Finding Genius Podcast

Lili Wang, Ph.D., has worked with viruses for 14 years and her latest focus is HIV. She's studying the amazing mechanics of the virological synapses of HIV, which allow the virus to transfer from infected to uninfected cell. But for this podcast, her job is to help Richard with his virus project, providing in-depth, enlightening answers to his questions. She discusses The evolution and coevolution of infectious diseases, The different entry mechanism of common infectious diseases and why such variety evolved, and The role viruses have played in our evolution and how she thinks they have molded what we are. Lili Wang, Ph.D. is a scientific researcher and instructor in the Department of Medicine at the Icahn School of Medicine at Mount Sinai. A member of the Benjamin Chen Laboratory, she's made solid progress in HIV research and continues her work in infectious disease microbiology. In this discussion, her virology background helps Richard grapple with his research questions with precise details of viral mechanics. She describes the coordinated manner with which viral cascades may work after cell entry and describes how evolution has continually refined these processes. She provides substantive explanations for the trigger systems and how receptors work for these different forms of entry viruses take. Especially interesting is her description of the "not deliberate, but still not random" nature of viral actions, a key moment in this interview and why researchers grapple with how to categorize viruses in the alive/not alive debate. She adds information about how viruses might use sensing mechanisms and then pivots to more categories, comparing the actions and coevolution of bacteria and viruses and how plasmids and extracellular vesicles fit in this picture of microorganisms. Finally, she gives an overview of the tight combined forces of our own microbiomes and viruses, bacteria, and phages, how the balance of these organisms keep us healthy and can be considered part of our very life: if they are disturbed or out of balance, we become ill. Listen in for more about how viruses work to make us who we are. For more information about her work, see her lab page and search for her in research aggregate sites. Available on Apple Podcasts: apple.co/2Os0myK

How do viruses hijack your body's cells? Why do they cause infectious disease in some people and not others, and what can they teach us about human biology? The COVID-19 situation is unprecedented, but the research questions it's triggered aren't the first of their kind. Tune in to discover: Why viral mechanisms that appear sophisticated might be simpler than you think, and how they are surprisingly error-prone How to understand the relationship between viral infection mechanisms and mechanisms of viral spread How genetic information and knowledge is passed to and from viruses With over 25 years' worth of research experience on the molecular biology of influenza viruses, Adolfo Garcia-Sastre is both a professor in the Department of Microbiology and Director of the Global Health and Emerging Pathogens Institute of Icahn School of Medicine at Mount Sinai. For Garcia-Sastre, studying viruses is a way of simplifying the study of more complex organisms, including humans. "Most people think that…viruses are smart, and that they come with very smart mechanisms…I am one of the few scientists that believe the opposite; I think that viruses are extremely dumb…they are just what they are because that's what they've evolved to," he says. He continues by explaining why he's developed this uncommon understanding of viruses, hitting on a number of compelling topics along the way, including viral latency, virus virulence and the balance between infecting a host and keeping it alive, the transfer of genetic information in the evolution and adaptation of infectious viruses, and why he views the question, "Are viruses alive?" to be one of mere semantics. Available on Apple Podcasts: apple.co/2Os0myK

