Kexin Yan

1 month ago | dx.doi.org | Fang Yuan |Kexin Yan |Yan Zhang |Yudong Li

Nov 12, 2024 | journals.plos.org | Agnes Carolin |Kexin Yan |Cameron Bishop |Bing Tang

Citation: Carolin A, Yan K, Bishop CR, Tang B, Nguyen W, Rawle DJ, et al. (2024) Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice. PLoS ONE 19(11): e0302344. https://doi.org/10.1371/journal.pone.0302344Editor: Engin Berber, Lerner Research Institute - Cleveland Clinic, UNITED STATES OF AMERICAReceived: April 25, 2024; Accepted: October 17, 2024; Published: November 12, 2024Copyright: © 2024 Carolin et al.

Jul 25, 2024 | biorxiv.org | Agnes Carolin |Cameron Bishop |Kexin Yan |Wilson Nguyen

AbstractThe severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes Coronavirus Disease 2019 (COVID-19), which can result in severe disease often characterised by a 'cytokine storm' and the associated acute respiratory distress syndrome. However, many infections with SARS-CoV-2 are mild or asymptomatic throughout the course of infection.

May 29, 2024 | biorxiv.org | David Frazer |Kexin Yan |Cameron Bishop |Agnes Carolin

AbstractThe severity of Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is often dictated by a range of comorbidities. A considerable literature suggests iron deficiency and iron overload may contribute to increased infection, inflammation and disease severity, although direct causal relationships have been difficult to establish.

May 8, 2024 | biorxiv.org | Kexin Yan |Troy Dumenil |Romal Stewart |Cameron Bishop

AbstractAngiotensin converting enzyme 2 (ACE2) serves as the primary entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, ACE2-independent entry has been observed in vitro for SARS-CoV-2 strains containing the E484D amino acid substitution in the spike protein. In this study, we conducted a whole genome CRISPR-Cas9 knockout screen using a SARS-CoV-2 strain containing the spike-E484D substitution (SARS-CoV-2MA1) to identify the ACE2-independent entry mechanisms.