Authors: Vineet Menachery The University of Texas Medical Branch, TX, USA)
Recent decades have seen the emergence of several zoonotic coronaviruses (CoV), from the first outbreak of SARS to the ongoing cases of MERS in the Middle East. However, with major advances in fields such as genomics and structural biology, can more be uncovered about coronaviruses and their emergence?
In this interview we speak to Vineet Menachery about his recent talk at the Microbiology Society’s Annual Conference (8–11 April, Belfast, UK) suggesting that coronavirus emergence is more complicated than receptor binding alone.
First, could you introduce yourself and give a brief summary your career to date?
I started as a PhD student at Washington University in Saint Louis (MO, USA). I was in the immunology program, but always interested in virology. I did my PhD with David Leib (Geisel School of Medicine at Dartmouth, NH, USA), who was a herpes virologist, and then from David’s lab, I went to Ralph Baric’s lab at the University of North Carolina (NC, USA) in 2010 to study coronaviruses.
So, I had been interested in type one interferon and interferon-stimulated genes and that is what I worked on initially when I was at Ralph’s lab. Then the opportunity came up to work with bat CoVs, which was obviously a great opportunity. My lab also works on the host side looking at aging in the context of SARS and MERS infections and we have funding from the NIH to work on that, in addition to our research on bat viruses.
Could you outline the research you’re presenting here?
So, in my talk I talked about a longitudinal study that had been done by Zhengli Shi’s group at the Wuhan Institute  on Chinese horseshoe bats, which led to a big shift in our thinking about these bat CoVs because it revealed they are much closer to the epidemic SARS strains than previously thought. Normally, we don’t evaluate anything beyond being reactive to the next emergent strain, but building on this study using our infectious clone system we had the opportunity to ask more questions – and that’s how this project started.
The study that I showed was using a chimeric approach – taking the spike protein of bat CoVs and putting them into the backbone of a virus we knew was functional. Coronaviruses are really large, so with generating the viruses there are any number of other things that could go wrong, such as incompatibilities, that might not allow that virus replicate even though the spike might be viable – by putting just the spike in a known backbone we could gain some insight into that. We chose a mouse-adapted strain for the backbone because then we could take the chimeric virus into animals, and what surprised us was that the SARS-like CoV spikes, WIV1 and SHC014, which were isolated from bats, caused robust disease.