Abstract
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is a novel coronavirus that emerged from Wuhan, China in late 2019 causing coronavirus disease-19 (COVID-19). SARS-CoV-2 infection begins by attaching to angiotensin-converting enzyme 2 receptor (ACE2) via the spike glycoprotein, followed by cleavage by TMPRSS2, revealing the viral fusion domain. Other presumptive receptors for SARS-CoV-2 attachment include CD147, neuropilin-1 (NRP1), and Myeloid C-lectin like receptor (CLR), each of which might play a role in the systemic viral spread. The pathology of SARS-CoV-2 infection ranges from asymptomatic to severe acute respiratory distress syndrome, often displaying a cytokine storm syndrome, which can be life-threatening. Despite progress made, the detailed mechanisms underlying SARS-CoV-2 interaction with the host immune system remain unclear and are an area of very active research. The process’s key players include viral non-structural proteins and open reading frame products, which have been implicated in immune antagonism. The dysregulation of the innate immune system results in reduced adaptive immune responses characterized by rapidly diminishing antibody titers. Several treatment options for COVID-19 are emerging, with immunotherapies, peptide therapies, and nucleic acid vaccines showing promise. This review discusses the advances in the immunopathology of SARS-CoV-2, vaccines and therapies under investigation to counter the effects of this virus, as well as viral variants.
Highlights
The recent emergence of Severe Acute Respiratory Syndrome Virus-2 (SARS-CoV-2) in December of 2019 in Wuhan, China causing coronavirus infectious disease-2019, referred to as COVID-19, reaffirms the clinical significance of zoonotic coronaviruses
SARS-CoV-2 has been characterized as causing severe respiratory distress that can lead to pneumonia and acute respiratory distress syndrome (ARDS), as well as clotting abnormalities and stroke [2,3]
With the emergence of the novel coronavirus, SARS-CoV-2, global public health structures were rapidly overwhelmed with COVID-19 cases, in part due to a lack of effective therapies against the virus and a lack of understanding of viral pathology
Summary
The recent emergence of Severe Acute Respiratory Syndrome Virus-2 (SARS-CoV-2) in December of 2019 in Wuhan, China causing coronavirus infectious disease-2019, referred to as COVID-19, reaffirms the clinical significance of zoonotic coronaviruses. Given that reduced ACE2 expression caused by SARS-CoV-2 is associated with inflammation and coagulation, patients with lower baseline levels of ACE2 may have a poorer prognosis from COVID-19, further diminishing the protective role of ACE2 in maintaining a balance between vasoconstriction and vasodilation [20] Other receptors such as CD147 and neuropilin-1 (NRP1) are under active investigation as potential receptors for SARSCoV-2 as well [12,13,14,21,22,23]. This correlates with FCS insertions in the hemagglutinin (HA) cleavage site of highly virulent influenzas that was cleaved by host furin protease [27,28] This could, in part, help explain the infection of cell types that may lack TMPRSS2, as priming of the S protein for fusion is an essential part of the infection process. The results of the studies that are defining the attachment and fusion of SARS-CoV-2 to host cells will better inform the development of therapeutics that may antagonize these processes that are essential the viral life cycle
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