Updated April 13, 2020

Background

A novel human coronavirus—now named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)—emerged from Wuhan, China, in late 2019 and is causing a pandemic.¹ Coronaviruses are enveloped RNA viruses that affect animals and humans.² Coronavirus particles range from 60 to 140 nanometers (0.06 to 0.14 micrometers), with an average of 0.125 micron, and have distinctive spikes of nine to 12 nanometers that give the appearance of “coronas” around the sun (figure 1). Cell death is observed 96 hours after inoculation on surface layers of human airway epithelial cells.²

Currently, there are six coronavirus species that cause human disease. Four of them—229E, OC43, NL63, and HKU1—often result in symptoms of the common cold.³ The other two strains—severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)—are zoonotic (originate from animals and cross over to humans), more serious, and sometimes linked to fatal illness.⁴

SARS-CoV-1 was the causal agent of the severe acute respiratory syndrome outbreaks in 2002 and 2003 in Guangdong Province, China.⁵ During this outbreak, approximately 8,098 patients were affected with 774 deaths, resulting in a mortality rate of 9%. This rate was much higher in elderly individuals, with mortality rates approaching 50% in those over age 60. Transmission of SARS-CoV-1 was relatively inefficient because it spread only through direct contact with infected individuals; once an individual exhibited symptoms, the virus spread. The outbreak was largely contained because it was easy to identify those individuals who were capable of spreading the disease. A few cases of super-spreading events occurred whereby individuals with higher viral loads and the ability to aerosolize the virus were able to infect multiple people. As a result of the relatively inefficient transmission of SARS-CoV-1, its outbreak was controllable through the means of quarantining individuals in households and health-care centers.⁶

The stability of SARS-CoV-2 is like SARS-CoV-1, with an 80% genetic makeup similarity. Both viruses bind to the human cell via the spike (S) protein to angiotensin-converting enzyme 2 receptor (ACE2) to gain entry, but there are a few differences (figure 2). First, higher viral loads have been detected in nasal passages and the upper respiratory tract of individuals infected with SARS-CoV-2, which mean coughs and sneezes may contain higher viral loads than its predecessor virus. Second, the potential for individuals infected with SARS-CoV-2 to shed and transmit the virus while asymptomatic is much greater, and those in the latent stages of the disease often shed the virus at a higher rate.⁷ Third—and most significantly—this new virus strain has been shown to be much more efficient at traveling more considerable distances and becoming aerosolized.

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