Thank you very much, Mr. Chair, and thank you to the committee for the opportunity to present.
My name is Keith Fowke, and I'm a researcher based at the University of Manitoba. I'm the head of my department of medical microbiology and infectious diseases, and I also function as the chair for CIHR's advisory committee on HIV/AIDS research.
As a university-funded and university-based researcher, mainly funded by the Canadian Institutes for Health Research since 2001, I'd like to make the point that federally funded, investigator-initiated research has benefits for reducing health care costs, including drug costs. I'll provide just one example of this potential.
I'll try to demonstrate that our research suggests that we may prevent new HIV infections using safe, affordable and globally accessible anti-inflammatory drugs like acetylsalicylic acid, or ASA, which is also known as Aspirin. Yes, that's right: I'll try to suggest to you today that it may be possible to prevent new HIV infections using Aspirin.
What's the scale of the problem that we're talking about? In 2018, there were 1.8 million people globally who were infected with HIV each year, the majority of whom were in sub-Saharan Africa. Globally, new infections have not declined very dramatically. Over the last 10 years, they have remained relatively flat. In the Canadian Prairies, we have a growing epidemic of HIV, especially in our indigenous communities.
HIV prevention methods, such as condom use, are not possible for everyone, especially when gender-based power differentials exist. Access to HIV medications that can be used to prevent HIV infections are not always available to everyone that needs them in the community. Therefore, we need new HIV prevention approaches to be added to our HIV prevention tool box.
My research, funded by CIHR and Grand Challenges Canada, focuses on understanding the mechanisms of why some Kenyan women, who are intensely exposed to HIV, fail to become infected. We have determined that these women have, in their genital tracts, naturally low numbers of the type of cell that HIV preferentially infects. Our goal has been to determine how to induce this reduction in genital tract HIV target cells in other women who are at risk of acquiring HIV.
At its most basic level, HIV infection requires a fit virus and a susceptible cell. Once that cell has been infected, usually in the genital tract, the virus quickly spreads throughout the body in a matter of a few days. Most HIV prevention efforts focus on trying to keep the virus away from the cells, focusing on things like condoms, or crippling the virus using anti-HIV drugs. However, we've taken the approach of trying to limit that HIV target cell from migrating to the genital tract in the first place. Without a susceptible target, HIV viruses are cleared from the genital tract and the body is not infected.
How can we prevent this HIV target cell from getting into the genital tract? The process of immune cells moving from the blood into tissue is called inflammation. We rationalized that perhaps using an anti-inflammatory drug would help reduce the number of target cells moving from the blood into the genital tract. When deciding which anti-inflammatory drugs to test, we chose to test drugs that were globally available and affordable and that had a strong track record.
ASA was the leading choice because it is an anti-inflammatory drug and hundreds of thousands of people safely use it daily for the prevention of cardiovascular disease. Most importantly, it's already there, sitting in every small kiosk throughout the world and in developing countries. When we asked Kenyan women, they said that Aspirin was highly desirable because it was already known in the community, and did not carry any of the stigmatization that other anti-HIV medications do.
To test our theory that ASA would actually reduce the number of HIV target cells, we conducted a small CIHR- and Grand Challenges Canada-funded pilot study in Nairobi. We gave 38 women low-dose Aspirin for six weeks and we measured the number of genital tract HIV target cells before and after the therapy. Interestingly, we observed a 35% reduction in the number of HIV target cells in the genital tract following six weeks of low-dose Aspirin.
While this does not prove that ASA will actually reduce HIV infections, we feel that it is logical that if there are fewer target cells in the genital tract, then should HIV be introduced, the probability of infection would be reduced.
What are the next steps? Currently we have a CIHR-funded study to assess the optimal dose of ASA that would be required and how long the effect would last. This will pave the way for larger clinical trials that are required to assess if anti-inflammatory drugs like ASA really can have an impact on reducing HIV infections.
Studies of the use of anti-HIV drugs in HIV prevention have demonstrated that the presence of genital inflammation can reduce the effectiveness of these drugs from 75% down to 10%. In other words, we have drugs that we already know have an impact on preventing HIV infection by targeting the virus, but if there is inflammation, it reduces their effectiveness. Much like in cancer, where cocktails of drugs are used to fight off cancer, we envision that people would be provided with a cocktail of HIV prevention approaches. By combining an anti-HIV medication that targets the virus and an anti-inflammatory drug that targets the target cell, we suggest that we could create an added benefit.
Our goal is to use a safe, affordable and globally available drug like Aspirin, which may reduce the number of HIV infections around the world and be added as one of the HIV prevention approaches that are used.
There are a couple of points to consider. We never started this research looking for a link with anti-inflammatory drugs and HIV; our investigator-initiated research was focused on trying to understand the mechanism of why some people weren't infected. The data led us to this hypothesis about inflammation being important, and therefore to looking at anti-inflammatory drugs.
The choice of which drugs to be used in this study was very conscious. We wanted drugs that were extremely safe and that were globally available and affordable. This often meant generically available drugs. Using this approach, should it prove to be effective and be actually rolled out into the wider community, the timelines for rollout would be significantly shortened because the drugs are already in the community.
Finally, repurposing existing drugs to fight new diseases in different ways has the potential to save on drug spending in the long term, but it would require some short-term investments in highly innovative fundamental research.
Thank you very much for your time.