For the first time in history, an American scientific team has succeeded in eliminating the AIDS virus from the genome of living animals.
And it is that since we have seen the growing AIDS epidemic pass through the world, scientists have focused their efforts on solving the problem of eliminating all traces of the human immunodeficiency virus (HIV) from a human body. Now, a method that combines treatment with advanced antiretrovirals and gene editing seems to show us the way to follow because in the latest study with rodents, scientists were able to eliminate HIV in five of the 13 transgenic mice in the experiment .
The HIV virus is a true master of disguise, transforming its appearance as it proliferates within the human body. Even if all else fails, the virus can hide its genetic blueprint within our own DNA, ready to emerge when a person’s immune system is compromised.
Thanks to its negative qualities, the best we can do is attack with an arsenal of pharmaceuticals designed to keep the deadly pathogen buried, preventing it from emerging and devastating the body’s immune system. Stopping antiretroviral drugs for a few weeks leads to the risk of a resurgence of infectious virus particles. But, so far, it is what we had.
Hope
Researchers at the University of Nebraska Medical Center and Temple University (USA) have shown that CRISPR-Cas9 gene editing technology is theoretically capable of finding those buried virus genes and destroying them in mice engineered to have human biochemistry.
But the CRISPR technique could not alone. The team had to pair it with long-acting, slow-release antiretroviral therapy so that genetic surgery would have the time to hunt down the viral genes and destroy them.
If we could apply the same approach to people, it would mean the possibility of abandoning daily retroviral medication and the variety of uncomfortable side effects that are associated with it. Given that nearly 40 million people around the world are currently living with the virus, such a cure would be a shocking advance in our society.
Unfortunately, CRISPR gene editing is still in an early stage as a medical technology , and we still don’t have a good idea of how much damage it can cause within a human body. However, compared to previous methods of selecting genetic sequences for deletion or dissection, CRISPR can be easily programmed to achieve an unprecedented level of precision.
This makes it an attractive tool for any researcher wishing to perform microsurgery at the molecular level. But the technology has landed with great controversies.
Even if we ask questions about the ethics of using it – or not – to change our own genes, there is concern that the CRISPR hardware is not as clean as expected, which could lead to changes that could increase the risk of cancer.
In context, any therapy based on such problematic technology becomes a question of risk versus probability of success.
It generally takes only a few days for HIV to reappear in untreated transgenic mice. But eight weeks after no treatment, there was no trace of the virus genes in 5 of the 13 infected subjects, implying a drug-free future for at least a lucky few.
It goes without saying that even mice designed to mimic our bodies are no substitute for real humans . Ongoing trials in primates could go a bit further by showing how much hope we should have for CRISPR as a way forward in HIV treatment.
Will we test this technique on humans?
The US Food and Drug Administration has in the past rejected a request from a biotech company to advance research on the treatment of sickle cell anemia based on CRISPR.
But we are on the way. Last December, another company received the green light to use the CRISPR method in a test to cure childhood blindness.
As it is, the final step towards a cure would be something to celebrate, and a lot, but for now, we must be cautious with the results and time will tell if it is the long-awaited AIDS cure.
Referencia: Sequential LASER ART and CRISPR Treatments Eliminate HIV-1 in a Subset of Infected Humanized Mice, Nature Communications (2019). DOI: 10.1038/s41467-019-10366-y , https://nature.com/articles/s41467-019-10366-y