Biologist Jeremy Bar studies the tri-partite symbioses formed between the bacteriophage, the bacterial hosts (prokaryotes), and the eukaryotic human cells. The human microbiota interact in all types of interdependencies from beneficial to harmful to somewhere in between. Dr. Barr offers a lively telling of what we've learned about bacteria and viruses as they make their way in the human microbiome. He discusses Why one virus infection in your gut might start a domino effect among microbes, affecting multiple biological processes, How a recent discovery provides fascinating evidence of quorum sensing among viruses and an ability to coopt bacterial systems to assess the best time to lyse, and How phage will even package bacterial DNA or other molecular information through horizontal gene transfer induction. Jeremy Barr is the head of the Bacteriophage Biology Research Group and a lecturer at Monash University in Australia. This podcast continues the series of interviews with contributors to Richard's book on virus behaviors. Dr. Barr begins with describing the beginnings of his biology interest as a kid obsessed with insects. When he studied biology in university, bacteriophages seemed to him as the insects of the microbiology world and he was hooked. His unique insight and fascination with lifecycle of bacteriophage lends an entertaining perspective to their discussion, such as a description of his favorite virus, the T4, using its threads to tap on a cell to perhaps sense its fitness for infection. He also has been involved with numerous recent studies that speak directly to virus characteristics and will broaden listener's concept of what viruses are capable of. He discusses viruses ability to sense how dense the bacteria population is outside its host cell to maximize their reproductive success and know whether it is better to stay in the cell or lyse. He addresses whether he thinks viruses should be considered alive, adding that they are arguably the most successful life forms on the planet and work at the most basal level of life. But, he comments, the argument whether they are or not really doesn't matter. They are everywhere, he says, transporting genetic material through space and time. Listen in to this dynamic conversation to hear more key moments in the bacteriophage life cycle. Find out more about his work by visiting his lab website. Available on Apple Podcasts: apple.co/2Os0myK

Returning guest Shiraz Shah specializes in bioinformatics. He uses microbial data analysis to uncover the complex and fascinating relationships between viruses, bacteria, and chronic conditions like childhood asthma. This conversation serves as part of a series in preparation for Richard's upcoming book on viruses, and Shiraz Shah shares his unique and valuable perspective on viral structure and functions gleaned from years of cutting-edge analysis. Topics include How CRISPR research and techniques are derived from bacteria snipping and retaining parts of viruses that infected the bacteria, How human DNA is part of the evolution arms race between bacteria and viruses, and How the presence of a type of prophage in a person's gut can make the difference in immune therapy cancer treatment and what this implies about the complex influence of viruses. Shiraz Shah is a senior researcher at the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC). Much of his graduate work focused on CRISPR-Cas9 bioinformatics. His current work involves analysis of data regarding bacteria hosts and viruses in the gut microbiome in particular. He explains how this analysis works at the level of genomics; for example, a virome sequencing might be compared to numerous other protein sequences in a search for significant patterns. COPSAC plans to take this collection of virus and bacteria data and follow the cohort of children for any corresponding organisms that might indicate causes or preventions of childhood asthma. This opens up into an enlightening conversation about the complex role of phages, which are viruses that use bacteria as their host cell. Viruses are everywhere, Dr. Shah asserts, and he believes our old view that viruses are predominantly dangerous, mostly causing sickness, is outdated. Most of us and the kids COPSAC studies are full of viruses without any sickness. So, what are those viruses up to? Replicating. And that effort makes for a sometimes commensal or mutualistic host relationship. Dr. Shah explains that scientists see a lot of prophages that are maintained over several generations and kept by bacteria because they help the host bacteria. He and Richard bring up examples involving cancer and cholera, where a phage's presence changes the bacterial response in a human body in numerous ways, sometimes beneficial or commensal, and sometimes towards more virulent behaviors. Dr. Shah and Richard also debate the level of intent, signaling, and quorum-sensing abilities of viruses. Near the end of their conversation, Dr. Shah explains that his present work, called viromics, may have as a significant impact as metagenomics. In a few years, scientists may therefore have a completely different and exciting view of viruses. Listen in for an expert's view of this new type of foundational research. For more about Shiraz Shah, see his page at COPSAC: copsac.com/home/about/staff/shiraz-shah/. Available on Apple Podcasts: apple.co/2Os0myK

