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2020 ; 6
(2
): 169-176
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A Review: Does Complement or the Contact System Have a Role in Protection or
Pathogenesis of COVID-19?
#MMPMID32405877
Maglakelidze N
; Manto KM
; Craig TJ
Pulm Ther
2020[Dec]; 6
(2
): 169-176
PMID32405877
show ga
INTRODUCTION: COVID-19 presentation may include a profound increase in cytokines
and associated pneumonia, rapidly progressing to acute respiratory distress
syndrome (ARDS). This so-called cytokine storm often leads to refractory edema,
respiratory arrest, and death. At present, anti-IL-6, antiviral therapy,
convalescent plasma, hydroxychloroquine, and azithromycin among others are being
investigated as potential treatments for COVID-19. As the disease etiology and
precise therapeutic interventions are still not definitively defined, we wanted
to review the roles that complement and the contact system may have in either the
treatment or pathogenesis of the disease. METHODS: We searched the recent
literature (PubMed) on complement and coronavirus; contact system and
coronavirus; bradykinin and coronavirus; and angiotensin receptor and
coronavirus. The manuscript complies with ethics guidelines and was deemed exempt
from institutional review board approval according to Human Subjects Protection
Office guidelines. RESULTS: Mouse models are available for the study of
coronavirus and complement. Although complement is effective in protecting
against many viruses, it does not seem to be protective against coronavirus. C3
knockout mice infected with SARS-CoV had less lung disease than wild-type mice,
suggesting that complement may play a role in coronavirus pathogenesis. Some
evidence suggests that the observed pulmonary edema may be bradykinin-induced and
could be the reason that corticosteroids, antihistamines, and other traditional
interventions for edema are not effective. Angiotensin-converting enzyme 2 (ACE2)
is a co-receptor for SARS-CoV-2, and studies thus far have not concluded a
benefit or risk associated with the use of either ACE-inhibitors or angiotensin
receptor antagonists. Activation of complement and the contact system, through
generation of bradykinin, may play a role in the SARS-CoV-2-induced pulmonary
edema, and our search suggests that further work is necessary to confirm our
suspicions.