Jan Kobal explores a potential new treatment for HIV
For decades HIV therapies have targeted the virus in the vain attempt to quell the spread of infection. However, a study from 2013 published in Nature out of the lab of Dr. Greg Towers, conducted by postdoctoral fellow Dr. Jane Rasaiyaah, has provided support for a paradigm shift in thinking with regards to HIV therapy.
Groundbreaking research out of the Division of Infection and Immunity in UCL, the Medical Research Council in Cambridge, and the Wolfson Institute in UCL proposes we should be targeting the host in order to “uncloak” HIV and thus let it be combatted by our own immune system. This is a much more promising treatment plan than trying to play catch up with how quickly HIV mutates and evades established therapies.
HIV in a developed world context has become less of a problem than it was 20 years ago. Drug cocktails against HIV have become much more efficient at keeping patients alive by targeting the spread of HIV in patients. This is at least until the virus mutates and a new cocktail needs to be designed for the patient. This has led to many patients being able to live full and productive lives. However, it has not at all eradicated the troubles associated with HIV in individuals who cannot afford therapy or simply do not have access to it. There is an ever-present need for a therapy that allows for the patient’s own immune system to mount a response against HIV.
Which is precisely what has been done by researchers from UCL and Cambridge.They have begun to develop a treatment that targets the components of a host cell that HIV requires in order to replicate and be infective, seeing as HIV is like any other virus in that it needs host cells in order to survive. They began to elucidate the therapy when they noticed that HIV evades our immune system by recruiting host proteins – proteins in our cells that are not foreign – that allow for it to be cloaked while it travels across our host cells to the nucleus where it can replicate.
Their claims were supported when they mutated the host proteins that HIV exploits and found that an innate immune response – the first line of defence – was mounted against HIV particles in a lab setting.
They then succeeded in developing a drug, called SmBz-CsA, that mimicked the mutated host proteins that HIV requires to survive. Treatment with the drug led to a complete suppression of HIV replication in a lab setting and a strong production of Interferon Beta, a molecule that is needed in natural human antiviral responses.
The implications of this paper are monumental. The scientific community might have an entire new avenue of HIV therapy research to explore if further experiments corroborate the theory that targeting host components will lead to HIV suppression. However, paradigm shifts in thinking have never been swift, especially not in a field as financially invested in as HIV research. It may be a while until we see more labs embracing this sort of an approach to combatting HIV. There is no denying its potential though.
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