Since the outbreak of the SARS-CoV-2, the spread of COVID-19 and its impact on public health have continued to ferment. Researchers around the world are working to deepen their understanding of coronaviruses with a view to quickly determine future treatment options and possible vaccine targets. As a global supplier of life sciences, during this special period, Elabscience® is committed to providing necessary products and services for researchers, developers and manufacturers to help them cope with 2019-nCoV.
SARS-CoV-2 structural proteins have important functions in pathogenesis as well as infectious virus assembly. These include spike protein (S protein), envelope protein (E protein), membrane protein (M protein) and nucleocapsid protein (N protein), which are all encoded by the 3’-end of the virus genome.
The recently sequenced genomes of SARS-CoV-2 strains combined with the comparative analysis of the SARS-CoV genome organization and transcription allowed us to construct a tentative list of gene products. It was suggested that SARS-CoV-2 had 16 predicted non-structural proteins (referred to nsp1-nsp16) constituting polyproteins pp1a and pp1ab, which were translated from ORF1a and ORF1ab of the virus genome.
The invasion of host cells is the most important part of coronavirus (CoV) infection. The envelope spike (S) glycoprotein is responsible for CoV cell entry and host-to-host transmission. For productive entry into host cells, viruses attach to specific cell surface receptor molecules. This is the case of CoV, whose use of distinct entry receptor molecules is responsible for their broad host range and tissue tropism.
After the virus invades the body, if the body cannot produce enough specific immune response to effectively remove the virus, it will continue to strengthen the non-specific inflammatory response to eliminate the virus in an inefficient way. This not only cannot effectively remove the virus but will aggravate infection, tissue ischemia and hypoxia and even necrosis, and eventually lead to non-specific inflammatory response out of control to trigger cytokine storms.