Compiled and edited by Laurence Gibson
Scientists in Auckland and Seattle have recreated part of the original ancestor
of HIV in an attempt to make a vaccine to stop the virus spreading, reports
the New Zealand Press Association.
Although still in embryonic form, the researchers believe the vaccine has the best chance of any that have been developed to contain HIV/Aids.
Auckland University Professor Allen Rodrigo said: “the virus mutates so quickly that any vaccine based on one of the current strains would quickly become ineffective.”
The genetic structure of HIV changes by about one per cent a year - about four million times faster than genes in any plant or animal species.
Rodrigo decided the only way to tackle such a constantly changing prey was to track down the common element in all varieties of the virus found in the Western world - their original common ancestor.
They found the likely structure of the ancestor by collecting genetic sequences of all main existing strains and arranging them in a ‘tree’, with each branch made up of strains with similar genetic sequences. Then they arranged the branches in groups of similar sequences, that ultimately led back to the original ‘trunk’.
Jim Mullins, from the University of Washington in Seattle, then took the genetic sequence of part of the ‘trunk’ and made all the chemical compounds (or proteins) that sequence would have produced in the original HIV ‘ancestor’.
He then injected this artificial HIV virus into rabbit cells, and the cells developed antibodies that fought off the latest natural strains of the virus. “It does seem to protect [against the virus],” commented Allen Rodrigo.
“This is very preliminary data. We have a synthetic vaccine of a synthetic virus that appears to create antibodies that can neutralise some of the kinds of HIV,” he added.
“I hope it will be broader than the existing vaccines that people are now trialling.”
Rodrigo believes the resulting vaccine would be only partial; not eliminating HIV, but weakening it so that people with the virus can live longer and not pass it on if they have children.
“The best strategy would be to immunise everyone with the hope that it would weaken the virus in people who get infected and prolong their life-span,” he said.
Treatment interruptions (TIs) can be a useful tool in HIV therapy when used correctly, the 43rd ICAAC Conference in Chicago heard in September.
The strategic use of long-term treatment interruptions seems to be a viable option, when performed under strict supervision. However they work best with patients who first start HIV therapy before their CD4 counts fall below 350 - suggesting a complete revamp of treatment guidelines.
The first study, from Italy, took 140 patients who all had CD4 counts over 500 and which had never been below 350. All had been receiving antiretrovirals for at least a year. The criterion for resuming treatment following their break was a decrease to less than 350 T-cells.
The average time to the above event was 104 weeks - a significant amount of time. This suggests that the use of treatment interruptions could influence when to start treatment. Over half of the patients are still off therapy.
In the second study, patients tolerated treatment interruptions well, with only two out of 114 patients (who had never had a viral load less than 350) experiencing viral rebound.
However, all patients with a low-point CD4 of less than 200 had to re-start therapy within 10 months of the break.
The conclusion? The use of long-term, immunologically driven, TIs could further enhance future therapeutic options for people living with HIV.
See also ‘when not to stop’.
Researchers reported last week that a new, two-step approach could bring the first hope of controlling a life-long Aids infection.
Dr Jerome Zack and colleagues, from the University of California, experimented with the technique to locate and kill dormant HIV-infected immune system cells in mice, and are now ready to test in monkeys.
Although modern treatments can keep HIV patients healthy indefinitely, they cannot reach latent virus that lurks inside the immune cells.
Dr Zack has devised a novel two-step system where, first, they partially activate the cells where the virus hides, then kill the cells before the virus can escape.
“About one in a million T-cells holds latent HIV that the antiretroviral drugs can’t touch,” Dr Zack told the Reuters news agency. “In order to make it visible, so you can attack it, you have to activate it.”
If all a patient’s T-cells were activated it could cause potentially deadly illnesses. So Zack’s team used two compounds to only partially activate the cells: interleukin-7 and prostratin.
“They hit a specific activation pathway but don’t fully turn on cells,” Zack said.
Once the cells have been partially activated, the scientists fire the ‘guided missile’ - an antibody spliced into a piece of diphtheria toxin. “Because the antibody is linked to a toxin molecule, it pops into the cell,” Zack continued. “The toxin kills that cell before lots of viruses are made.”
The novel approach has cleared 70-80 per cent of the reservoir of latent T-cells in mice without mistakenly attacking healthy cells. Nevertheless, it remains difficult to extrapolate how well the technique will be tolerated by humans.
Once tested on people, Zack envisions the approach could be used along with HAART to stem the virus within the body, but warns against thinking that the technique offers the possibility of a complete cure.
 photo: courtesy WHO/p virot |
A bog-standard smallpox vaccination could provide the unlikely key that protects people from Aids, it emerged last week.
Although initially dismissed as a “crazy idea,” the early test results remain encouraging.
Originally, the work was based on an observation that Aids first began to spread rapidly across central Africa - the first place to be identified as having HIV infection - when smallpox was eliminated and people stopped vaccinating against it.
“My first reaction was, this sounds like some kind of crazy idea. But after some analysis I realised it was not so crazy,” said Ken Alibek, a former research scientist for the Soviet biological weapons programme.
“It would be a great way to protect people because the vaccine has been safely produced, is already in production, and has been used successfully on a global scale to eradicate smallpox,” he said.
In the study, the team took samples from 10 people who had the smallpox vaccination, and 10 who had not.
Once HIV was introduced to the blood of those who were vaccinated, the virus either slowed considerably, or failed to grow completely.
Despite the small sample, these results are, according to Professor Alibek, “statistically significant”, although he has come under fire for issuing the press release before the experiment was reviewed by his peers.
Pete Hotez, from the Department of Microbiology in Washington, described the release as “totally perverting the whole scientific process.”
But Professor Alibek remained unruffled by the controversy, by insisting: “The university has a right [to issue a press release]. You want to involve all interested parties. This is a way of attracting money. Many foundations claim they exist for helping HIV-infected people, and this would, I hope, interest them.”
George Mason University has already filed patent applications on the smallpox vaccine’s therapeutic use against HIV. Laurence Gibson
