Podcast Categories: Viruses

  • Shining a Light on COVID-19 Virus Detection

    Shining a Light on COVID-19 Virus Detection

    Out with the old, in with the new COVID-19 virus detection method? A faster, more cost-effective, and more sensitive test may soon replace the status quo. Press play to discover:

    • How to deactivate the covid-19 virus without destroying the outer spike proteins, and how to test whether it’s truly been deactivated
    • How this novel detection method discriminates between specific viruses and other particles in the body
    • How soon this COVID-19 virus detection method could be available for commercial use

    Brian T. Cunningham is a professor in the Department of Electrical and Computer Engineering at the University of Illinois at Urbana-Champaign, and for the past several months, he’s been working on a novel detection method for the COVID-19 virus that’s faster and more sensitive than the PCR test. How does it work? The method uses engineered nucleic acid molecules that can bind to the spike proteins on the surface of the COVID-19 virus, and capture the virus on a nanostructured surface called a photonic crystal. When light is shined on this surface, the scattering between the light and virus particles is amplified, which then allows for a special microscope to immediately count the number of virus particles present. The COVID-19 virus is detected by virtue of the unique shadow it casts when light is scattered off its surface.

    Initially, this method had actually been published for the detection of the Zika virus, and when COVID-19 hit, Cunningham and his team began adapting the method to detect the COVID-19 virus. The same method is also being used for HIV viral load monitoring, which is a proposal that’s recently been funded by the NIH.

    A paper submitted to Nature Communications detailing the method was just accepted, which means it will soon be published and available to the public.

    Press play for all the details and visit http://nano.illinois.edu/ to learn more.

    Available on Apple Podcasts: apple.co/2Os0myK

  • An Evolutionary Arms Race Between Bees and Viruses: Who Will Win?

    An Evolutionary Arms Race Between Bees and Viruses: Who Will Win?

    Is it possible to breed a species of bee with total viral immunity? Maybe, and the research being done in Michelle Flenniken’s lab could pave the way for it to happen.

    Tune in to discover:

    • Whether bees might utilize a form of preventative medicine
    • In what way a honeybee model for insect immunity might be superior to the status quo fruit fly model
    • Why the term “honeybee viruses” might be misleading

    Michelle Flenniken is Assistant Professor in the Plant Sciences Department and Co-Director of the Pollinator Health Center at Montana State University whose primary research is focused not only on understanding the impact of viruses on honeybees, but on the molecular mechanisms that bees have evolved to combat viral infections.

    Longitudinal monitoring projects looking at the prevalence and abundance of 16 pathogens across several bee colonies over time have led to interesting and useful findings. For instance, Flenniken’s lab has shown that bees that are infected with viruses have perturbation in the genes that are important for metabolic processes, and that even in so-called asymptomatic bees, there are more than a billion copies of RNA viruses per bee. The hypothesis that follows this finding is that this viral load could be energetically taxing on bees—even if the bees appear phenotypically normal.

    More recent research in Flenniken’s lab has shown that a bee’s immune response is stimulated by double-stranded RNA, which is a molecule that viruses produce when replicating; this molecule stimulates RNA interference in bees—an antiviral mechanism. This has shown to be true also in bumblebees, but is not the case in the fruit fly, which is the go-to model for studying insect immunity. This has opened the door to more exciting and new research that Flenniken and her lab are gearing up to conduct.

    If antiviral mechanisms in bees can be fully understood, then it may be possible to identify the genes associated with fighting off viral infection, which would make it possible to breed honeybees that are resistant or immune to viral infections.

    Flenniken discusses the details of all this and more, including viral transmission in bees and across species, whether different castes of bees are differentially impacted by viruses, host-pathogen interaction studies, and which viruses most commonly impact bees.

    Check out https://plantsciences.montana.edu/directory/faculty/1524085/michelle-flenniken to learn more.

    Available on Apple Podcasts: apple.co/2Os0myK

  • Politics Playing Medicine: A Closer Look at COVID-19

    Politics Playing Medicine: A Closer Look at COVID-19

    “I felt I had to stand up and be heard at least by the local council; it was never my intention that the video clip would go viral internationally….I gave my opinion, which seems to have struck a chord for many people internationally,” says Dr. Roger Hodkinson.

