Finding Genius Podcast

Podcast Categories: Viruses

  • Virus as Puppet Master: Phage Communication with Charles Bernard

    Virus as Puppet Master: Phage Communication with Charles Bernard

    Curious about one of the newest discoveries in the nature of viruses? This discussion explores an exciting find in virus behavior and their ability to communicate: quorum sensing by bacteriophages.

    Listen and learn

    • What a team in Israel discovered in 2017 about viral communication that set the groundwork for Charles Bernard’s research, 
    • How the importance of virus and host balance dictates virus survival and therefore initiates this communication regarding density, and
    • What therapeutic applications might develop from viruses using quorum sensing to control bacteria life cycles. 

    Charles Bernard is a PhD student at Sorbonne Université in Paris, working on microbiome communication. He says that quorum sensing means the “minimal number of bacteria or viruses to be present for a collective behavior to be efficient and therefore triggered.” But what is viral communication? An important discovery was made in Israel in 2017 when a lab found that a temperate bacteriophage communicates by taking over the cellular machinery of their host bacteria.

    It signals to other viral particles in a way that determines the host-to-bacteriophage density. In other words, the virus must decide whether to replicate quickly via a lytic cycle or slow down and keep its host alive through a lysogenic cycle, which protects the host. That decision is determined by the ratio of bacteria to bacteriophage: the more bacteria, the better the lytic tradeoff works. The less bacteria, the more host the virus needs to preserve to be able to survive.

    The genome of the bacteriophage contains genes that produce a signal and a receptor. They use this back-and-forth from within the bacteria to discover the ratio. In other words, they’re assessing their odds to determine which replication cycle they should enter. Charles has continued looking at other bacteriophage communications and has been the first to find a bacteriophage with two different communication signals. These findings can translate to therapies by using bacteriophages to control bacteria.

    For example, if phages can signal in such a way to prevent bacteria from producing spores, scientists could control certain bacterial infection rates.  As Charles says, “who gets to decide when it is time to sporulate? We used to think it was the bacteria, but, in fact, maybe it is the phages manipulating its host’s biology . . . like a puppet master. ”

    For more, see his lab’s website: Team AIRE.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • HIV Clarified: Viral Pathogenesis Steps with Researcher Guido Van Marle

    HIV Clarified: Viral Pathogenesis Steps with Researcher Guido Van Marle

    HIV’s effect on the gut immune cells appears significant. This implies that gut-associated lymphoid tissue (GALT) stands as a possible viral replication reservoir. Virologist Guido Van Marle is researching how and why this happens and how gut infection affects systemic infection.

    Listen in as he and Richard explore every step of HIV infection.

    They discuss

    • What the difference between the acute and dormant stage is and why it’s termed dormant rather than latent,
    • Why some infected individuals are long-term non progressors and others develop AIDS, and
    • What happens when the virus attacks the gut-associated lymphoid tissue and why this is significant.

    Guido Van Marle is an associate professor in the Department of Microbiology, Immunology, and Infectious Diseases at the University of Calgary.

    He focuses on viruses, specifically molecular virology techniques of West Nile Virus and the HIV-1 life cycle. He offers listeners numerous molecular mechanism examples of HIV.

    He takes special care to designate the different stages of viral infection, explaining how in the early stage, called the acute or primary infection phase, the virus replicates and destroys some of the immune system cells. When it moves into the dormant stage, this activity dies down and the immune system is able to rebound.

    Significantly, the gut immune cells don’t rebound the way other systems do.

    In fact, his research has found that there is high load of infection going on in these gastrointestinal tract cells in that early acute phase post-HIV transmission, which means the area experiences a lot of cell death and inflammation: this allows pathogens to enter the tract and exit into the blood stream.

    He explains the molecular mechanisms of biology that lead to leaky gut in this process. Furthermore, when doctors deliver antiviral therapy, and the patient’s immune cells increase in number, they don’t increase as much in the gut. He has focused on this area of infection for his research with the hopes of understanding disease progression as a whole.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • Fighting Perinatal Infection with Phage Therapy

    Fighting Perinatal Infection with Phage Therapy

    This podcast explores how one researcher is working to keep babies safer without turning to antibiotics. Group B Streptococcus (GBS) presence in the mother is a leading cause of neonatal morbidity and mortality. Doctors often treat mothers with antibiotics to curb the infection, which presents its own complications. Richard interviews a microbiologist working on alternatives.

