A coronavirus (CoV) commonly known as SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) and causing COVID-19 (coronavirus disease of 2019) has become a pandemic following an outbreak in Wuhan. Although mutations in the SARS-CoV-2 spike glycoprotein (SGP) are obvious from comparative genome studies, the novel infectious nature of the virus, its new varients detected in the UK, and outside and recovery–death ratios of COVID-19 inspired us to review the mechanisms of the infection, replication, release, and transmission of progeny virions and the immune response in the host cell. In addition to the specificity of SARS-CoV-2 binding to angiotensin-converting enzyme 2 receptor and transmembrane protease serine 2, the varied symptoms and severity of the infection by the original and mutated forms of the virus suggest the significance of correlating the host innate and adaptive immunity with the binding of the virus to the mannose receptor via lipopolysaccharides (LPSs), toll-like receptors via LPS/proteins/RNA, and sialic acid (Sia) via hemagglutinin, or sugar-acid segments of glycans. HA-to-Sia binding is considered based on the innate Sia N-acetylneuraminic acid and the acquired Sia N-glycolylneuraminic acid in the epithelial cells and the sialidase/neuraminidase- or esterase-hydrolyzed release and transmission of CoVs. Furthermore, the cytokine storms common to aged humans infected with SARS-CoV-2 and aged macaques infected with SARS-CoV encourage us to articulate the mechanism by which the nuclear capsid protein and RNAs bypass the pattern recognition-induced secretion of interferons (IFNs), which stimulate IFN genes through the Janus-activated kinase-signal transducer and activator of a transcription pathway, leading to the secretion of antiviral proteins such as myxovirus resistance protein A/B. By considering the complexities of the structure, and the infectious nature of the virus and the structures and functions of the molecules involved in CoV infection, replication, and immune response, a new interface among virology, immunology, chemistry, imaging technology, drug delivery, and nanoscience is proposed and will be developed. This interface can be an essential platform for researchers, technologists, and physicians to collaborate and develop vaccines and medicines against COVID-19 and other pandemics in the future.

在武汉爆发之后，通常被称为SARS-CoV-2（严重急性呼吸系统综合症冠状病毒2）并导致COVID-19（2019年冠状病毒病）的冠状病毒（CoV）已成为大流行病。尽管从比较基因组研究中可以明显看出SARS-CoV-2穗糖蛋白（SGP）的突变，但该病毒的新颖感染性，在英国发现的新变体以及COVID-19的外部和恢复-死亡比激发了我们综述子代病毒粒子的感染，复制，释放和传播机制以及宿主细胞中的免疫反应。除了SARS-CoV-2与血管紧张素转化酶2受体和跨膜蛋白酶丝氨酸2结合的特异性外，病毒的原始和突变形式导致的感染症状和严重程度的变化表明，将宿主的先天免疫和适应性免疫与病毒通过脂多糖（LPSs），通过LPS的toll样受体与甘露糖受体的结合相关联的重要性/蛋白质/ RNA和唾液酸（Sia）通过血凝素或聚糖的糖酸片段。基于先天的Sia N-乙酰神经氨酸和上皮细胞中获得的Sia N-糖基神经氨酸以及唾液酸酶/神经氨酸酶或酯酶水解的CoV释放和传递，考虑了HA与Sia的结合。此外，感染SARS-CoV-2的老年人和感染SARS-CoV的老年猕猴常见的细胞因子风暴，促使我们阐明核衣壳蛋白和RNA绕过模式识别诱导的干扰素（IFN）分泌的机制。通过Janus激活的激酶信号转导子和转录途径的激活子刺激IFN基因，从而导致分泌抗病毒蛋白，例如粘液病毒抗性蛋白A / B。考虑到结构的复杂性，病毒的传染性以及与CoV感染，复制和免疫反应有关的分子的结构和功能，在病毒学，免疫学，化学，成像技术，药物输送，提出并将会发展纳米科学。