In late December 2019, the World Health Organization declared
the illness resulting from the new virus, COVID-19, a Public Health
Emergency of International Concern. By early March 2020, the novel
coronavirus—now named SARS-CoV-2—had infected more than 90,000
people worldwide and killed at least 3,100.Note: COVID-19 is the disease, SARS-2-CoV is the virus.
Like other coronaviruses, SARS-CoV-2
particles are spherical and have proteins called spikes
protruding from their surface. These spikes latch onto human cells,
then undergo a structural change that allows the viral membrane to
fuse with the cell membrane. The viral genes can then enter the host
cell to be copied, producing more viruses. Recent work shows that,
like the virus that caused the 2002 SARS outbreak, SARS-CoV-2 spikes
bind to receptors on the human cell surface called
angiotensin-converting enzyme 2 (ACE2).
The researchers found that the
SARS-CoV-2 spike was 10 to 20 times more likely to bind ACE2
on human cells than the spike from the SARS virus from 2002. This may
enable SARS-CoV-2 to spread more easily from person to person than
the earlier virus.
Despite similarities in sequence and
structure between the spikes of the two viruses, three different
antibodies against the 2002 SARS virus could not successfully bind to
the SARS-CoV-2 spike protein. This suggests that potential vaccine
and antibody-based treatment strategies will need to be unique
to the new virus.[It also suggest that more 'novel' mutations may occur in the future.]
Clinical information here - https://forsythkid.blogspot.com/2020/03/coronavirus-covid-19-clinical.html
Clinical information here - https://forsythkid.blogspot.com/2020/03/coronavirus-covid-19-clinical.html
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