    Listen and learn

    • How GBS transmission happens and what screening processed is used,
    • What different strains of GBS exist and are they equally infectious, and
    • How phage therapy may be the best solution to decrease infection rates while leaving the microbiome of the baby balanced and healthy.

    In this episode, Richard speaks with a researcher specializing in perinatal microbiology and infections of the perinatal period. She examines how these infections can modify the outcome for mothers and babies. By looking at the epidemiology and how GBS strains change regarding capsule type and other factors in different regions, she hopes to learn more about the bacteria to utilize a bacteriophage for infecting the bacteria.

    What’s a bacteriophage versus a virus? One way to understand the difference is to consider the host: bacteriophages are viruses that infect bacteria. The bacteriophage life cycle is intertwined with the host bacteria, and many researchers are looking at bacteriophages in the human body as a treatment alternative to antibiotics.

    Because antibiotics are used to treat bacterial versus viral infections and can kill beneficial organisms inhabiting the baby, phage therapy may benefit babies in multiple ways. GBS transmission occurs during the vaginal birth process if the mother has the bacteria. While some babies can remain healthy despite this, others are infected with harmful results including death.

    Therefore, widespread screening is in place, testing the mother.

    Generally a mother is given antibiotics a few hour before labor.

    This microbiologist is researching candidate phages for therapy and also trying to understand more about natural exposure to phages during pregnancy. Listen in for more about this dynamic and potentially life-saving work.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • The Elusive HIV Reservoir with Researcher Matt Gartner

    The Elusive HIV Reservoir with Researcher Matt Gartner

    In addition to HIV prevention, one of the biggest topics for HIV research is finding a cure. While antivirals are able to control and suppress the virus, it’s still able to keep its foothold in infected subjects. This podcast talks to one researcher who’s helped scientists understand that persistence.

    Listen and learn

    • How HIV infection manifests as productive and latent infections,
    • What his study showed about the lack of viral evolution and means of proliferation, and
    • What stands as one of the more promising potentials for a cure, namely the “shock and kill” approach.

    Matt Gartner is a research officer with Subbarao Group, researching common infectious diseases. His PhD work focused on infectious diseases microbiology, most specifically HIV. Like many infectious viruses, after the transmission of HIV, the virus usually undergoes a latent period.

    However, the latent period has a couple of mysterious characteristics.  Dr. Gartner studied the ability of HIV to establish a strong latent reservoir, which allows the virus to persist in people even if they’re on antivirals. He explored two questions in his work: how does HIV establish this reservoir and how is this reservoir being maintained even under antiviral retro therapy.

    His research found very little signs of virus evolution, suggesting the antiviral drugs are good at blocking replication. But they found a large percentage of sequences in the patient that were identical, which has important implications: this points to a proliferation of immune cells copying the same strain.

    Dr. Gartner thinks that a patient’s immune response helps the reservoir expand when it responds and replicates to attack a specific pathogen. As it replicates, it produces clones of the HIV retrovirus. While this means “any particular cure strategy will be very difficult to carry out,” he discusses one that has potential called the “shock and kill” strategy. Listen in for more about this theory and other details on HIV infection mechanisms.

    For more about his work, he suggests searching PubMed and ResearchGate.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • Viral Translation Strategies: Aurelie Rakotondrafara Talks Plant Viral Infections

    Viral Translation Strategies: Aurelie Rakotondrafara Talks Plant Viral Infections

    It’s all in the translation, especially for plant viruses. This podcast takes an interesting look at virus expressions in plants and their ability to coopt cellular machinery for their own purposes.

    Listen and learn

    • The basics methods a virus uses to infect a plant cell, including insect-vector mechanics,
    • The challenges a virus faces inside the cell to use the ribosomal translation factors, and
    • The ways this knowledge may be used to speed production of vaccines. 

    Aurelie Rakotondrafara is an associate professor of biology at the University of Wisconsin in Madison. She brings an infectious awe to all things viral as she discusses the ways plant viruses work in this episode, from viral gene transfer to viral resistance in plants. Her particular focus is on viral gene expression—how viruses manage to outcompete other cell molecules to make proteins.

