Abstract
SARS-CoV-2 is the most recent coronavirus which crossed the species barrier in 2019 and provoked a still ongoing and dangerous pandemic known as coronavirus disease 2019 (COVID-19). The SARS-CoV-2 infection has triggered an impressive amount of clinical and experimental studies to identify an effective and safe therapy to stop the pandemic spread. Hence, numerous trials and studies have scrutinized the analogies between SARS-CoV-2 and other corona viruses or the host-virus interactions and their similarities with immune system disorders. Still, the pathogenic mechanisms behind SARS-CoV-2 have been partially deciphered and the current therapies have not yet met the initial enthusiastic expectations. So far COVID-19 therapies have targeted various pathogenic mechanisms, namely the neutralization of ACE2 receptors or SARS-CoV-2 spike protein epitopes, the disruption of the endocytic pathways using hydroxychloroquine, arbidol, or anti-Janus kinase inhibitors, the inhibition of RNA-dependent RNA polymerase using nucleotide analogues such as remdesivir, immunosuppressive drugs or molecules acting on the immune response (corticoids, interferons, monoclonal antibodies against inflammatory cytokines, mesenchymal stem cells) and convalescent plasma administration together with numerous drugs with unproven effect against SARS-CoV-2 but with potential antiviral activities (antiretrovirals, antimalarial drugs, antibiotics, etc.). Nevertheless, these therapies have been associated with side effects and contradictory results. At the same time a specific SARS-CoV-2 vaccine is a long-term solution requiring clinical validation and important investments together with appropriate strategies to promote the confidence in the safety of the new vaccine. The article revises the current state of SARS-CoV-2 therapeutic options but advises towards a more cautious and individualized treatment approach centred on the clinical features, immune particularities, and the risk-benefit balance.
Highlights
Coronaviruses (CoVs) are a large group of RNA viruses belonging to the subfamily of Coronaviridae, the family Coronaviridae, order Nidovirales
Three species of CoVs have been responsible for important and severe respiratory outbreaks in humans, namely the severe acute respiratory syndrome coronavirus (SARS-CoV) which lead to the 2002–2003 outbreak, the Midde East respiratory syndrome coronavirus (MERS-CoV) in 2012 and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) associated with the ongoing pandemic referred to as CoV disease 2019 (COVID-19) (Huang et al, 2020)
As of June 2020, remdesivir, a nucleoside analogue has gained an authorization for emergency use in hospitalized patients with severe forms of COVID-19 in the United States and Europe, while dexamethasone is recommended in specific situations and umifenovir, a-interferon, lopinavir/ritonavir, ribavirin, and chloroquine phosphate has been added to the Guidelines for the Diagnosis and Treatment of COVID-19 in China (Youyao and Yizhen Chen, 2020)
Summary
Coronaviruses (CoVs) are a large group of RNA viruses belonging to the subfamily of Coronaviridae, the family Coronaviridae, order Nidovirales. SARS-CoV-2 is a large, enveloped, single-stranded RNA virus with a positive-sense It entails 16 non-structural proteins (Nsp) which are essential for viral replication and 4 other structural proteins namely the spike, membrane, envelope and nucleocapsid, which mediate the cell invasion and immune response (Alsaadi and Jones, 2019; Gordon et al, 2020). Receptor Recognition as a Therapeutic Target The CoV-2 S protein is a type I transmembrane protein It contains two ectodomains: a receptor-binding subunit (RBD) S1 which ensures the viral biding to angiotensin-converting enzyme 2 (ACE2) receptor and a membrane-fusion subunit S2 (Wan et al, 2020; Zhang et al, 2020; Zhou P. et al, 2020). While the correlation between the outcome of SARS and serum or tissue concentration of ACE2 or ACEIs/ARBS
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