    He’s not an anti-vaxxer, he’s not a so-called conspiracy theorist: he’s a well-recognized and accomplished physician who isn’t willing to compromise his ethics and integrity by corroborating the mainstream media message simply because he’s being intimidated and threatened into doing so.

    Press play to hear him expound on the opinion that drew international attention, and to discover:

    • Why the innovative mRNA vaccine for COVID-19 may work, but also might backfire and create dangerous complications that emerge within the coming months or years
    • What the Danish mask study showed about the effectiveness of masks in preventing transmission of COVID-19
    • How and to what extent the consequences of the response to COVID-19 have harmed more people than the virus itself

    Dr. Roger Hodkinson completed a pathology residency in the 1970s at the University of British Columbia in Vancouver and has since practiced as a general pathologist with a special interest in molecular diagnostics and hematopathology. Among other accomplishments, he is a serial entrepreneur who has established a number of startup medical businesses, he has dealt in several international medical diagnostic markets, and previously served as a member of the committee on laboratory accreditation and as chairman of a test committee in general pathology at the Royal College of Physicians and Surgeons of Canada, which sets the annual pathology board examination for Royal College.

    According to Dr. Hodkinson, the COVID-19 situation we’re in today is being amplified by two primary drivers: (1) the testing of the asymptomatic population with an enormous number of false positives, which feeds public paranoia; and (2) the lack of any counter-narrative because of systematic intimidation at all levels.

    “Physicians are being intimidated with the threat of losing their license to practice, like myself. There is intimidation at a political level…there is a concerted attempt at all levels to suppress any counter-narrative to the idiocy that is currently going on,” says Dr. Hodkinson.

    He continues by going back to the beginning and exploring how all this began. Fast-forward to the current day, he discusses details about the vaccine, which was rushed to the market with completely new technology, and is being given first to some of the most vulnerable members of the population. With grave consequences, it’s “politics playing medicine,” says Dr. Hodkinson. He discusses censorship by big tech companies, shares his opinion on what could happen in the near and long-term future, and shares practical, safe, and simple practices for proactively protecting our health.

    Available on Apple Podcasts: apple.co/2Os0myK

  • Stopping Superbugs: Steffanie Strathdee Talks Phage Therapy Research

    Stopping Superbugs: Steffanie Strathdee Talks Phage Therapy Research

    “This is the worse superbug you can get,” said her husband’s doctors when diagnosing him with a life-threatening multidrug resistant bacterial infection.

      But Steffanie Strathdee put her research skills to work and eventually was able to convince doctors to treat him with an experimental phage therapy that ended up saving his life.

    Listen and learn

    • Why no other solution was working to cure her husband of this superbug,
    • How the history of phage therapy versus antibiotics has played out, and
    • Why the problem of antibiotic resistance may be addressed by utilizing bacteriophages.

    Steffanie A. Strathdee is the Associate Dean of Global Health Sciences and the Harold Simon Professor in the Department of Medicine at the University of California San Diego School of Medicine. She helped found and co-directs UCSD’s new center for Innovative Phage Applications and Therapeutics (IPATH) and also works with the Global Health Institute and the International Core of UCSD’s Center for AIDS Research.

    An infectious disease epidemiologist, she’s also the author of The Perfect Predator, which tells the story of her husband’s struggle with a superbug and the successful effort to help him recover with phage viruses. Phages are viruses that infect bacteria, and are emerging as a potential winner as scientists struggle with how to prevent superbugs from causing deadly infections. 

    She gives listeners a fascinating history of how politics and war kept phage therapy out of American medicine for decades. First discovered by a French Canadian microbiologist, their adoption by Russians pre-World War II marked them as off-the-table for the American medical field. But they are emerging again as having great potential, and Steffanie Strathdee helps enlighten listeners by describing the process and why they can be effective.

    First, scientists are able to pick and choose their phages, testing to make sure what bacteria the phages will infect. They can get specific, killing only the bacteria they want to target. Ideally, they’ll collect a couple of different phages for the best chances of success, then make isolates of them.  The most difficult stage is the purification, she says. Scientists are moving ahead, designing clinical studies.