    The primary goal for any virus, whether animal or plant, is to enter their obligate host cell and replicate. But plant cells have an impenetrable cell wall; unlike with animal viruses, there’s no endocytosis or similar entry method. They often use a vector to put them inside the cell—the majority of plant viruses are transmitted by insects, who are able to penetrate the cell wall and secrete the virus.

    Aurelie Rakotondrafara’s research focuses on what the viruses do once they are inside that cell as they work to coopt the cell’s ribosomes. The plant uses ribosomes to make their own proteins and the virus needs to work a complex strategy to trick the ribosomes into making their proteins instead. The majority of plant viruses are RNA viruses, and they are competing with a million of the plant’s mRNA that are already floating in the cytoplasm.

    Dr. Rakotondrafara studies the unique strategies that the viruses use to do this. She discusses some of these tricky strategies and mentions one particular wheat virus she studies in detail. That virus has such a tremendous ability to translate that researchers may see if it can be used to speed the production of vaccines.

    For more about her work, see her lab’s web page: rakotondrafaralab.russell.wisc.edu.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • The Mosaic of Life: Virus-Host Cell Interaction and Evolution with James A. Shapiro

    The Mosaic of Life: Virus-Host Cell Interaction and Evolution with James A. Shapiro

    A winner of an episode, this is the last in a series of interviews for Richard’s upcoming Understanding Viruses book. Professor James A. Shapiro treats listeners to his thoughts on virus behaviors and characteristics gleaned from researching virus-host relationships and virus-cell interactions.

    Listen and learn

    • How virus evolution over time is really a story of the weaving of life systems pulling from all directions,
    • What are surprising characteristics of viruses such as primordial vector activity, how frequently viruses lend advantages to their hosts, and other significant virus evolution impact factors, and
    • How to consider if viruses are living or nonliving and why Professor Shapiro pushes for a more non reductionist view on the origin and evolution of viruses .

    James Shapiro is a professor in the Department of Biochemistry and Molecular Biology at the University of Chicago. In addition to numerous publications, he’s a part of the website The Third Way of Evolution, which considers evolution in the era of genomics and epigenomics.

    As Richard holds this final interview to investigate how viruses persist, James Shapiro offers his own fascinating answers to questions such as are viruses alive, do they participate in quorum-sensing, and why so many differing incubation periods. For example, not only are endogenous retroviruses responsible for mammal placenta formation, these retroviral proteins are unique for each order of mammal.

    This diverges from the classic view of evolution that starts with a characteristic branching out into other organisms. It’s as if “the placenta was invented over and over again,” he adds.

    As he addresses the huge variety in viral behavior, he says that many factors determine this variety—viruses can recombine with each other, for example, and produce recombinant viruses. The holobiont model exemplifies this: a large organism like a human isn’t just human cells but also microbial cells living on and in us.

    We can think of viruses in our genome as holobiont elements: we should take a systemic view of entity development, with mosaics and amalgams determining multiple aspects of life.

    He adds, “we can’t reduce what happens in life to some simple formula that is good for every from of life, because variety is an inherent aspect of the living world.” Listen in for more rich conversation about the stuff of life. 

    For more about James A. Shapiro, see his website: shapiro.bsd.uchicago.edu.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • Insidious HIV: Dr. Masci Shares Story of AIDS through the Decades

    Insidious HIV: Dr. Masci Shares Story of AIDS through the Decades

    Joseph R. Masci began his time at Mt. Sinai when doctors were first confronted with HIV patients who had developed AIDs. He brings his intimate knowledge of this treatment and its evolving history to listeners in this episode.

    Listeners will learn

    • What doctors met at the bedside of an AIDS patient in terms of opportunistic infections and how the medical community became a second family to those suffering,
    • How this retrovirus works through reverse transcriptase and a decades-long latency period, and
    • How treatments and HIV prevention evolved into today’s effective combination on an infectious disease microbiology level.

    Joseph R Masci is a clinical professor in the Infectious Diseases, Environmental Medicine and Public Health, and Global Health divisions at Mount Sinai. He started his training at Mount Sinai in 1980 when experts in infectious diseases were first confronted with a rapidly expanding population of AIDs patients.

