COVID-19: Are we dealing with a multisystem vasculopathy in disguise of a viral infection?

Abstract

After the emergence of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV) in the last two decades, the world is facing its new challenge in Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) pandemic with unprecedented global response. With the expanding domain of presentations in COVID-19 patients, the full range of manifestations is yet to unfold. The classical clinical symptoms for SARS-CoV-2 affected patients are dry cough, high fever, dyspnoea, lethal pneumonia whereas many patients have also been found to be associated with a few additional signs and clinical manifestations of isolated vasculopathy. Albeit a deep and profound knowledge has been gained on the clinical features and management of COVID-19, less clear association has been provided on SARS-CoV-2 mediated direct or indirect vasculopathy and its possible correlation with disease prognosis. The accumulative evidences suggest that novel coronavirus, apart from its primary respiratory confinement, may also invade vascular endothelial cells of several systems including cerebral, cardio-pulmonary as well as renal microvasculature, modulating multiple visceral perfusion indices. Here we analyse the phylogenetic perspective of SARS-CoV-2 along with other strains of β-coronaviridae from a standpoint of vasculopathic derangements. Based on the existing case reports, literature and open data bases, we also analyse the differential pattern of vasculopathy related changes in COVID-19 positive patients. Besides, we debate the need of modulation in clinical approach from a hemodynamical point of view, as a measure towards reducing disease transmission, morbidity and mortality in SARS-CoV-2 affected patients.

JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy

“…It has high ACE2 expression through which SARS-CoV-2 gain access to enter the host cell. They also constitute CD147 (Extracellular matrix metalloproteinase inducer), TMPRSS2, and sialic acid receptor [ 32 ]. They undergo viral replication and apoptosis via Fas/FasL or TRAIL-PR-5 dependent mechanisms.…”

The Enigma of Endothelium in COVID-19

“…As the clinical, pathological and molecular features of COVID-19 patients are unfolding in investigational studies, several researchers are hypothesizing and reviewing a vascular-centric pathogenesis of COVID-19. A summary of such recent reviews and short reports is provided in Table 1 ( Alvarado-Moreno and Majluf-Cruz, 2020 ; Amraei and Rahimi, 2020 ; Cure and Cure, 2020 ; Froldi and Dorigo, 2020 ; Guler et al, 2020 ; Gupta et al, 2020 ; Gustafson et al, 2020 ; Mangalmurti et al, 2020 ; Marchetti, 2020 ; Mondal et al, 2020 ; Panfoli, 2020 ; Pons et al, 2020 ; Sardu et al, 2020b ; Teuwen et al, 2020 ). Hence, undoubtedly, an assessment of endothelial dysfunction in patients with COVID-19 to stratify the patients based on severity holds immense relevance.…”

Acute reversible renal failure requiring temporary dialysis in a patient with COVID-19

“…There are multiple proposed mechanisms for the development of vasculopathy, hypercoagulability and acute kidney injury in patients with COVID-19 infection. They may include direct cytopathic effects of the virus on endothelial cells and kidneys, cytokine storm, hypotension leading to renal hypoperfusion or renal medullary hypoxia [ [5] , [6] , [7] ].…”