ACE2 role in SARS-CoV-2 infectivity and Covid-19 severity
- Author:
Elena Azizan
1
Author Information
1. Department of Medicine, The National University of Malaysia (UKM) Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000, Kuala Lumpur, Malaysia
- Collective Name:Morris Brown
- Publication Type:Review
- Keywords:
angiotensin-converting enzyme 2;
ACE2;
SARS-CoV-2;
Covid-19;
coronavirus
- From:The Malaysian Journal of Pathology
2020;42(3):363-367
- CountryMalaysia
- Language:English
-
Abstract:
In 2003, it was discovered that the entry receptor for the Severe Acute Respiratory Syndrome
coronavirus (SARS-CoV) is a protein called the angiotensin-converting enzyme 2 (ACE2). This
protein is present in a number of cell types, including those from the respiratory tract. Soon after the
emergence of SARS-CoV-2 that is responsible for the disease Covid-19, scientists found that ACE2
was also used by the new coronavirus to infect cells. This opened some interesting possibilities to
explain the striking variation in risks of catching and dying from Covid-19. The best recognised of
these are the much higher risk of serious illness in older than younger people, in men than women,
and in those with pre-existing comorbidities such as hypertension and cardiovascular diseases. There
are several ways in which the ACE2 protein might contribute to this variation. The most obvious
would be if there is more ACE2, there would be more entry points for the virus to infect the cell,
e.g. in older people or in men. However, the evidence for this is rather small, partly because it is
not that easy to obtain representative healthy tissues. Alternatively, it could be related to ACE2
membership of a family of proteins that has one end of the protein anchored inside the cell while
most of the protein protrudes from the outside of the cell which therefore can be shed when cleaved
by proteases at the cell membrane. Herein we review current evidence and theories of ACE2 role
on SARS-CoV-2 infectivity and Covid-19 severity.
- Full text:5.2020my01082.pdf
