2020, Number S1
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Acta Pediatr Mex 2020; 41 (S1)
Pathophysiology of multi-organ damage in SARS-CoV-2 infection
López-Pérez GT, Ramírez-Sandoval MLP, Torres-Altamirano MS
Language: Spanish
References: 71
Page: 27-41
PDF size: 738.41 Kb.
ABSTRACT
SARS-CoV-2 could originate from unknown bats or intermediate hosts and cross the
species barrier to humans. Virus-host interactions affect viral entry and replication. The
virus genome encodes four essential structural proteins, the spike glycoprotein, the
small envelope protein, the matrix proteins, and the nucleocapsid protein. The SARSCoV-
2 glycoprotein S binds to the host cell receptors of the enzyme, the conversion of
angiotensin 2 (ACE2), which is a critical step for virus entry. It is expressed more in men
than in women, probably by estradiol and testosterone that can influence ACE activity
in different ways. In the viremia phase, it passes from the salivary glands and mucous
membranes, especially the nasal and larynx, to the lungs and other organs with the
same ACE2 receptors, such as the heart, liver, and even the central nervous system. It
can reach the intestines, which can explain the symptoms and is detected in the stool
from the beginning of the infection. Comorbidities such as immunodeficient status, old
age, systemic arterial hypertension, diabetes mellitus or chronic lung diseases, obesity
or smoking are key to viral pathogenesis. When the immune system is inefficient to
effectively control the virus in the acute phase, it can evolve into a macrophage activation
syndrome that results in the dreaded cytokine storm that puts the patient in a
very critical condition. Understanding the pathophysiology of SARS-CoV-2 infection
is the cornerstone to provide timely diagnosis and implement appropriate treatment
for patients, limiting the spread of the virus and ultimately eliminating the presence
of the virus in humanity.
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