    Listen in for more exciting news about this life-saving treatment.

    For more, see the Innovative Phage Applications and Therapeutics (IPATH) website.

    Available on Apple Podcasts: apple.co/2Os0myK

  • The Death Rattle of Citrus Plants: Understanding a Unique RNA Plant Virus

    The Death Rattle of Citrus Plants: Understanding a Unique RNA Plant Virus

    Over the past century, one virus has been responsible for the death of over 100 million trees in the world, posing an agricultural problem particularly in regions of Asia, South America, and South Africa; this virus is called Citrus tristeza virus (CTV).

    Press play to learn about it, and discover the following:

    • What role aphids play in the transmission of CTV from tree to tree
    • How ‘movement proteins’ interact with host proteins to facilitate the spread of virus within the plant
    • How viruses alter the expression of plant genes, and what effect this can have on the plant
    • How plant viruses travel from cell to cell within the host

    In the Department of Plant Biology at the University of Florida, Associate Professor Svetlana Y. Folimonova, PhD, has been working with CTV for several years now, which is a virus that primarily affects citrus plants and trees. In some plant varieties, it causes no disease (or mild disease), while in others it causes severe disease, to such a degree that infection by the virus spreads throughout the entire plant and causes death.

    In addition to the significant agricultural impact of this virus, Dr. Folimonova explains that the virus is fundamentally interesting in that it is among the largest of all RNA viruses, with a non-segmented genome comparable to the size of the virus causing COVID-19. At about 20,000 nucleotides, its genome is about twice as large as the average size of RNA viruses. It also has a unique shape, which can be described as filamentous—very long and narrow, with a “rattlesnake” structure.

    Dr. Folimonova discusses how the virus enters plant cells, what happens once the virus is inside plant cells, the two main types of disease caused by CTV, how the virus alters many organelles within plant cells, as well as the structure of plasmodesmata—microscopic channels that pass through the walls of adjacent plant cells—to facilitate movement of the virus within the plant.

    The primary practical goal of Dr. Folimonova’s work is to determine how diseases caused by CTV can be controlled. She discusses possible solutions, which leads to a conversation about cross-protection in plants, superinfection exclusion, and more.

    Learn more by searching for Dr. Folimonova on Google Scholar, and by visiting https://plantpath.ifas.ufl.edu/people/faculty-pages/svetlana-folimonova/.

    Available on Apple Podcasts: apple.co/2Os0myK

  • Utilizing Mycoviruses for Healthy Plants: Shinyi Marzano Researches Fungal Viruses

    Utilizing Mycoviruses for Healthy Plants: Shinyi Marzano Researches Fungal Viruses

    That grey fuzz you find on your strawberries after a day or two in the fridge has researchers busy in the lab. White and grey molds often harm crops and Shinyi Marzano is working to inhibit these pathogens that often strike greenhouse crops like lettuce, tomatoes, and strawberries.

    Listen and learn

    • How her work zeros in on the arms race between plant and fungi, looking for weak spots in fungi progression,
    • Why this has led her to research RNA silencing pathways in fungi and properties of mycoviruses, and
    • How blocking the RNA silencing mechanism of fungi might give the mycoviruses the upper hand, freeing the plant from these pathogens.

    Shinyi Marzano is a molecular biologist and recently started working with USDA’s Agricultural Research Service. She focuses on green house and high tunnel production, both of which are used for crops highly susceptible to these white and grey molds.

    Plants are especially susceptible during flowering to white mold, when sexually-produced spores germinate after they’ve attached to flower petals. The fungi’s mycelium forms and grows, causing a systemic infection that leads to stem rot. Grey mold is particularly a problem for fruit crops, spreading rapidly and ruining the fruit production.

    Shinyi and her colleagues are studying both the RNA silencing process the fungi initiates as well as the mycoviruses that infect the fungi. RNA silencing in plants is really a function of the fungi. When they sense the double-stranded RNA that’s produced by many mycoviruses, they attempt to silence or inhibit the RNA by releasing proteins that cut up the RNA strands, creating small pieces of what’s called virus-derived small RNA.

