"The other thing we found is that the viruses [HCoV-EMC, SARS, and the common cold virus] are all similar in terms of host responses: they don't provoke a huge innate immune response," Thiel says. This is an indication that HCoV-EMC is already well adapted to the human host and that the virus uses that same strategy other coronaviruses use for evading the host's non-specific immune mechanisms.
The authors asked themselves whether boosting this weak immune response might diminish the virus' ability to infect airway epithelial cells. They found that pre-treating the cells with lambda-type interferons, proteins that are released by host cells in response to infection and enable communication between cells to mount an immune response, significantly reduced the number of infected cells. This is encouraging from a treatment standpoint, note the authors, since interferons have also shown a good deal of promise for treating SARS and another viral illness, Hepatitis C.
Thiel and co-author Ronald Dijkman emphasize that their work with HCoV-EMC would not have been possible without the efforts of many different research groups from Switzerland, Germany, The Netherlands, and Denmark.
Ongoing collaboration is crucial, they say. Future research to head off outbreaks of HCoV-EMC and other emerging diseases requires cooperation and trust among scientists and health agencies, a goal that is not always achieved. The future of this virus is uncertain, Thiel points out, but access to samples fr
|Contact: Jim Sliwa|
American Society for Microbiology