Abstract
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.
Highlights
The human bocavirus (HBoV) is the fourth most common virus detected in respiratory infections [1] and the second autonomous human parvovirus causing respiratory tract infections in all age groups [2, 3].The virus is able to form covalently closed circular DNA that is thought to represent episomal structures persisting in the infected cells [4,5,6]
The bronchoalveolar lavages (BALs) were archived for routine purposes and stored at -80°C before they were subjected to the current analyses
All BALs were routinely tested for all relevant respiratory pathogens, but except for the detection of persisting herpes viruses (HHV), no pathogen other than HBoV
Summary
The human bocavirus (HBoV) is the fourth most common virus detected in respiratory infections [1] and the second autonomous human parvovirus causing respiratory tract infections in all age groups [2, 3]. The virus is able to form covalently closed circular (ccc) DNA that is thought to represent episomal structures persisting in the infected cells [4,5,6]. This assumption could explain the relatively high percentage of asymptomatic HBoV-positive patients in addition to those with primary infection, as the virus persists in a productive but subclinical state [7, 8]. Because it was shown previously that parvoviruses are able to integrate into the host genome [9, 10], and especially parvovirus B19 is associated with several cancers [11,12,13,14,15,16,17,18], colorectal and lung cancer
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