In this podcast, returning guest and computational biologist and author Eugene V. Koonin and Richard examine intriguing angles of virus behavior. Dr. Koonin is a contributor to Richard's upcoming book on viruses, and Richard sees him as a cornerstone of his own biological knowledge. An expert on the origin and evolution of life, Dr. Koonin graces listeners with fascinating ideas, such as Where viruses sit in the continuum of the evolution of life on earth in relation to ancient replicons and the first cells, What his definition of a virus is and how that collides with the categories of living/nonliving, and How he describes the "sensing" abilities of viruses and explains virus competition and identity. Eugene V. Koonin is a senior investigator at the National Center for Biotechnology Information (NCBI), the National Library of Medicine, and the National Institute of Health. He's the author of several books, including Logic of Chance: The Nature and Origin of Biological Evolution. One of a series where Richard interviews contributors to an upcoming book, this conversation explores Dr. Koonin's early days of studying virology and how far science has since come in understanding the machinations involved. It was, in fact, his first studies on virus genomes and trying to decipher those codes that lead him into his present focus on computational biology. Richard steers him towards several important questions on the nature of viruses and this gives Dr. Koonin opportunities to speak on some of their most surprising characteristics. He asserts that viruses are an intrinsic part of the biological realm and have their own evolutionary fate or trajectory; in other words, they experience their own selective factors that in turn shape their evolution. In this sense, he adds, they are substantially independent from their host; however, they are also completely dependent on their host for energy production. Therefore, they have same characteristics of life and yet are missing others. It is the tension in this mix of evolutionary force and obligate nature that makes them worthy of such discussions. Listen in to enjoy this intelligent entry into virus behaviors. For more about his work, search his name in science publication aggregates and see his website at NCBI: ncbi.nlm.nih.gov/research/groups/koonin/. Available on Apple Podcasts: apple.co/2Os0myK

Without glycogen, we couldn't go very far. Dr. Sullivan is a specialist in the glycogen molecule, which stores glucose, our energy source. In this podcast, he describes exciting discoveries and future research centered on glycogen presence that might help explain the connection between diabetes and kidney disease. Listen and hear answers to these questions and more: How does diabetes affect the kidneys? How do glycogen molecules differ in the liver of diabetic patients and why is that important? What does glycogen do to the kidney that might lead to diabetic kidney disease stages? Mitchell Sullivan is pursuing a postdoc at the University of Queensland in a group that investigates glycation, diabetes, and how diabetic bodily systems handle extra glucose. Dr. Sullivan in particular follows glycogen formation in the organs. He's just setting out on a new study connecting diabetes and kidney health by focusing on glycogen presence in the kidneys of diabetics. Normally, glycogen is in the liver and muscle tissue, waiting to supply us with different kinds of energy needs. But microscopy shows glycogen in the kidneys of diabetic patients that likely leads to damage and inflammation. The findings may lead to better therapeutics and prevention measures, from a more effective diabetes and kidney disease diet to medical interventions. Listeners will have the privilege of hearing straight from Dr. Mitchell the hypothesis for this study that's just begun. He explains with clarity why the structure of this glycogen in diabetic kidneys differs from its normal form and is significantly insoluble in this form. Furthermore, it sticks together in clumps of starch-like granules in the thick ascending limb of the nephron. He's investigating if these cells that aren't accustomated to glycogen become overwhelmed and the glycogen gets stuck, leading to damage and inflammation that make for one of the common kidney failure causes. What's most interesting is that his PhD work on glycogen in the liver and muscle tissue of diabetics makes this hypothesis seem more likely. Listen in to hear why that's the case and more about this study that might bring scientists that much closer to improving diabetes and kidney health. To find out more about Dr. Mitchell's work, search his name in research aggregates, see his information page with Queensland University, and feel free to email him: mitchell.sullivan@mater.uq.edu.au. Available on Apple Podcasts: apple.co/2Os0myK

