s immune cells, although in a latent, non-replicating state. Patients must take the drugs for life to prevent this store of virus from reawakening.
Now, U.S. government and university researchers report finding a way to reduce this low level of dormant HIV much further.
Led by University of Texas scientists, they gave four patients who were already taking combinations of standard AIDS drugs an additional compound. It is valproic acid, a medication long established to prevent convulsions. The four patients took valproic acid by mouth twice daily for 16 to 18 weeks. The researchers found a 75 percent drop in the number of the dormant HIV cells in three of them. When the treatment ended, the number of cells rebounded to earlier levels.
At McGill University in Montreal, Canada, AIDS researcher Jean-Pierre Routy, who was not involved in this study, says it is too early to talk of a cure for HIV, but he calls the results promising for their potential to deplete latent HIV reservoirs in the body.
“We can start to attack the virus where it is hiding,” he said. “We can hope one day that we can kill it or remove it from the body or kill the cells infected by the virus. So, yes, it’s a glimpse of hope for sure.”
The researchers present their findings in this week’s edition of the medical journal Lancet. They write that while the results are not definitive, they suggest that new approaches will allow the cure of HIV in the future.
But other scientists are cautious about the findings. Johns Hopkins University physician John Siliciano, who helped discover dormant HIV cells in the 1990s, told the Associated Press that to be useful, a drug has to kill virtually all of the cells, not merely 75 percent of them.
Rockefeller University AIDS researcher David Ho calls the finding a step forward, but a modest one. He told an NBC television Today Show interviewer that the ways of measuring HIV in this test are not precise, so the drop could be less than 75 percent.
“It [the virus] is extremely difficult to get rid of, so scientists do not want to raise false hope,” said Mr. Ho. “It’s a very interesting observation, but we have to be cautious to see if this observation could be confirmed.”
The researchers who reported the study say they are experimenting on larger groups of HIV patients. They say that, if their findings are substantiated, eliminating the virus in a person could occur in stages, beginning with standard combination therapy to suppress it, followed by drugs like valproic acid to complete the job.
Monday, May. 23, 2005
An indigenous pharmaceutical company, Fidson Healthcare Limited, has made a breakthrough in the production of anti-retroviral drug for the management of Human Immuno-Deficiency Virus (HIV) and Acquired Immuned Deficiency Syndrome (AIDS).
The new drug, Virex Anti-retroviral, was approved by the National Agency for Food and Drug Administration and Control (NAFDAC) Thursday, prompting the company to go into full production of the drug.
Speaking to Vanguard at their Ikorodu Road, Lagos office, the marketing manager of the company, Mr Ijimakin Eboh Ola, said that the breakthrough in the production of anti-retroviral drug is just the beginning of many good things to come from the company.
He explained that the feat by Fidson Healthcare Ltd was the first of its kind in the whole of West Africa.
According to him, the journey for the production of the highly demanded drug started four years ago and the breakthrough came this year.
“We have one of the best research facilities in the industry and Virex anti retroviral drug is just the first and a lot of others will follow,” he said.
Continuing, he explained that there is no known cure for HIV/AIDs as all drugs available are aimed at bringing the viral load to the lowest level, adding that evidence has shown that Virex can do it.
The marketing manager, who stated that his company will continue to research towards finding a cure for the disease, explained that the only way to grow in the industry is through research.
“We are committed to research, which is a continuous thing in our company” he said.
On why they went into the research for HIV/AIDS anti-retroviral drugs, Mr Ola explained that three things brought them into it, which he describe as the three A’s (Affiordability, Availability and Accessibility).
According to him, though there could be other anti-retroviral drugs by multi-national pharmaceutical companies, yet they are not affordable, available and accessible to the over one million HIV carriers in the country.
He therefore said that Fidson Healthcare will ensure that all the three A’s problems faced by the patients are solved.
“Whatever this is in the market today, our brand will be better priced, and available” eh stated.
Virex according to him comes in five viriants including for children and adults and could prevent transmission of HIV from mother to child.