In science, as in many other walks of life, what is unexpected is often what is most interesting and important. The idea, first mooted in 2011 by Julian Gold of the Prince of Wales Hospital in Sydney, Australia, that HIV infection—or maybe the drug treatment used to fight it—might protect against multiple sclerosis (MS), was certainly unexpected. Now, in a study just published in the Journal of Neurology, Neurosurgery and Psychiatry, Dr Gold has confirmed his suspicion. That is interesting. It may also be important.
Dr Gold’s original motive for investigating the connection between the two diseases was casual observation. He treats people with HIV and has several acquaintances with MS. This led him to realise he had never come across a case of somebody with both. A literature search confirmed the lack of connection. Of the 700,000 published papers on HIV and AIDS, and the 300,000 on MS; not one referred to a patient who had the pair of them. Eventually, he tracked down a single instance—and, tellingly, that individual had started to shrug off the symptoms of MS when he began taking antiretroviral drugs to combat his HIV.
This finding led a Danish team to compare 5,000 HIV-positive people with a control group of 50,000 of their uninfected peers. Unfortunately (for science, if not for the individuals involved) even these large numbers did not yield enough instances of subsequent multiple sclerosis for a statistically significant result to emerge. Dr Gold therefore decided to throw the kitchen sink at the problem. He and his colleagues turned to the English Hospital Episode Statistics, which record all interactions between the people of England and hospitals belonging to their country’s National Health Service.
The team used this database to identify and track everyone in England with HIV who was discharged from hospital between 1999 and 2011, and to provide similar information on multiple sclerosis both for these people and for a group of uninfected controls. In total, Dr Gold and his colleagues found 21,207 HIV-positive individuals in the database and compared them with 5,298,496 controls of similar ages and ethnic backgrounds.
The rate of onset of MS in the controls suggested that about 18 cases should have developed among the HIV-positive patients. In fact, the team found only seven. That result was indeed statistically significant. It suggests those infected and undergoing treatment are 60% less likely to develop MS than their uninfected peers. Moreover, further analysis showed this value leapt to 80% among those who had been infected and treated for more than five years.
Dr Gold’s results do not indicate whether it is the infection or its treatment that is suppressing MS. Either sounds plausible. The immediate cause of MS’s symptoms (which range from clumsiness of movement to depression) is that the sufferer’s immune system is attacking his central nervous system—specifically, the fatty sheaths that insulate the nerve cells in it. HIV meddles with many sorts of immune-system cells and signalling pathways that are associated with multiple sclerosis, so this could be why the disease wanes in those infected with it. On the other hand, though the underlying cause of MS is unknown, many people suspect it is triggered by a yet-to-be-determined virus. If that is true, it may be that the antiviral drugs given to those with HIV are bringing relief by attacking this unknown culprit too.
If this second idea is the right one, it means a treatment for MS looks eminently plausible; it may simply be a question of repurposing some existing drugs. If HIV itself is the protective agent, devising a treatment will be harder. Dr Gold’s discovery would still be a useful pointer, though, to the molecular-biological crack into which a suitable pharmacological crowbar could be inserted. Either way, then, this does look like an important result, derived ultimately from an unexpected observation.
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