Dr. Reid specializes in host pathogen interactions studies such as investigating the chikungunya virus infection and Ebola virus microbiology. A returning guest, he and Richard discuss all things virus in this episode as Dr. Reid will contribute to Richard's upcoming book on viruses. Their conversation covers Why it's significant that all life forms have associated viruses, including ancient bacteria discovered recently in glacial inlands that have phages (viruses that infect bacteria); What implications exciting virus discoveries may hold, such as the giant Mimivirus, which may prove an evolutionary bridge; and How we can investigate virus characteristics like means of entry and coopting of cellular machinery to better understand means of replication and evolutionary success as well as how cellular machinery works in the first place. St. Patrick Reid is an assistant professor in the Pathology and Microbiology Department in the University Of Nebraska Medical Center College Of Medicine. In a previous podcast, he and Richard discuss chikungunya diagnosis and pathology and Ebola virus symptoms and behavior. He begins this discussion explaining his journey into the field, which includes exciting postdoc work in France on Ebola. Now his researcher involves host pathogen interactions and he's particularly interested in different host proteins a virus has to recruit to replicate. The conversation takes a turn into exploring what scientists have assumed about viruses compared to recent discoveries that may take that knowledge in new directions. For example, he talks about ancient phage discoveries in glacial bacteria and phage-bacteria coevolution. He describes an interest in how viruses that infect bacteria allow those bacteria to live in a community of other bacterium. The viruses actually play a role in enabling those bacteria to survive. He discusses numerous other virus characteristics and implications, from DNA versus RNA viruses and what that dictates regarding habits like latency. He also addresses when that understanding changes with new discoveries, such as finding Ebola virus in chimps months after infection. They also talk a little virus philosophy and cover topics like what enables virus entry into cells and how tropism works. For more about Dr. Reid and his work, see his website at the university, unmc.edu/pathology/faculty/bios/reid.html, and follow him on Twitter as @StPatrickReid3. Available on Apple Podcasts: apple.co/2Os0myK

While Dr. Jospeh Masci could speak on numerous specific issues in the realm of infectious diseases microbiology, today's discussion centers on a general exploration of virus behaviors and characteristics. In this podcast, he addresses Why he centered his work on the study of common infectious diseases and those with special urgency such as HIV/AIDS and COVID-19; How varied virus behaviors are, from the speed at which they infect to their morphology and their means of infection; and How these behaviors indicate even more mystery about the history of virus origin, relationship to the evolution of bacteria, and intracellular-dependence. Joseph R. Masci is a clinical professor of Medicine, Infectious Diseases, Environmental Medicine and Public Health, and Global Health at Mount Sinai. His expertise includes HIV/AIDS diagnosis and treatment, general infectious diseases, tropical medicine, and emergency preparedness. He's currently coauthoring a book with Richard about viruses. He begins by describing how he was inspired by the infectious disease faculty in medical school and went on to work in the area, meeting the AIDS crisis and bioterrorism concerns post 9/11, and now is heavily focused on investigating COVID-19. The conversation turns into speculations about whether viruses should be considered alive and if that designation ultimately maters. This opens up a deep dive into virus behaviors. One particular characteristic that varies by virus and therefore effects infectious disease treatment is latency or the dormant stage. He discusses how such a period is quite common in many viruses, commenting that HIV can have long latency while cold viruses might hold dormancy for only a day or two. He connects this with how the virus takes hold in human cells and why this timing differs according to the virus mechanisms. They also discuss what factors dictate virulence and when passage from human to human increases or decreases the virulent attributes with specific examples. He adds that it's important to consider what the host contributes to the interaction as well as other organisms and compounds. The discussion also delves into virus origins, the nature of bacteria and virus coevolution, signaling between viruses, and the possibility of viruses working together with job-specific attributes. For more, see his NIH work and his website at Mount Sinai: mountsinai.org/profiles/joseph-r-masci. Available on Apple Podcasts: apple.co/2Os0myK

