Acute respiratory distress syndrome: a life threatening associated complication of SARS-CoV-2 infection inducing COVID-19

Abstract

Acute Respiratory Distress Syndrome (ARDS) is a form of respiratory failure in human. The number of deaths caused by SARS-CoV-2 infection inducing this severe pneumonia (ARDS) is relatively high. In fact, COVID-19 might get worsen in ARDS and provoke respiratory failure. A better understood of ARDS key features and the pathophysiological injuries of the pulmonary parenchyma are linked to lessons learned from previous severe diseases associated previous coronaviruses outbreaks (especially SARS-CoV and MERS-CoV) and more the ongoing SARS-CoV-2. The ARDS mechanism includes a diffuse alveolar damage associated disruption of alveolar capillary membrane, pulmonary edema, damaged endothelium and increased permeability. A diffuse inflammation, with acute onset, on the lung tissue accompanied by release of biochemical signal and inflammatory mediators (TNFa, IL-1 and IL-6) leading to hypoxemia, low PaO 2 /FiO 2 ratio and the chest radiological expression of bilateral infiltrates in ARDS. The ongoing outbreak could lead to a better understood of ARDS pathophysiology and prognostic. An overview is also highlighted about the seven coronaviruses proved to infect human especially those having ability to cause severe disease SARS-CoV, MERS-CoV and SARS-CoV-2. In this review, we focused on the major pathological mechanisms leading to the ARDS development as a result of viral infection, severe COVID-19 worsening.

Chloroquine and Hydroxychloroquine Interact Differently with ACE2 Domains Reported to Bind with the Coronavirus Spike Protein: Mediation by ACE2 Polymorphism

“…The global COVID-19 pandemic is still an ongoing challenge because SARS-CoV-2 infection constitutes a serious threat both to human life and socioeconomic development [ 5 ]. Two vaccine types are authorized and recommended for use and some other COVID-19 vaccines are undergoing large-scale (phase 3) clinical trials [ 20 ].…”

“…This could be correlated with the geographical distribution of ACE2 genotype which has been previously reported [ 43 ]. For its entry within the cell, SARS-CoV-2 uses both ACE2 and the ganglioside-attached sialic acids [ 5 , 40 ]. Further studies on the interactions of CQ and HCQ with ganglioside-attached sialic acids could give general ideas about the possible actions of these drugs on the virus entry.…”

“…It has caused the worldwide COVID-19 (coronavirus disease 2019) pandemic. Currently, there are no specific drugs or vaccines available and people are still dying mainly with acute respiratory distress syndrome (ARDS) which is one of the main severe complications of COVID-19 [ 5 ]. Throughout the ongoing COVID-19 pandemic, the use of CQ and HCQ has been allowed in several countries to treat the SARS-CoV-2 infected people.…”

“…It has been reported that both CQ and HCQ interfere with various cellular levels and might have a wide range of antiviral potencies even on cancer cells [ 2 , 6 , 7 ]. In fact, both inhibit the SARS-CoV-2 viral replication [ 8 ], decrease antigen processing and its presentation [ 9 , 10 ], and decrease the cellular activity via low secretion of inflammatory cytokines and type 1 interferon [ 5 ]. CQ and HCQ might also interfere with angiotensin-converting enzyme 2 (ACE2) receptor which is involved in COVID-19 and its symptoms [ 11 ].…”

COVID‐19 pandemic: mechanism, diagnosis, and treatment

“…For most infected patients, this infection is restricted to the upper respiratory tract 20 . Third and final, the Acute Respiratory Distress Syndrome (ARDS) and Hypoxia stage, in which the virus reaches, infects, and damages the alveoli in the lungs, which release interferons that signal the nearby healthy cells to release antiviral peptides 21 . The antiviral peptides cause the breakdown of the virus.…”