Coronavirus

Coronavirus infections historically were associated with mild upper respiratory tract diseases in infants, children, and adults. Human coronavirus (HCoV)-OC43 and HCoV-229E were associated with 15–30% of common colds in winter and occasionally linked with lower respiratory tract disease in populations with chronic underlying diseases. HCoV research was complicated by the lack of a reverse genetic system or animal model. These viruses propagated poorly, and the number of reagents was limited. However, coronaviruses are capable of rapid host switching and evolution in changing ecologies (1), suggesting that their diversity and role in human disease were underappreciated. The 21st century heralded the arrival of the more pathogenic coronaviruses, like severe acute respiratory syndrome (SARS)-CoV.

https://web.archive.org/web/20180604062832/https://www.pnas.org/content/102/23/8073

• Feb, 2008 - Difference in Receptor Usage between Severe Acute Respiratory Syndrome (SARS) Coronavirus and SARS-Like Coronavirus of Bat Origin¹⁾

• Feb 6, 2020 - Persistence of coronaviruses on inanimate surfaces and their inactivation with biocidal agents²⁾

Humanized mice develop coronavirus respiratory disease Ralph Baric and Amy C. Sims PNAS June 7, 2005. 102 (23) 8073-8074; https://doi.org/10.1073/pnas.0503091102

In 2013, researchers at the Wuhan Institute of Virology published a paper saying that Dr. Zhengli Shi and EcoHealth Alliance's Dr. Peter Daszak found CoVs that were 95% identical to human SARS-CoV in Chinese horseshoe bats. Further, these CoVs “were able to use human angiotensin-converting enzyme 2 (ACE2) receptor for docking and entry.”³⁾

Between 2004 and 2020, there were at least four incidents in which a SARS-CoV leaked from a laboratory.⁴⁾ During the COVID-19 pandemic, debate has raged over a lab leak hypothesis.