SEP 11, 2019 12:00 PM PDT

Understanding Astrovirus Pathogenesis: Who Knew Viruses Had Toxins?

C.E. Credits: P.A.C.E. CE Florida CE
Speaker
  • Full Member (Professor) Department of Infectious Diseases, St Jude Children's Research Hospital
    Biography
      Dr. Schultz-Perry's introduction to influenza pathogenesis began as a postdoctoral fellow with Dr. Virginia Hinshaw at the University of Wisconsin. Given her PhD training as a cellular biochemist with an emphasis on wound healing and extracellular matrix-growth factor interactions in the Department of Pathology at the University of Alabama-Birmingham, her postdoctoral studies focused on understanding the viral and cellular factors involved in influenza virus-induced apoptosis.

      She was specifically interested in how highly pathogenic avian influenza (HPAI) viruses induced extensive damage. These studies led to a faculty position at the Southeast Poultry Research Lab (USDA-ARS) studying HPAI. The timing of the move corresponded to the 1997 HPAI outbreak in humans in Hong Kong.

      During her 5 years at the USDA, she was intimately involved in the H5N1 outbreak in terms of diagnostics, epidemiology, surveillance, and pathogenesis and worked closely with the CDC. They were also one of the first laboratories to begin working with turkey pneumovirus; closely related to human metapneumovirus. In 2002, she accepted a tenure-track faculty position at the University of Wisconsin School of Medicine and Public Health where her laboratory continued to focus on pathogenesis. She also identified and characterized a novel antiviral peptide that blocks influenza attachment. Their patent was recently licensed by a small influenza company.

      After receiving tenure at Wisconsin, St. Jude offered her a faculty position that she could not refuse. At St. Jude, her laboratory is part of the Center for Excellence in Influenza Research and Surveillance and the World Health Organization Collaborating Center. They are continuing with basic research studies but have also initiated surveillance efforts throughout Latin America.

    Abstract

    immunocompromised populations where the virus can cause systemic and even fatal infections. Indeed, we have shown that astrovirus infections are more prevalent than norovirus in our pediatric oncology population with many patients being long-term shedders. Due to the lack of cell culture systems and animal models for most astrovirus family members, little is known about pathogenesis. Our group demonstrated that the human astroviruses cause intestinal epithelial cells to lose cell-to-cell junctions resulting in increased membrane permeability (i.e. leaky gut). The virus does not have to replicate to induce membrane permeability. The outer viral coat protein, or capsid, is all that was required. To determine if this could also happen in vivo, animal models were orally inoculated with species-specific astrovirus or astrovirus capsid and intestinal permeability and clinical disease was monitored. Like cells in culture, the astrovirus capsid protein alone caused a loss of membrane permeability, relocalization of sodium transporters and diarrhea. Our initial work suggests the virus disrupts the barrier by causing the epithelial cells to change and undergo epithelial to mesenchymal transition.


    Learning Objectives:

    1. Recognize the importance of astroviruses.

    2. Illustrate how a viral toxin could cause diarrhea without causing damage to the intestinal cells.

     


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