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Abstract
The novel coronavirus designated as SARS-CoV-2 is the etiological agent of coronavirus disease 2019 (COVID-19), which rendered the care of the global health powerless and plunged the world economy into a historic decline. This disease is characterized by different clinical pictures; ranging from asymptomatic mild phase to severe illness with acute respiratory distress syndrome (ARDS), in addition to having no specific therapy. The protective immunity involving solid CD4+ T-cells, viral specific CD8+ T-cells and the neutralizing immunoglobulins have been established in most of the convalescent COVID-19 individuals. On the other hand, the host immune response to severe COVID-19 infection has been attributed to the inflammatory cytokine storm, and to influx of the activated immune cells to the lungs; leading to severe pneumonia, extensive ARDS and finally to death. Despite of this, the protective and pathogenic aspects of the human immunity have not been fully elucidated. Recent attempts conducted by several published research works have focused on information derived from the immune responses to the severe acute respiratory syndrome-related coronavirus diseases (mainly; SARS and MERS). However, these works lack sufficiency due to variations in the transmissibility, virulence, host-virus interactions and the immune evasion mechanisms. Hence, adequate understanding of the host immune response mechanisms to SARS-CoV-2 will generate the impetus towards effective control and preventive measures. The objectives of this article were to provide an overview of the host immune responses to SARS-CoV-2 infection, the viral immune evasion strategies, and to define certain knowledge gaps that require further studies.
Highlights
Coronaviruses are spherical-shaped enveloped, non-segmented positive-sensed RNA viruses, which belong to the subfamily Coronavirinae of the familyCoronaviridae
Shi et al, (2020); Shurin et al, (2020); Thevarajan et al, (2020) added that the host immune responses in COVID-19 seem to be in two-stages; a protective response observed in most patients with mild or no clinical symptoms, and pathogenic response characterized by hyper-activation of some subsets of immune cells; increased viral propagation, inflammatory cytokine storm (ICS), acute respiratory distress syndrome (ARDS) and massive destruction of the affected tissues, which are observed in severe COVID-19 patients when the protective response is impaired
The COVID-19 pandemic caused by severe acute respiratory syndrome (SARS)-CoV2 is a multifactorial pathophysiological process involving pro-inflammatory cytokines; chemokines, blood cells, activated immune cells and residential tissue cells
Summary
Coronaviruses are spherical-shaped enveloped, non-segmented positive-sensed RNA viruses, which belong to the subfamily Coronavirinae of the family. Recent studies conducted by Cleri et al, (2010); Naeem, (2014); Rokni et al, (2020); Yang et al, (2020a) reported that these viruses are responsible for the major epidemics in the past two decades. Infections with the latter group have been reported to cause severe immunopathological responses, which result in fatal pneumonia. Liang et al, (2020); Shah et al, (2020) reported that significant efforts have been made to unravel the immunity surrounding this pandemic; much of these efforts were predictive knowledge derived from the host immune responses to acute respiratory syndrome-related coronavirus diseases, severe acute respiratory syndrome (SARS) and Middle-East respiratory syndrome (MERS). It highlights some gray areas of research requiring further exploration
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