    Imagine facing large numbers of HIV patients with no antiretroviral drugs available and no effective treatment for at least 10 years down the road.

    He and his colleagues offered emotional support in addition to soothing the opportunistic infections that the virus enabled. They created a special area, a “living room” in their hospital for these patients who were isolated from their families and became their second families. They put on concerts and memorial services for them. He says that the epidemic was “sudden, tragic and not treatable like today.

    “

    Because Dr. Masci was in it for the long haul, he’s able to explain to listeners each stage of advancing treatment and an eventual measure for preventing the transmission of HIV. Along the way he explains the mechanics of infectious viruses, how HIV has especially insidious traits through its ability to become part of infected person’s DNA and its long latency period. As with other common infectious diseases like Epstein Barr, once a person has it, they can’t get rid of it.

    He talks listeners through treatments like AZT, nucleosides, and the effective protease inhibitor drugs. He makes the vital point that much of the world doesn’t have access to these very effective drugs and that many still die from AIDs in low income countries. He then is able to take the basics he’s established through the podcast and establish some comparisons with COVID-19 and its treatment.

    Listen in for some of the most important medical history of our time. 

    For more about his work, find his publications in PubMed and ResearchGate.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • Computing COVID: Computational Biology Research with Oak Ridge National Laboratory’s Dan Jacobson

    Computing COVID: Computational Biology Research with Oak Ridge National Laboratory’s Dan Jacobson

    Working on COVID-19? This podcast is for you. This episode offers a valuable conversation with a comprehensive yet detailed understanding of SARS CoV-2 pathogenicity.

    Listen in as a front-line researcher discusses the computational biology of COVID-19 from three directions: the viral action, the human response, and environmental influences on both.

    Listen and hear

    • The viral biology of pathways this particular coronavirus inhibits and disrupts, such as the RAS and Kallikrein systems,
    • How this disruption leads to bradykinin storms and hydrogel formation in the lungs, which impede oxygen exchange and cause organ distress, and
    • What therapeutics directly address these disruptions and other patterns they are hopeful this computational and systems biology will reveal.

    Daniel A. Jacobson is a computational systems biologist at Oak Ridge National Laboratory. Oak Ridge is part of the national laboratory system in the U.S., and has access to world-wide data and top researchers. His lab is tracking all the SARS CoV-2 sequence data from around the world and finding significant patterns that may impact pathogenicity and looking at evolutionary patterns that may give insights. He shares an invaluable level and type of information with listeners in this conversation, explaining exactly how COVID-19 infects cells and what pathways it disrupts.

    For example, he explains how after looking at the “dynamic tension” points in normal systemic pathways, they were able to identify how this virus disrupts specific aspects of the RAS pathway, kallikrein system, and vitamin D reception in infected patients.

    The resulting bradykinin storm and increased hyaluronic acid leads to the symptoms doctors find so difficult to overcome such as hydrogel in the lungs.

    But there’s good news too: they’ve identified a number of pharmaceuticals that can help in these metabolic pathways, even down to vitamin D regulation. Currently, researchers have identified three different drugs that do what the lab’s mechanistic models predicted and help patients suffering from the virus. He adds that they are expanding their list, hoping to identify a larger battery of drugs that will also help.

    He says there’s a significant push to join forces with clinical colleagues and explore multiple common therapies. He also discusses the mutation patterns.

    They are identifying how the virus changes over the course of the pandemic and trying to infer how those changes will impact pathogenicity. Then they can observe how those changes are promulgating in the human population.

    Finally, they are also plugging in environmental components.

    Find their papers in eLife, Molecular Biology and Evolution, and bioRxiv and google them for more.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • A Viral Arms Race in the Body: Past, Current, and Future Coronaviruses

    A Viral Arms Race in the Body: Past, Current, and Future Coronaviruses

    As the cell employs its machinery to shut down the virus that’s inside it, the virus makes proteins to shut down the cell’s efforts. The scene is set, but how will this arms race end? The answer depends on many, many factors.

