Next Article in Journal
Twelfth International Foamy Virus Conference—Meeting Report
Previous Article in Journal
Crosstalk between Autophagy and Type I Interferon Responses in Innate Antiviral Immunity
Article Menu
Issue 2 (February) cover image

Export Article

Open AccessArticle
Viruses 2019, 11(2), 133;

Non-Structural Protein 2B of Human Rhinovirus 16 Activates Both PERK and ATF6 Rather Than IRE1 to Trigger ER Stress

State Key Laboratory for Infectious Disease Prevention and Control, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, 155 Changbai Road, Beijing 102206, China
Author to whom correspondence should be addressed.
Received: 17 December 2018 / Revised: 26 January 2019 / Accepted: 29 January 2019 / Published: 1 February 2019
(This article belongs to the Section Antivirals & Vaccines)
Full-Text   |   PDF [2404 KB, uploaded 2 February 2019]   |  
  |   Review Reports


To understand the underlying mechanisms of endoplasmic reticulum (ER) stress caused by human rhinovirus (HRV) 16 and non-structural transmembrane protein 2B, the expressions of ER chaperone glucose-regulated protein 78 (GRP78) and three signal transduction pathways, including protein kinase RNA-like ER kinase (PERK), activating transcription factor 6 (ATF6) and inositol-requiring enzyme 1 (IRE1), were evaluated after HRV16 infection and 2B gene transfection. Our results showed that both HRV16 infection and 2B gene transfection increased the expression of ER chaperone GRP78, and induced phosphorylation of PERK and cleavage of ATF6 in a time-dependent manner. Our data also revealed that the HRV16 2B protein was localized to the ER membrane. However, both HRV16 infection and HRV16 2B gene transfection did not induce ER stress through the IRE1 pathway. Moreover, our results showed that apoptosis occurred in H1-HeLa cells infected with HRV16 or transfected with 2B gene accompanied with increased expression of CHOP and cleaved caspase-3. Taken together, non-structural protein 2B of HRV16 induced an ER stress response through the PERK and ATF6 pathways rather than the IRE1 pathway. View Full-Text
Keywords: HRV16 2B protein; endoplasmic reticulum stress; PERK; ATF6; IRE1 HRV16 2B protein; endoplasmic reticulum stress; PERK; ATF6; IRE1

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Song, J.; Chi, M.; Luo, X.; Song, Q.; Xia, D.; Shi, B.; Han, J. Non-Structural Protein 2B of Human Rhinovirus 16 Activates Both PERK and ATF6 Rather Than IRE1 to Trigger ER Stress. Viruses 2019, 11, 133.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top