Abstract
A sudden outbreak of COVID-19 caused by a novel coronavirus, SARS-CoV-2, in Wuhan, China in December 2019 quickly grew into a global pandemic, putting at risk not only the global healthcare system, but also the world economy. As the disease continues to spread rapidly, the development of prophylactic and therapeutic approaches is urgently required. Although some progress has been made in understanding the viral structure and invasion mechanism of coronaviruses that may cause severe cases of the syndrome, due to the limited understanding of the immune effects caused by SARS-CoV-2, it is difficult for us to prevent patients from developing acute respiratory distress syndrome (ARDS) and pulmonary fibrosis (PF), the major complications of coronavirus infection. Therefore, any potential treatments should focus not only on direct killing of coronaviruses and prevention strategies by vaccine development, but also on keeping in check the acute immune/inflammatory responses, resulting in ARDS and PF. In addition, potential treatments currently under clinical trials focusing on killing coronaviruses or on developing vaccines preventing coronavirus infection largely ignore the host immune response. However, taking care of SARS-CoV-2 infected patients with ARDS and PF is considered to be the major difficulty. Therefore, further understanding of the host immune response to SARS-CoV-2 is extremely important for clinical resolution and saving medication cost. In addition to a breif overview of the structure, infection mechanism, and possible therapeutic approaches, we summarized and compared the hematopathologic effect and immune responses to SARS-CoV, MERS-CoV, and SARS-CoV-2. We also discussed the indirect immune response caused by SARS and direct infection, replication, and destroying of immune cells by MERS-CoV. The molecular mechanisms of SARS-CoV and MERS-CoV infection-induced lymphopenia or cytokine storm may provide some hint toward fight against SARS-CoV-2, the novel coronavirus. This may provide guidance over using immune therapy as a combined treatment to prevent patients developing severe respiratory syndrome and largely reduce complications.
Highlights
Coronaviruses belong to the Coronaviridae family of the subfamily Coronavirinae
In this review, we discuss three coronaviruses, Severe Acute Respiratory Syndrome (SARS)-CoV, Middle East respiratory syndrome (MERS)-CoV, and SARS CoV-2, from an immunological point of view. We describe their structure and protein composition, mechanisms of entering host cells, and mechanisms to evade innate immune responses
The recent outbreak of the SARS-CoV-2 infection has caused a worldwide crisis in the epidemiology and medical systems
Summary
Coronaviruses belong to the Coronaviridae family of the subfamily Coronavirinae. The viruses of this family have a broad range of animal hosts, and zoonotic transfer between species is common. In this review, we discuss three coronaviruses, SARS-CoV, MERS-CoV, and SARS CoV-2, from an immunological point of view We describe their structure and protein composition, mechanisms of entering host cells, and mechanisms to evade innate immune responses. Coronavirus S protein is a large multifunctional class I viral transmembrane protein, whose size varies from 1,160 amino acids in Infectious Bronchitis Virus (IBV) in poultry to 1,400 amino acids in Feline Coronavirus (FCoV) [11] It is a trimer located on the virion surface, giving the virion a crownlike appearance. The amino acid sequences of the M protein are diverse in different coronaviruses, the structural similarity is maintained overall [15] It has a short N-terminal glycosylated domain outside the virion and a much larger C-terminal domain inside the virion that extends 6–8 nm into the viral particle [16]. Recent studies suggest that the M protein exists as a dimer in the virion, and may adopt two different conformations allowing it to promote membrane curvature, as well as bind to the nucleocapsid [14]
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