Human Coronavirus: Host-Pathogen Interaction.
By T. S. Fung, D. Liu. Annual Review of Microbiology, 2019
887 citations recorded by the source corpus.
Human coronavirus (HCoV) infection causes respiratory diseases with mild to severe outcomes. In the last 15 years, we have witnessed the emergence of two zoonotic, highly pathogenic HCoVs: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). Replication of HCoV is regulated by a diversity of host factors and induces drastic alterations in cellular structure and physiology. Activation of critical signaling pathways during HCoV infection modulates the induction of antiviral immune response and contributes to the pathogenesis of HCoV. Recent studies have begun to reveal some fundamental aspects of the intricate HCoV-host interaction in mechanistic detail. In this review, we summarize the current knowledge of host factors co-opted and signaling pathways activated during HCoV infection, with an emphasis on HCoV-infection-induced stress response, autophagy, apoptosis, and innate immunity. The cross talk among these pathways, as well as the modulatory strategies utilized by HCoV are also discussed. Expected final online publication date for the Annual Review of Microbiology Volume 73 is September 9, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
Subfields: Animal Science and Zoology, Cell Biology, Infectious Diseases
View Paper: https://www.semanticscholar.org/paper/43a4e0e3cb22981f76e372cba0e9e0ce40932dd1
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Citations in the corpus
- SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues (2020, neutral): “Overall, our data provide motivation to better understand the trade-offs of antiviral and/or IFN therapy in humans infected with SARS-CoV-2 in order to balance host restriction, tissue tolerance, and viral enhancement mechanisms (Davidson et al., 2015; Fung and Liu, 2019; Imai et al., 2005; Iwasaki ”
- Structures of Human Antibodies Bound to SARS-CoV-2 Spike Reveal Common Epitopes and Recurrent Features of Antibodies (2020, positive): “The neutralizing antibody response to coronaviruses is primarily directed against the trimeric spike glycoprotein (S) on the viral membrane envelope, which serves as the machinery to fuse the viral and host cell membranes (Fung and Liu, 2019).”
- The reactome pathway knowledgebase 2022 (2021, positive): “First, starting in March 2020 we curated the infection process mediated by the SARS-CoV-1 coronavirus (10).”
- Autophagy in inflammation, infection, and immunometabolism (2021, background): “Both coronaviruses and autophagy involve formation of intracellular double membranes, albeit they differ (Cottam et al., 2011; Cottam et al., 2014; Fung and Liu, 2019; Gassen, 2020; Prentice et al., 2004; Reggiori et al., 2010).”
- Type I and Type III Interferons – Induction, Signaling, Evasion, and Application to Combat COVID-19 (2020, background): “two decades, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS) (Fung and Liu, 2019).”
- Amplification-free detection of SARS-CoV-2 with CRISPR-Cas13a and mobile phone microscopy (2020, positive): “To confirm the specificity of our crRNAs, we tested themagainst a set of other respiratory viruses, including alphacoronavirus HCoV-NL63 and betacoronaviruses HCoV-OC43 and Middle East respiratory syndrome coronavirus (MERS-CoV), which are among seven coronaviruses that infect human hosts and cause ”
- Current Status of Epidemiology, Diagnosis, Therapeutics, and Vaccines for Novel Coronavirus Disease 2019 (COVID-19) (2020, background): “In general, 15-30% of common colds are caused by human coronaviruses (HCoVs) including HCoV229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1 [5].”
- Predicting commercially available antiviral drugs that may act on the novel coronavirus (SARS-CoV-2) through a drug-target interaction deep learning model (2020, background): “…of the translated polyprotein with viral 3C-like proteinase, 3) replication of gRNA with the viral replication complex that consists of RNA-dependent RNA polymerase (RdRp), helicase, 3 0 -to-5 0 exonuclease, endoRNAse, and 2 0 -O-ribose methyltransferase, and 4) assembly of viral components [11].”