Felipe Diaz-Griffero, PhD, studies the early events of HIV infection. A native of Chile, he earned a master’s in plant virology by pursuing a combined program between the Pontifical Catholic University of Chile and the Max Planck Institute of Molecular Physiology in Germany, followed by a PhD in retrovirology at Albert Einstein College of Medicine. He later completed postdoctoral fellowships at New York University’s School of Medicine and the Dana-Farber Cancer Institute at Harvard Medical School. Dr. Diaz-Griffero joined the Einstein faculty in 2010, where he is Professor of Microbiology & Immunology, the Elsie Wachtel Faculty Scholar and a member of the Einstein-Rockefeller-CUNY Center for AIDS Research. He now leads two National Institutes of Health-funded studies into cell proteins that keep viral replication in check.
When did you first become interested in HIV?
In high school, in the late 1990s. I was doing volunteer work in a hospital in La Paz, Bolivia, and heard about an HIV patient who was placed in quarantine because everyone was afraid, and nobody knew what to do. I asked the infectious disease specialist how I could help. He welcomed me into his lab and trained me how to do ELISAs [assays for detecting viruses and other substances in the blood].
Thanks to antiretroviral therapy (ART), most people with HIV have near-normal lifespans. What else is needed in terms of treatment?
The problem is that ART can have many side effects, from fatigue to cognitive issues to liver damage. Not surprisingly, many patients don’t comply with treatment—with disastrous consequences. ART suppresses viral replication, but since the virus integrates into the genome of host cells, it never goes away. If you stop taking the drugs, the infection comes roaring back and you risk infecting others. Another issue with ART is that some HIV strains are developing resistance to one or more components of the ART drug cocktail. So while we’ve made great progress in treating HIV, it’s not enough.
Is the only solution a therapy that eliminates HIV altogether from our cells?
Or at least a therapy that allows people to live with HIV symptom-free—a so-called functional cure. Perhaps we can learn from our fellow primates, like African green monkeys, who have found a way to coexist with viruses similar to HIV. The virus in infected green monkeys does not get out of control, and they don’t develop symptoms.
Is there any benefit to coexisting with retroviruses?
In evolutionary terms, yes. Retroviruses drive primate evolution by introducing regulatory sequences into the genome, some of which can be beneficial. For the most part, primates have learned how to control these pathogens rather than eliminate them. One way cells control retroviruses is with host-cell proteins called restriction factors, which I started studying as a postdoc. When HIV or other viruses infect cells, restriction factors are the cells’ first line of defense against viral replication. Unfortunately, in the case of HIV, our restriction factors aren’t very good at keeping the virus in check. Most ARTs developed so far do not target this early part of the HIV life cycle.