Human Immunodeficiency Virus (HIV) has affected approximately 37.9 million people in the world as reported by HIV’s official website in 2018.
Of those who are infected, roughly 96% are adults (15 and older).
Although HIV can be fatal and was the seventh leading cause of death globally in 2000, new forms of treatment have substantially increased survival rates and it was no longer on the World Health Organization’s top 10 global causes of death list in 2016.
Much of this improvement is attributed to the substantial amount of research that has been conducted in the years since the virus was first observed in 1981.
UW research professors Dr. Florian Hladik and Dr. German Gornalusse, who both work in the department of obstetrics and gynecology, published a paper that gives insight into how to prevent HIV from reemerging after treatment ceases.
For both Hladik and Gornalusse, a passion for the sciences arose early in their careers as they were navigating their lives in their home countries.
“I began research in Austria, where I did med school and Ph.D.,” Hladik said. “But then I started to become interested in infectious diseases. At the time, [the] HIV epidemic was going global.”
Gornalusse, on the other hand, explored other career paths — including business — before settling on the sciences.
“I changed my plans,” Gornalusse said. “I applied for a job in Texas and did my Ph.D. in epigenetics of a receptor that has to do with HIV.”
Both came to the United States in the early 2000s with the intention of continuing their research careers in the area of infectious diseases.
In late 2016, Hladik and Gornalusse, along with other collaborators, began the conversation about how to find the tissues where HIV is easily reactivated and the biological mechanisms that allow the virus to reemerge.
The virus’s reappearance is due to the presence of latently infected cells which are largely silent during treatment but can become activated after the end of treatment. These cells then start to produce a new virus, which then infects neighboring cells, allowing HIV to arise once again.
By using biopsies from benign surgeries that were available to them, they were able to identify that the cells in the cervix have maximum reactivation capacity.
“These [HIV-infected T lymphocyte] cells are working as hotspots and constantly reactivating,” Gornalusse said.
However, they believe that the cervix is just one of many hotspots in the body, and areas that are structured very similarly, like the gastrointestinal tract, may also have similar mechanisms for reactivation.
By tracking all these hotspots, and by determining the processes by which HIV reactivates in these areas, they hope to pave the path toward more effective therapies and treatments.
“If we find where and how, and if somebody else finds good curative therapy, we can merge there,” Hladik said. “A patient gets their curative therapy and then our information hopefully will help to make the few remaining cells in the body not reactivate HIV.”
Theoretically, destroying those few infected cells that remain will ensure that the virus is not reactivated in the body. However, they agree that deriving an actual cure in the form of a drug may be a long-term goal. Nonetheless, Hladik and Gornalusse believe that their research can still be used to provide more basic solutions, like counseling.
As their colleagues in the sciences reacted positively to the research, Hladik and Gornalusse are thinking of the next steps. Gornalusse has already submitted a grant for supplementary research to extend the model and improve the deficiencies in their first paper. Moreover, they plan to work toward directly developing cures in the form of drugs, this time in collaboration with bioengineers and other scientists.
Through research and corroboration among different scientists, Hladik and Gornalusse believe that an actual solution, whether that be a cure or treatment, may be underway.
“If you treat HIV effectively, you essentially interrupt the epidemic,” Hladik said.
Reach contributing writer Sheharbano Jafry at science@dailyuw.com. Twitter: @SheharbanoJafry
