Type 3 hypersensitivity in COVID-19 vasculitis

Abstract

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Denovo designing, retrosynthetic analysis, and combinatorial synthesis of a hybrid antiviral (VTAR-01) to inhibit the interaction of SARS-CoV2 spike glycoprotein with human angiotensin-converting enzyme 2

“…Similarly, blockage of IL-6 and granulocyte macrophage-colony stimulating factor inhibits monocyte-macrophage recruitment and differentiation to the lungs, and blocks the inflammatory response ( Gómez-Rial and Martinón-Torres, 2020 ). In addition to that, deposition of immune complexes (ICs) inside vascular walls can also induce cytokine storm ( Roncati et al, 2020 ) hence status of ICs may be too critical for design and immune-based treatments like plasma therapy and vaccine ( Vuitton et al, 2020 ). To make the situation more complicated, there is an activation of complement C3 during lung injury, and C3-targeted intervention by compstatin-based complement C3 inhibitor AMY-101 prevents complement-mediated inflammatory damage in COVID-19 patients ( Mastaglio et al, 2020 ).…”

Necrotising Vasculitis in Covid-19: watch out for bowel perforation

“…Necrotizing vasculitis has been described as a common histopathological nding in SARS-CoV-2 infected patients [4], with typical features. Enteric and bowel involvement, however, is not yet clear: some authors suggest it is present in up to 50% of the cases [5]. Furthermore, SARS-Cov-2 has been detected in samples from faeces suggesting that virus can actively infect and replicate in the GI tract [6] leading to different forms of colitis; a common feature for the other member of coronavirus family.…”

“…Furthermore, SARS-Cov-2 has been detected in samples from faeces suggesting that virus can actively infect and replicate in the GI tract [6] leading to different forms of colitis; a common feature for the other member of coronavirus family. Nowadays, exact mechanism of viral infection causing intestinal symptomatology is not yet understood, Angiotensin-Converting Enzyme 2 (ACE 2) receptor, known as the SARS CoV-2 receptor on human, is expressed not only by lung but also by intestinal epithelium: mouse models shows that ACE2 receptor modi cations can be associated with higher rate in colitis, suggesting that receptor modi cation due to virus infection can increase risk of developing intestinal in ammation and colitis [5]. It is also known that COVID-19 patient, especially with more severe forms of disease, suffered for an acute systemic in ammatory response due to cytokine storms that can develop a multiple organs injury [7], often driven by vasculitis as initial damage.…”

“…We, here, describe a possible critical complication of the still largely unknown disease related to SARS-CoV-2 infection. Many Covid 19 patients presents GI symptoms together with respiratory ones (2,5).…”

Cryoglobulins: Identification, classification, and novel biomarkers of mysterious proteins

“…Roncati et al reported scientific evidence that in COVID-19, vasculitis indicates that a life-threatening escalation and switch from humoral immunity (type 2 T-helper immune response) to type 3 hypersensitivity has taken place. The deposition of immune complexes inside the vascular walls could induce a severe inflammatory state with the consequent inflammatory amplification ascribed as cytokine storm syndrome [120] . Type 3 hypersensitivity represents an immunopathogenic mechanism of disease that involves immune complexes deposition inside tissues and blood vessels, inducing a severe inflammatory state by the action of complement anaphylatoxins (C3a and C5a) that ultimately leads to tissue damage.…”