    Shinyi is looking at mechanisms to disarm the pathogen host of those essential proteins that are part of the RNA silencing pathway. The fungal pathogen would then be susceptible to those mycoviruses. She explains other interesting avenues, including delivery means of these mycoviruses.

    For more about her work, she recommends searching Google Scholar.

    Available on Apple Podcasts: apple.co/2Os0myK

  • Global Health Laws and Reform Amid COVID-19

    Global Health Laws and Reform Amid COVID-19

    Every continent on the planet has now been touched by the COVID-19 virus, launching the world into an unprecedented state of lockdowns and the many negative consequences that follow from it. Orders to wear masks, socially distance, and limit large gatherings have not only brought to the table a whole layer of global and public health law, but illuminated health and racial inequalities.

    Press play to learn the following:

    • What aspects of global health law are ripe for reform in light of the COVID-19 pandemic
    • The effect of and reason behind contradictory messages from the CDC and WHO regarding the appropriate response to and science of the COVID-19 virus
    • Are travel restrictions and lockdowns actually effective at preventing spread of the COVID-19 virus?
    • Why lockdowns should be a last resort, and what should be changed in the coming weeks and months to mount a better, more effective response to COVID-19

    Lawrence Gostin is University Professor at Georgetown University and Founding O’Neill Chair in Global Health Law. Since the beginning of the pandemic, his focus has been almost exclusively on the COVID-19 response in the US and globally. In addition to discussing the sheer unequalness illuminated by COVID-19, he talks about the hope he sees in human ingenuity and science, and the vaccines that are being administered in the US and Europe.

    He explains what a “global health law” is, and discusses international law in the form of international health regulations, such as the WHO treaty by which 196 states are bound, including the US.

    This treaty deals with matters such as how to detect, report, and response to novel infectious disease.

     Gostin also shares his opinion about what might lay ahead of us in the coming months, what he sees as the light at the end of the tunnel, his conviction that another pandemic will inevitably emerge, why he believes the WHO should be granted additional powers, and more.

    Tune in for all the details.

    Available on Apple Podcasts: apple.co/2Os0myK

  • Diving Into Lipid Droplets, Exploring Early Viral Infections

    Diving Into Lipid Droplets, Exploring Early Viral Infections

    Can the immune response to viral infection be strengthened to the point that the impact of the infection is greatly reduced, and later or latent infection is prevented? This is the question at the crux of Ebony Monson’s research in the Department of Physiology, Anatomy & Microbiology at Latrobe University in Australia.

    Tune in to learn:

    • Why ‘lipid droplets’—previously thought to be only a storage location for lipids—may actually play a critical role in the immune response to viral infection
    • What happens from the moment a virus enters the body to the time it creates pathogenesis in the host
    • What significant functions interferon and cytokines fill during viral infection, and what leads to an exaggerated immune response that actually harms the host

    Monson’s work focuses primarily on viruses that infect humans—flaviviruses specifically, such as Zika, dengue, and hepatitis C. She studies the innate immune response that’s produced immediately after an infection, with the goal of better understanding how this innate immune response can be enhanced or augmented.

    Monson recently finished her PhD, which demonstrated that during early viral infection, there is an accumulation of new lipid droplets within the cytoplasm of cells, and an increase in the size of existing lipid droplets. Furthermore, Monson demonstrated that these lipid droplets are necessary for an effective interferon response during viral infection, and that without them, there would be a much more exaggerated immune response.

    Prior to this research, no one thought much of lipid droplets, as they were largely assumed to be unimportant in the development or progression of the immune response. Monson explains how these lipids can be broken down and can actually become toxic to the host, how they move around in the cell, how they grow and become depleted, and a number of other topics which are the subject of ongoing research.

    Tune in for all the details.

    Available on Apple Podcasts: apple.co/2Os0myK

  • Targeting Rhabdoviruses and Related Pathogens with Yves Gaudin

    Targeting Rhabdoviruses and Related Pathogens with Yves Gaudin

    The rabies virus kills at least 60,000 people a year, worldwide. Because it is far more prevalent in lower economic status countries, it doesn’t receive adequate funding for better vaccines or treatment.

    Researchers like Yves Gaudin are trying to change this. He works on understanding the mechanisms of rhabdovirus transmission.

