Effects of rhinovirus species on viral replication and cytokine production

Kazuyuki Nakagome, Yury A. Bochkov, Shamaila Ashraf, Rebecca A. Brockman-Schneider, Michael D. Evans, Thomas R. Pasic, James E. Gern

Research output: Contribution to journalArticlepeer-review

64 Scopus citations

Abstract

Background Epidemiologic studies provide evidence of differential virulence of rhinovirus species (RV). We recently reported that RV-A and RV-C induced more severe illnesses than RV-B, which suggests that the biology of RV-B might be different from RV-A or RV-C. Objective To test the hypothesis that RV-B has lower replication and induces lesser cytokine responses than RV-A or RV-C. Methods We cloned full-length cDNA of RV-A16, A36, B52, B72, C2, C15, and C41 from clinical samples and grew clinical isolates of RV-A7 and RV-B6 in cultured cells. Sinus epithelial cells were differentiated at the air-liquid interface. We tested for differences in viral replication in epithelial cells after infection with purified viruses (108 RNA copies) and measured virus load by quantitative RT-PCR. We measured lactate dehydrogenase (LDH) concentration as a marker of cellular cytotoxicity, and cytokine and/or chemokine secretion by multiplex ELISA. Results At 24 hours after infection, the virus load of RV-B (RV-B52, RV-B72, or RV-B6) in adherent cells was lower than that of RV-A or RV-C. The growth kinetics of infection indicated that RV-B types replicate more slowly. Furthermore, RV-B released less LDH than RV-A or RV-C, and induced lower levels of cytokines and chemokines such as CXCL10, even after correction for viral replication. RV-B replicates to lower levels also in primary bronchial epithelial cells. Conclusions Our results indicate that RV-B types have lower and slower replication, and lower cellular cytotoxicity and cytokine and/or chemokine production compared with RV-A or RV-C. These characteristics may contribute to reduced severity of illnesses that has been observed with RV-B infections.

Original languageEnglish (US)
Pages (from-to)332-341.e10
JournalJournal of Allergy and Clinical Immunology
Volume134
Issue number2
DOIs
StatePublished - Aug 2014
Externally publishedYes

Bibliographical note

Funding Information:
Supported by National Institute of Health grants U19 AI104317 and P01 HL070831 , and by the Banyu Fellowship Program sponsored by Banyu Life Science Foundation International (K. Nakagome).

Funding Information:
Conflicts of interest: K. Nakagome has received research support from the National Institutes of Health (NIH) and from Banyu Life Science Foundation International . Y. A. Bochkov, S. Ashraf, R. A. Brockman-Schneider, M. D. Evans, and T. R. Pasic have received research support from the NIH . J. E. Gern has received consultancy fees from Merck, GlaxoSmithKline, Biota, Centocor, Boehringer Ingelheim, MedImmune, Theraclone, and Gilead; and has received research support from the NIH , Merck , AstraZeneca , and GlaxoSmithKline .

Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.

Keywords

  • Asthma
  • cellular cytotoxicity
  • chemokine
  • cytokine
  • rhinovirus

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