In a unique case, one MS patient went without symptoms for more than 12 years after contracting HIV and starting treatment with antiretroviral drugs.
The results of a study published this week in the Journal of Neurology, Neurosurgery and Psychiatry suggest that people who are HIV positive may have a much lower risk of developing multiple sclerosis (MS). Could HIV be tamping down the immune system, preventing MS relapses, or are the drugs given to HIV patients making the difference?
Researchers first noticed dramatic changes in a single HIV-positive MS patient who began taking antiretroviral drugs, said Julian Gold of the Albion Centre at Prince of Wales Hospital in Sydney, Australia, in an interview with Healthline.
“He was diagnosed with MS before he had the HIV,” explained Gold. “His MS progressed really very rapidly and he had quite a bad outlook.” The man couldn’t use interferon and had a number of relapses in the first and second years after diagnosis. Then he became infected with HIV.
But after years of relentless MS attacks that were causing his disease to rapidly progress, the man started taking antiretroviral therapy to combat HIV, and that, said Gold, “was when we saw his MS subside.” His MS symptoms disappeared for more than 12 years after he began antiretroviral treatment.
A Danish research team tried to find out if the antiretroviral drugs the man had taken could be an effective treatment for MS. While their results are encouraging, the study population was small and more research is needed.
Gold’s team decided to pick up where the Danish researchers left off. They did this by looking at all episodes of hospital care between 1999 and 2011 in England.
They compared the records of more than 21,000 HIV-positive people to those of a control group of nearly 5.3 million people treated for other conditions or injuries.
Over a seven year span, they compared the number of MS cases in both groups. Compared to those who did not have HIV, those who did were 62 percent less likely to develop MS. After having HIV for one year, patients were 75 percent less likely to develop MS, and after five years that number rose to 85 percent, suggesting a correlation between having HIV and being protected from MS.
But was it the HIV virus that caused this protective effect, or might antiretroviral drugs be staving off MS?
“There are patients with HIV who are not on treatment who are [having relapses] of their MS,” Gold pointed out, “so it’s hard to actually know.”
In the original case that sparked this research, being initially infected with HIV did not change the course of the patient’s MS. This suggests that the key was starting antiretroviral drugs.
Gold admitted this theory seems reasonable, “but certainly from a scientific point of view we need to be careful in what we say. It’s very important that we don’t give people unrealistic expectations. So, I think that what we need to do is to look at the evidence, follow it through. We’re doing a clinical trial at the moment in London and we’ll see what it shows.”
Gold’s team is so certain there’s a viral component to MS — either causing the disease or triggering it — that their new phase II study is testing the antiretroviral drug raltegravir as a therapy for MS. Researchers will track a small group of 24 patients with active MS by taking monthly MRI scans of their brains. They plan to publish their findings early next year.
The trouble with studying viral triggers of MS, Gold said, “is that unless you can stop the infection and see the outcome, then you really don’t know if it’s the cause. So up until now, even though a lot of viruses have been suggested in MS, there’s never been any way of stopping them or preventing them, and therefore you never really know if they are involved in MS or not.”
If the team is successful, Gold said, it could pave the way for new treatment options for MS and might bring us closer to defining a cause.
“I think this work, with the antiretroviral drugs, is particularly exciting,” said Gold, “because we know that they do inhibit or stop almost completely the production of retrovirus, so I think that there may be renewed optimism in this area.”