SARS-CoV-2 and Coronavirus Disease 2019: What We Know So Far

Abstract

In December 2019, a cluster of fatal pneumonia cases presented in Wuhan, China. They were caused by a previously unknown coronavirus. All patients had been associated with the Wuhan Wholefood market, where seafood and live animals are sold. The virus spread rapidly and public health authorities in China initiated a containment effort. However, by that time, travelers had carried the virus to many countries, sparking memories of the previous coronavirus epidemics, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and causing widespread media attention and panic. Based on clinical criteria and available serological and molecular information, the new disease was called coronavirus disease of 2019 , and the novel coronavirus was called SARS Coronavirus-2 (SARS-CoV-2), emphasizing its close relationship to the 2002 SARS virus (SARS-CoV). The scientific community raced to uncover the origin of the virus, understand the pathogenesis of the disease, develop treatment options, define the risk factors, and work on vaccine development. Here we present a summary of current knowledge regarding the novel coronavirus and the disease it causes.

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): An overview of viral structure and host response

“…This virus can enter the human body through its receptors, ACE2 which are found in various organs such as heart, lungs, kidneys, and gastrointestinal tract, thus facilitating viral entry into target cells. The process of CoV entering into the host cell begins through the attachment of the S glycoprotein to the receptor, the ACE2 in the host cells (such as in type II pneumocytes in the lungs) [15]. This attachment occurs in the binding domain of S protein of SARS-CoV-2 receptors which are present at 331 to 524 residues, and can bind strongly to human ACE2 and bat ACE2 [13].…”

“…This attachment occurs in the binding domain of S protein of SARS-CoV-2 receptors which are present at 331 to 524 residues, and can bind strongly to human ACE2 and bat ACE2 [13]. The entry and binding processes are then followed by fusion of the viral membrane and host cell [11] After fusion occurs, the type II transmembrane serine protease (TMPRSS2) that is present on the surface of the host cell will clear the ACE2 and activate the receptor-attached spike-like, S proteins [15].…”

“…The entry of the virus into the host cell triggers stimulation of the host's immune response, which will first be encountered by innate immune system cells via antigen presenting cells (APC), e.g. dendritic cells and macrophages as frontline of the immune system [15,26]. infection.…”

“…IL-17 is a proinflammatory cytokine that also is increased when SARS-CoV2 infection occurs. These cytokines further recruit neutrophils and monocytes to the site of infection and activate several other pro-inflammatory cytokines and chemokines including IL-1, IL-6, IL-8, IL-21, TNF-β, and MCP-1 [15,26,30,31].…”

“…Next, activation of Th1 cells could stimulate CD8 + T cells, which are one of the effectors of T cells that will target and kill cells infected with CoV. At the same time, CD4 T cells could stimulate humoral immune responses by producing antigen-specific antibodies via activating T-dependent B cells [15,28,30].…”