In just the last few years, the boundaries of genetic research have been expanded due to a set of tools referred to as CRISPR.
CRISPR gene editing uses a process modeled after the system bacteria uses as a defense against viruses which remembers them when it encounters them in the future.
Researchers say one of them, CRISPR-Cas9, is faster, more accurate, affordable and efficient than other common genome methods, and there’s plenty of potential to help all sorts of medical conditions.
One of the latest might be HIV.
A team from Northwestern University recently announced that they were able to identify a section of the virus that has a vital role in how it infects human blood cells and replicates itself.
This exploration can potentially lead to more discoveries about the virus operates and perhaps eventually lead to a cure.
Although there was strong attention to combatting HIV/AIDS in the 1980s and 1990s, public perception has shifted as well as funding toward other medical conditions. Plus, combinations of medications and similar therapeutics allow people with HIV to live normal lives with lower risk of moving into the fatal AIDS infection. The most common is ART, or a cocktail of anti-retroviral medication.
Still, more than 37.1 million people worldwide with HIV as of 2020, according to HIV.gov. Of these, 1.7 million are children 14 and under, and 36 million are adults. The organization also reports that 1.5 million globally were infected in 2020, which is an encouraging 31 percent decline since 2010.
The Northwestern research team was able to identify more than 80 separate genes that are involved in the process of how HIV infects cells and continues to grow and spread.
The study was headed by Dr. Judd Holquist, who as lead researcher, felt that attention to research, especially related to CRISPR gene editing, may be able to lead to better, more permanent solutions to help people rather than having them take antiretroviral medications indefinitely without a cure.
It was published recently in Nature Communications, an open-access journal, as “A functional map of HIV-host interactions in primary human T cells.”
Dr. Holquist and the research team looked at 426 genes known to be involved in HIV. Using CRISPR gene editing, the research looked closer at 364 and found 86 candidate hosts factors that could alter HIV infection. About 40 of the factors weren’t previously known to play a functional role in replication of HIV cells.
“The first step identified which genes are important, and the next step identifies why these are important,” he said.
Part of the reason that these type of research efforts continue toward a cure is due to equity issues. While wealthier people with HIV in developed countries, such as the U.S., can afford the medication, those who can’t pay for it have a greater risk of complications as well as spreading the virus.
Holquist said he’s excited to continue the research but said that his team isn’t interested in creating gene editing therapeutics.
What he would like to see, however, is more potential collaboration between other researchers especially as these genes are explored, especially the ones that are involved in infection and replication. But this can help open more doors.
“We’re looking at decades of research just to understand one individual gene, and this research identified many of them,” he said.
