The science of success

2013-10-13 06:00

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What will it take to cure diseases like TB, malaria and HIV, or at least make sufferers’ lives far easier?

Hard work, a spot of luck and some very dedicated South African scientists. City Press examines some of the health innovations where SA is leading the way. Zinhle Mapumulo and Steve Kretzmann report

Five years ago, a University of Cape Town (UCT) team realised that too many HIV-positive people were developing end-stage kidney failure, which meant they needed transplants.

But being HIV-positive meant you didn’t qualify for a transplant, so Dr Elmi Muller and her team got to work.

Muller and her team explored the idea of pioneering organ donation between HIV-positive people at Cape Town’s Groote Schuur Hospital.

Between September and November 2008, they performed four kidney transplants from HIV-positive donors to HIV-positive recipients.

The recipients were on antiretroviral (ARV) treatment and had undetectable viral loads. The two donors had never taken ARVs, but their kidneys functioned normally.

Since then, several other kidney transplants of this nature have taken place at Groote Schuur. The team monitors recipients to see if there are any long-term complications.

Muller, the principal investigator, says the preliminary results are encouraging.

“Twenty-four kidney transplants have been performed at Groote Schuur in the past four years and all of them have been a success,” she says. If the final results show that kidney transplants can be performed on an HIV-positive person using organs from someone else with the virus – with minimal or no complications over a long period – this could seriously reduce the burden placed by end-stage kidney failure on the health system, especially when it comes to dialysis. Taking the sting out of malaria Each year, more than 600 00 people die of malaria worldwide. But Professor Kelly Chibale and his

team at UCT’s Drug Discovery and Development Centre (H3-D) believe they’ve found an effective single-dose cure for all strains of the disease.

It is too early to cry “cure”, but Chibale and his team have a compound that has been through preclinical trials – a significant milestone in itself – and if all goes well, will enter the first phase of clinical trials next year.

“The standard period to get to where we are is six years but we were blessed to have done it in two,” says Zambian-born Chibale, who is the founder and director of H3-D and holds the research chair in drug discovery at the science and technology department.

If it is a cure, the involvement of Swiss-based nonprofit organisation Medicines for Malaria Venture means it could be available at $1 (R10) or less per treatment.

The clinical trials will take another six years or more, says Chibale, but if the compound is found to be safe and effective, it will have a massive impact on disease control in Africa.

Since positive preclinical trial results were released in June last year, Chibale and his team have been figuring out exactly why and how the compound, called MMV390048, works. They are researching the backup molecules needed for the inevitable resistance that will develop against the drug should it be used as a cure. They have also been researching more cost-effective ways of manufacturing it to make it commercially viable. TB or not TB? Protein holds the key It took four years of trial and error for a team of researchers from UCT to solve a mystery that baffled scientists for years.

Their discovery is key to understanding the ability of the tuberculosis bacterium to cause disease. In future, it may even help biochemists develop new and powerful drugs that will stop latent TB from becoming active.

About one-third of the world’s population has latent TB, which means they are infected by the bacteria but are not yet ill with the disease.

Our local team, led by Dr Digby Warner and Dr Krishnamoorthy Gopinath from UCT’s Molecular Mycobacteriology Research Unit, identified a protein that allows the bacterium to scavenge and take vitamin B12 in the body of a person infected with TB.

Humans need vitamin B12 to form red blood cells and to help the brain and nervous system function. If an infected person has a vitamin B12 deficiency, there is an increased risk of them developing TB.

Scientists have known for years that a protein called Rv1819c played a critical role in the ability of the mycobacterium tuberculosis to cause TB – but they weren’t sure what that role was.

Through intensive laboratory tests, the UCT researchers, working with scientists from Switzerland, Lithuania and the US, unravelled the mystery. Warner explains that the study identified Rv1819c as a possible vitamin B12 transporter.

This discovery, he says, means it’s possible that the tuberculosis bacterium “scavenges B12 during host infection” – so the TB bug scoffs the protein and makes you, the latent sufferer, more likely to start showing active symptoms of the disease.

The science of coincidence

It could become one of the most powerful weapons in the fight against HIV and Aids – and it was discovered by accident.

Scientists from the National Institute for Communicable Diseases (NICD) were searching for clues as to how the body of an HIV-infected person can produce powerful antibodies that can kill most strains of the HI virus.

It started with two women from KwaZulu-Natal who enrolled in different HIV trials conducted by the Centre for the Aids Programme of Research about eight years ago.

The pair was HIV negative when they enrolled in the study, but became infected once the trial was under way.

Their blood was taken shortly after they’d been infected, and the samples were kept at the NICD laboratory.

Further tests, conducted years later, revealed that the women had started producing broadly cross-neutralising antibodies.

These are very powerful and can kill up to 88% of HIV strains from across the world.

The team, led by Dr Penny Moore and Professor Lynn Morris, decided to use the blood samples to determine which part of the HI virus is targeted by broadly cross-neutralising antibodies.

While conducting tests, they discovered that the women’s antibodies targeted a specific sugar on the HI virus, known as “332”.

They then went back and studied the first blood samples taken shortly after the women were infected.

To their surprise, they discovered the virus that infected the women carried no 332 sugar, even though

later antibodies were binding to that particular sugar.

The women’s stories and the powerful antibodies hidden in their blood might, scientists believe, be the first step on the road towards developing an HIV vaccine.

If they are right, the vaccine would combat HIV1, the most common strain of the virus in the world.

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