Coronavirus biology and replication: implications for SARS-CoV-2
By P. V’kovski, A. Kratzel, Silvio Steiner, H. Stalder, V. Thiel. Nature Reviews Microbiology, 2020
2,828 citations recorded by the source corpus.
The SARS-CoV-2 pandemic and its unprecedented global societal and economic disruptive impact has marked the third zoonotic introduction of a highly pathogenic coronavirus into the human population. Although the previous coronavirus SARS-CoV and MERS-CoV epidemics raised awareness of the need for clinically available therapeutic or preventive interventions, to date, no treatments with proven efficacy are available. The development of effective intervention strategies relies on the knowledge of molecular and cellular mechanisms of coronavirus infections, which highlights the significance of studying virus–host interactions at the molecular level to identify targets for antiviral intervention and to elucidate critical viral and host determinants that are decisive for the development of severe disease. In this Review, we summarize the first discoveries that shape our current understanding of SARS-CoV-2 infection throughout the intracellular viral life cycle and relate that to our knowledge of coronavirus biology. The elucidation of similarities and differences between SARS-CoV-2 and other coronaviruses will support future preparedness and strategies to combat coronavirus infections. In this Review, Thiel and colleagues discuss the key aspects of coronavirus biology and their implications for SARS-CoV-2 infections as well as for treatment and prevention strategies.
Subfields: Infectious Diseases
View Paper: https://www.semanticscholar.org/paper/590d0827b156947e1f0563d39644ec71cf8f36d8
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Citations in the corpus
- Host cell-intrinsic innate immune recognition of SARS-CoV-2 (2021, neutral): “Virion assembly and budding occurs along the ER-to-Golgi network, and new virions are released by exocytosis [6].”
- Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant (2021, background): “Detection of the N* sgRNA in B.1.1.7 infected cells can be explained by a triple nucleotide change spanning amino acids R203K/G204R (28881 GGG>AAC), which creates a novel TRS, near a downstream start codon, predicted to generate a short C-terminal form of N called N* 40,47 , which may have innate im”