    Listeners can tune in to explore the following:

    • How to study the way in which obesity, diabetes, and host immunosuppressive states alter the trajectory of viral disease like that caused by SARS-CoV-2
    • Whether it’s possible to create drugs that can combat viruses that don’t yet exist
    • How SARS-CoV-2 enters cells, with a play-by-play look at what exactly is does prior, during, and after entry
    • What evidence suggests that SARS-CoV-2 had been replicating in humans for a while—potentially months—before anyone knew about it

    Since 2004, Matthew Frieman, PhD has been researching coronaviruses. In 2009, he established his own research lab at the University of Maryland School of Medicine, where he is an associate professor in the area of microbiology and immunology. First it was SARS-CoV, then MERS-CoV, and now SARS-CoV-2, the virus causing COVID-19. With each new coronavirus, he learns a little bit more about the tricks they use to enter and infect cells. He also learns more and more about therapeutics which could potentially combat the current virus and viruses to come.

    A focal point of the research in Frieman’s lab is on the role of comorbidity in disease progression, and how an understanding of this in lab mice might be reflected in humans. For instance, why do those with underlying conditions appear significantly more vulnerable to SARS-CoV-2, and more likely to suffer severe symptoms? His research is also focused on developing a broadly antiviral drug not only for SARS-CoV-2, but for viruses that emerge in the future.

    The conversation covers the similarities and differences between SARS-CoV-1 and SARS-CoV-2, two primary entry methods of SARS-CoV-2, the role of the ACE2 receptor and TMPRSS2 protease, why more virions per cell means fewer ACE2 receptors, which means decreased capacity for lung tissue repair, how cells detect the presence of a virus and respond accordingly,  characteristics of viral spread, structure, and function, virus-host interactions, research aimed at combining antibodies to create a dual antiviral effect against SARS-CoV-2, and so much more.

    Visit https://www.medschool.umaryland.edu/profiles/Frieman-Matthew/ and follow Frieman on Twitter @MattFrieman.

    Available on Apple Podcasts: apple.co/2Os0myK

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  • Viruses in Every Step of Life: Virus-Host Cell Interaction with Shervin Takyar

    Viruses in Every Step of Life: Virus-Host Cell Interaction with Shervin Takyar

    Another in the Finding Genius Podcast series on viruses, this captivating conversation with Yale University’s Dr. Takyar explores interesting avenues of the virus-host relationship, offering listeners a glimpse into a top researcher’s understandings of viral characteristics and behavior.

    Listeners will hear

    • How his answer to the inevitable question, “are viruses living” provides a new spin,
    • Why a recent study shows that viruses do message each other as translated through cellular machinery, and
    • What his own research may show regarding a virus’s ability to affect surrounding cells in such a way to increase the potential for tumor growth by creating a niche.

    Seyedtaghi “Shervin” Takyar, MD, PhD, is a Yale Medicine pulmonologist and an associate professor of Pulmonary, Critical Care, and Sleep Medicine. His work on disease research his given him an interesting perspective on virus-cell interaction and Richard brings him into this continuing look at viral behaviors. They begin by addressing if viruses are living or nonliving and this gives Dr. Takyar a chance to provide a rich answer in which he says, on the one hand, they are akin to a program in a computer if a computer were consider “life.”

    On the other hand, he adds, nature doesn’t have rigid lines, and he would say viruses are at the very least a footprint of life. He explains each of these analogies in more depth and ends his answer with, “it is more interesting to find their place in life,” rather than label them as one or the other. The rest of the podcast examines this place.

    The origin and evolution of viruses follows the pattern of life: virus evolution over time just means they’ve found those places that fit best. He explains various behavior with similar language. For example, a virus incubation period depends on their environment.

    They may not express parts of their genome until the right time comes. The right time inside the cell is dictated by a lot of actors—like aging, for example—the increased mortality in older folks with SARS CoV-2 is because those states are codes for the virus: certain parts of the process that it needs to grow are available and this triggers replication.

    He shares a brand new behavior confirmed by researchers next, that viruses use the factory inside cells to talk to each other.

    Scientists have shown that bacteriophages use the translation machinery inside the bacteria to translate their message to other viral particles.

    Dr. Takyar shares more of his thoughts with listeners on topics from quasi-species to speculations on viral epigenetics.

    For more about Dr. Takyar and his research, start with his lab website: medicine.yale.edu/lab/takyar.

    Available on Apple Podcasts: apple.co/2Os0myK

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