Xu Qi
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Xu Qi has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Benjamin A. Krishna
Department of Medicine, University of Cambridge, Cambridge, CB20QQ, UK
2 shared publications - Christine M. O'COnnor
Infection Biology, Sheikha Fatima bint Mubarak Global Center for Pathogen and Human Health Research, Cleveland Clinic Research, Cleveland Clinic
2 shared publications - Michael C. Kelly
Infection Biology, Sheikha Fatima Bint Mubarak Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA; Case Comprehensive Cancer Center, Cleveland, OH, 44106, USA
2 shared publications - Vargab Baruah
Infection Biology, Sheikha Fatima bint Mubarak Global Center for Pathogen and Human Health Research, Cleveland Clinic Research, Cleveland Clinic
2 shared publications
Latest Publications
- Open Access
- 16 April 2025
- Published by Elsevier in Antiviral Research
- Vol. 238, 106169
Inhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34+ Kasumi-3 cells
- 16 April 2025
- Published by Elsevier in Antiviral Research
- Vol. 238, 106169
Open AccessInhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34+ Kasumi-3 cells
- Open Access
Inhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34 + Kasumi-3 cells
Reactivation of latent human cytomegalovirus (CMV) can lead to severe complications in individuals with dysregulated immune systems. While antiviral therapies for CMV are approved, these compounds are limited by their toxicity and inability to specifically target the latent reservoir or prevent reactivation. Herein we show that CMV reactivation in Kasumi-3 cells, a CD34 + hematopoietic cell line, requires mitogen-activated protein kinase (MAPK) activation. Importantly, pharmacological inhibition of the MAPK signaling pathway, including MEK and ERK, restricts viral reactivation in Kasumi-3 cells. In sum, our findings show MAPK signaling is critical for CMV reactivation, revealing a potential avenue for therapeutic intervention to prevent viral reactivation and downstream pathogenesis that is often detrimental for immunosuppressed and immunocompromised patients.
Open AccessInhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34 + Kasumi-3 cells
Reactivation of latent human cytomegalovirus (CMV) can lead to severe complications in individuals with dysregulated immune systems. While antiviral therapies for CMV are approved, these compounds are limited by their toxicity and inability to specifically target the latent reservoir or prevent reactivation. Herein we show that CMV reactivation in Kasumi-3 cells, a CD34 + hematopoietic cell line, requires mitogen-activated protein kinase (MAPK) activation. Importantly, pharmacological inhibition of the MAPK signaling pathway, including MEK and ERK, restricts viral reactivation in Kasumi-3 cells. In sum, our findings show MAPK signaling is critical for CMV reactivation, revealing a potential avenue for therapeutic intervention to prevent viral reactivation and downstream pathogenesis that is often detrimental for immunosuppressed and immunocompromised patients.