Presenter
Amy Proal
Dr. Proal is a microbiologist and President/Chief Scientific Officer of PolyBio Research Foundation - a non-profit studying how viral, bacterial, and fungal infections contribute to chronic diseases and aging processes. She directs PolyBio's LongCovid Research Consortium: an international scientific collaboration to rapidly and openly study LongCovid, with a focus on the persistence of the SARS-CoV-2 virus in tissue. She also serves as Scientific Director of Mount Sinai's CoRE clinic, where she oversees the development of research studies and clinical trials aimed at controlling persistent infection, inflammaging, and metabolic dysfunction.
Abstract:
This talk will explain how common viruses accumulated by humans over the course of a lifetime (the human virome) contribute to diseases of aging and inflammaging. These viruses, which include the herpesviruses, have evolved a wide range of mechanisms to directly hijack the activity of the human genome and human metabolism. They also modulate the immune response to drive aging processes. For example, the amyloid beta “plaque” that accumulates in the Alzheimer’s brain is now being studied as an immune peptide that forms in response to viral pathogens in brain tissue.
Indeed, proteins encoded by persistent viruses have been shown to distort human longevity signaling networks. For example, one analysis uncovered dozens of viruses encoding proteins experimentally demonstrated to interact with proteins from pathways associated with human aging, including cellular senescence. Viral infection can also have profound effects on host cell processes relevant to telomere biology and genome maintenance, with human herpesvirus 6 (HHV-6) capable of driving telomere dysfunction by directly integrating into host telomeric DNA.
Human virome-driven contributions to diseases of aging and general aging processes have been impacted by the COVID-19 pandemic. I lead the PolyBio LongCovid Research Consortium. We are increasingly studying the SARS-CoV-2 virus as capable of long-term persistence in a wide range of human body and brain sites. We may consequently be seeding the human population with yet one more virus that can drive human genome, metabolic, and senescence-related dysfunction under certain conditions.
