Friday, 21 October 2016 16:33

Zika and enterovirus D68

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Published in Zika Diaries
Structure of enterovirus D68. Structure of enterovirus D68.

When Zika virus grabbed the attention of my laboratory at the beginning of 2016, we had been searching for a new object of interest after many years of working on poliovirus. We had been doing experiments with enterovirus D68 (EV-D68), but were stymied in our ability to study the neurovirulence of that virus. As a consequence of our work on Zika virus, that problem might have been solved.

Enterovirus D68 was first isolated from patients with severe respiratory disease during the 1960s in California. In the summer and fall of 2014, the virus caused an outbreak in the United States. A total of 1,153 people in 49 states and the District of Columbia had respiratory illness caused by EV-D68, mainly among children. During these outbreaks, acute flaccid paralysis similar to that caused by poliovirus was reported to correlate with EV-D68 infection in young children, suggesting that the virus might invade the central nervous system.

Enterovirus D68 is classified in the picornavirus family, and shares features with both polioviruses (which cause paralysis but not respiratory disease) and rhinoviruses (which cause respiratory disease but not paralysis). Like human rhinoviruses, EV-D68 initiates infection in the the respiratory tract, but not the intestinal mucosa like poliovirus. Transmission of EV-D68 is by respiratory aerosols (like rhinoviruses), not faecal-oral contamination as for poliovirus. Unlike poliovirus, EV-D68 has not been found in the stool of infected patients.

Although EV-D68 infection has been associated with paralysis in young children, it is not clear if the virus is responsible for this condition. Therefore it is important to determine if EV-D68 is neurovirulent—if it is able to replicate in and destroy neural cells. Until recently we had no clear path to answering this question.

Our work on Zika virus has lead to the establishment of two different systems in our laboratory for studying viral neurovirulence. I previously described our finding that Zika virus can replicate in human cortical neurons produced from human embryonic stem cells. I’ve also described our use of embryonic mice to determine if Zika virus can infect the brain. Both systems could be used to study EV-D68 neurovirulence.

That’s how a research laboratory should work: progress made on one project (Zika virus) can be used to advance our understanding of a different virus (EV-D68). Even though our laboratory is small, we can work on two very different viruses because the experimental approaches are similar.

Last modified on Friday, 21 October 2016 17:41
Vincent Racaniello

Vincent Racaniello, Ph.D. is Professor of Microbiology at Columbia University Medical Center. As principal investigator of his laboratory, he oversees the research that is carried out by Ph.D. students and postdoctoral fellows. He also teaches virology to graduate students, as well as medical, dental, and nursing students.

Vincent entered the world of social media in 2004 with virology blog, followed by This Week in Virology. Videocasts of lectures from his undergraduate virology course are on iTunes University and virology blog. You can find him on WikipediaTwitter, Facebook, and Instagram. His goal is to be Earth’s virology professor. In recognition of his contribution to microbiology education, he was awarded the Peter Wildy Prize for Microbiology Education by the Society for General Microbiology. His Wildy Lecture provides an overview of how he uses social media for science communication.