Coronavirus disease 2019 (COVID‐19): An overview of the immunopathology, serological diagnosis and management

Abstract

SARS‐CoV‐2 is a novel human coronavirus responsible for the Coronavirus disease 2019 (COVID‐19) pandemic. Pneumonia and acute respiratory distress syndrome are the major complications of COVID‐19. SARS‐CoV‐2 infection can activate innate and adaptive immune responses and result in massive inflammatory responses later in the disease. These uncontrolled inflammatory responses may lead to local and systemic tissue damage. In patients with severe COVID‐19, eosinopenia and lymphopenia with a severe reduction in the frequency of CD4+ and CD8+ T cells, B cells and natural killer (NK) cells are a common feature. COVID‐19 severity hinges on the development of cytokine storm characterized by elevated serum levels of pro‐inflammatory cytokines. Moreover, IgG‐, IgM‐ and IgA‐specific antibodies against SARS‐CoV‐2 can be detected in most patients, along with the viral RNA, forming the basis for assays that aid in patient diagnosis. Elucidating the immunopathological outcomes due to COVID‐19 could provide potential targets for immunotherapy and are important for choosing the best clinical management by consultants. Currently, along with standard supportive care, therapeutic approaches to COVID‐19 treatment involve the use of antiviral agents that interfere with the SARS‐CoV‐2 lifecycle to prevent further viral replication and utilizing immunomodulators to dampen the immune system in order to prevent cytokine storm and tissue damage. While current therapeutic options vary in efficacy, there are several molecules that were either shown to be effective against other viruses such as HIV or show promise in vitro that could be added to the growing arsenal of agents used to control COVID‐19 severity and spread.

Anticardiolipin and other antiphospholipid antibodies in critically ill COVID-19 positive and negative patients

“…3 4 One of the salient features of COVID-19 is the development of thrombotic events associated with severe morbidity and mortality. [5][6][7][8] In the context of systemic inflammation and dysregulated immunity, 9 some reports have linked APLA to these thromboses, 10 11 severe COVID-19 6 12 and release of neutrophil extracellular traps. 6 However, APLAs are also described in a variety of other infectious diseases 13 and critically ill patients have high rates of thromboembolism that were not linked to APS or APLA 14 (critically reviewed in ref.…”

Novel Therapeutical Approaches to Managing Atherosclerotic Risk

“…Recently, new anti-inflammatory treatment strategies of atherosclerosis have been introduced. Some of these drugs have recently been used for the suppression of the inflammatory cascade induced by some viruses, others for the treatment of inflammatory bowel diseases, and some others for systemic autoimmune inflammatory diseases [ 81 , 82 ]. Tocilizumab, a monoclonal antibody that blocks IL-6 receptors, has reduced myocardial damage and systemic inflammation, although there was a serious safety concern due to a significant increase in LDL-cholesterol levels soon after starting treatment [ 83 ].…”

An Update on the Pathogenesis of COVID-19 and the Reportedly Rare Thrombotic Events Following Vaccination

“…Currently, we know that the manifestations and developments of COVID-19 are caused by overlapping and complex interactions of different pathophysiological mechanisms. 41,42 In this regard, one of the proposed mechanisms is down regulation of ACE2 over the course of COVID-19 infection. In a healthy person, angiotensinogen, produced in the liver, is cleaved by renin, resulting in formation of angiotensin I (AT-I).…”