Lung Infection by Human Bocavirus Induces the Release of Profibrotic Mediator Cytokines In Vivo and In Vitro

PLoS One. 2016 Jan 25;11(1):e0147010. doi: 10.1371/journal.pone.0147010. eCollection 2016.


Human Bocavirus subtype 1 (HBoV1) is associated with respiratory diseases and may contribute to chronic lung diseases by persisting in the infected host. Here the question was addressed if HBoV infections could contribute to fibrogenesis processes as suggested by previously published clinical observations. Cytokine profiles induced by HBoV infection in CuFi-8 air-liquid interphase cell cultures and in bronchoalveolar lavage fluid (BALF) of 20 HBoV-positive and 12 HBoV-negative patients were analysed by semi-quantitative Western spot blot analyses. Although lots of cytokines were regulated independently of HBoV status, several cytokines associated with lung fibrosis and tumour development, e.g., EGF, VEGF, TARC (CCL17), TNF-α, TNF-β, TIMP-1, were clearly upregulated in the HBoV-positive cohort. These findings suggest that the development of lung fibrosis might be triggered by HBoV induced cytokine expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Alveolar Epithelial Cells / metabolism
  • Alveolar Epithelial Cells / virology
  • Bronchoalveolar Lavage Fluid / chemistry
  • Cells, Cultured
  • Chronic Disease
  • Coinfection
  • Cytokines / biosynthesis
  • Cytokines / metabolism*
  • HEK293 Cells
  • Human bocavirus / physiology*
  • Humans
  • Lung / virology*
  • Lung Diseases, Interstitial / complications
  • Lung Diseases, Interstitial / physiopathology
  • Lung Diseases, Interstitial / virology
  • Middle Aged
  • Parvoviridae Infections / physiopathology*
  • Pneumonia, Viral / complications
  • Pneumonia, Viral / physiopathology*
  • Pneumonia, Viral / virology
  • Pulmonary Fibrosis / etiology
  • Pulmonary Fibrosis / physiopathology
  • Pulmonary Fibrosis / virology
  • Retrospective Studies
  • Up-Regulation


  • Cytokines

Grant support

This study was supported by research grants from the Else Kröner-Fresenius Stiftung (Germany) (grant number A100_2013 to VS), the Beatrix-Lichtken-Stifung (Germany) (grant for HBoV Research to OS), and the Private University of Witten/Herdecke (internal grant to VS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.