    Listen and learn

    • How rhabdoviruses enter cells and install their viral factories, which are protected by liquid phase separation, 
    • Why the polymerase is key to making the viral particle infectious, and
    • How their efforts to destabilize the liquid phase separation that contains the viral factory is one main avenue to a possible treatment.

    Yves Gaudin is a researcher with CNRS and the Institut de Biologie Intégrative de la Cellule. CNRS is France’s National Center for Scientific Research. He’s a virologist studying the rhabdovirus family, which includes the rabies virus, Chandipura virus (CHAV), and vesicular stomatitis virus (VSV). He describes two central mechanisms that characterize this family.

    First the rhabdovirus causes a particular entry process and requires a polymerase for infection: the glycoprotein, which makes a spike around the virion, recognizes the cell receptor and attaches.

    This triggers endocytoses and an eventual fusion event allows the viral genome and polymerase is to be released into the cytoplasm. The polymerase immediately copies that genome into an mRNA, which then hijacks the cellular machinery. The polymerase presence is vital to infection—without it, the viral particle would be inert, so targeting that polymerase offers one attack possiblity.

    Second, his lab has characterized the chemical nature of viral factory itself. It is distinguished by liquid phase separation—it is housed inside a compartment that separates it, like oil in water, from the cell cytoplasm. The interaction between this factory and our innate immune system spreads the infection, using the pathway to the synthesis of interferon, and so on.

    This liquid phase separation helps the virus keep its identity in the cell and provides another focus for fighting these viruses. They hope to find small molecules that could destabilize this liquid phase separation or utilize some other weakness such as their sensitivity to temperature.

    Here is the website where Yves Gaudin article is freely available: https://www.nature.com/articles/s41467-017-00102-9

    In the section entitled additional information, listeners can find the movies: https://www.nature.com/articles/s41467-017-00102-9#additional-information

    Available on Apple Podcasts: apple.co/2Os0myK

  • Memory’s Neuronal Networks Incorporate Ancient Virus: Jason Shepherd Explains

    Memory’s Neuronal Networks Incorporate Ancient Virus: Jason Shepherd Explains

    We know how artificial intelligence “remembers,” utilizing data encoding techniques to translate information into a complex pattern of 1s and 0s. But human memory storage continues to pose many fascinating mysteries. Researchers like Jason Shepherd are tackling these neuroscience puzzles on a molecular level. His lab investigates how our neural network is able to store information and retain a lifetime of memories despite the short life of proteins within cells.

    Listen and learn

    • What the mechanisms and basic maps are for short-term to long-term memory conversion,
    • How his lab is researching a specific gene utilized in this encoding and modulation between cells called ARC, which they believe evolved from an ancient viral infection, and
    • Why a better understanding of the Arc capsid function holds a key to the entire process.

    Jason Shepherd is an associate professor of neurobiology and anatomy and an adjunct associate professor of ophthalmology and visual sciences at the University of Utah School of Medicine. He works at the molecular level to understand how the cells in our brain are able to store information and experiences over a lifetime.

    He reminds listeners that when we learn, there’s a specific set of cells that are active and encoding that experience. What is data encoding for the brain? Well, there’s a consolidation period when those active neurons become connected to each other through synaptic connections. Scientists call this synaptic plasticity, when the connections between cells that’ve retained the experience are wired together. That specific circuit is activated when we recall the memory and they think that plasticity process stores the memory.

    That’s where the master regulator gene called Arc comes in. If the gene is removed from mice, they cannot remember anything for long periods of time. The short to long-term memory conversion requires this gene, and based on its appearance, they think it evolved from an ancient viral element that infected an ancestor. It’s retained a lot of the viral biology, such as utilizing a capsid.

    Because scientists have learned so much about retroviruses like HIV, Shepherd and his team are able to use that knowledge in how they approach Arc research. The gene enables signaling from one cell to another through this capsid, which viruses usually use to transfer their own genetic material. He’s taking a focused look at what exactly the capsid enables.

    For more, see his lab’s website at shepherdlab.org and find him on Twitter as @JasonSynaptic.

    Available on Apple Podcasts: apple.co/2Os0myK

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