The COVID-19 situation isn't the first of its kind—not entirely, at least. For as many times as you've heard voices claiming it's triggered the "new normal," you should have also heard the voices of reason and evidence and logic, which assert that it's really more like an old normal, yet one that is causing unprecedented levels of damage to the underpinnings of society. Why haven't you heard these voices? Because they've been censored and suppressed by those who stand to gain by spreading fear and lies. Press play to learn the following: How big pharma has impacted the news media in profound and extremely consequential ways, and how this relates to the COVID-19 situation How the AIDS panic of the 1980s eerily parallels that of COVID-19, and which players have played a starring role in both Where the funding for scientific research on infectious diseases comes from, and how this influences who can conduct research (i.e. who has a voice in medical science) Ken McCarthy, a pioneer in the movement to commercialize the internet, an expert on internet advertising and marketing, and former student of neuroscience at Princeton University, presents an eye-opening look at COVID-19 in the context of global history. It's one you won't hear on the news, and for good reason, which McCarthy explains in depth. This explanation leads to so many others, such as how to develop and inseminate brilliant propaganda, what it takes to actually implement a war, what it means to put a human being on a ventilator, how to understand the Nuremberg Code in the current context of COVID-19, the truth about Bill Gates' record as a businessman, the surprising role in and influence on bioethics wielded by Christine Grady, Anthony Fauci's wife, the very real prospect of digital IDs as vaccine schedule verification, the important distinction between central and commercial banks, and more. Visit kenmccarthy.com for more information. Some Important Links to Explore: Fauci's First Fraud: https://www.youtube.com/watch?v=wy3frBacd2k&feature=emb_logo The New York Problem: https://www.youtube.com/watch?v=qXD1UR2dmZ0&feature=emb_title Ken McCarthy's top CoVid videos: https://www.brasscheck.com/video/the-covid-con-dismantled/ Ken McCarthy's top Brasscheck videos: https://www.brasscheck.com/video/the-hiv-aids-fraud-dismantled/ Available on Apple Podcasts: apple.co/2Os0myK

This is a unique show in the Finding Genius series. Podcast founder and host Richard Jacobs sites Perry Marshall's ideas as the impetus for starting the Finding Genius podcast. In this discussion listeners can learn more about why and hear about an upcoming symposium Marshall has helped construct on cancer and evolutionary biology. He explains What the basic ideas of his book Evolution 2.0 are, namely an argument for a new model for evolution that better fits organisms' active adaptations; How cancer is evolution gone wild and why better cancer treatment necessitates adopting this new conception of evolution; and Which topics and speakers will appear in the Cancer and Evolution Symposium and a preview of several exciting findings they will present. Perry Marshall is an author and highly influential business consultant with an electrical engineering background. In this discussion, he connects the foundational ideas in Evolution 2.0 with cutting-edge cancer science. Marshall lost his father to cancer at age 17 and has followed theories behind its treatment ever since. He reminds listeners that common cancer therapy treatment only works routinely with early stage cancer. Alternatively, he says that when cancer reaches stages 3 and 4, survival chances are not that much better than they were in 1930. Therefore, there must be a lag in how we are addressing serious cancer diagnoses. This lag is connected with a traditional view of passive evolutionary theory rather than theories like that of Professor Henry Heng, who claims evolution is actively engineered by organisms themselves; in addition, they are able to pass those engineered traits to their offspring. Henry Heng is one of the speakers at the upcoming Cancer and Evolution Symposium along with Columbia University Medical Center's Azra Raza and evolutionary theorist James Shapiro from the University of Chicago. Dr. Heng connects this theory of evolution and cancer, noting that treatments like chemo destroy about 98% of the cancer cells while the few remaining develop massive wholesale restructuring of their DNA and are then more equipped to spread and survive. Importantly, this restructuring is active rather than a random accident of mutations. Marshall explains these ideas in more detail and discusses other topics covered by the speakers. He describes the symposium as a world-class collection of cancer and evolutionary theorists coming together to address cancer evolution and disable the cancer treatment lag. The symposium will work via Zoom and takes place October 14th through 16th. To sign up and learn more, see the symposium website: cancerevolution.org. Available on Apple Podcasts: apple.co/2Os0myK