The VP1 unique region of human parvovirus B19 and human bocavirus induce lung injury in naïve Balb/c mice.

Both human parvovirus B19 (B19V) and human bocavirus (HBoV) are known to be important human pathogens of the Parvoviridae family. Our earlier investigation demonstrated that both B19V-VP1u and HBoV-VP1u have a significantly disruptive effect on tight junctions (TJs) in A549 cells, implying the essen...

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Bibliographic Details
Main Authors: Chun-Yu Lin, Yu-Han Chung, Ya-Fang Shi, Bor-Show Tzang, Tsai-Ching Hsu
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC6095614?pdf=render
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Summary:Both human parvovirus B19 (B19V) and human bocavirus (HBoV) are known to be important human pathogens of the Parvoviridae family. Our earlier investigation demonstrated that both B19V-VP1u and HBoV-VP1u have a significantly disruptive effect on tight junctions (TJs) in A549 cells, implying the essential role of parvovirus in airway infection and lung injury. However, no direct evidence that B19V-VP1u and HBoV-VP1u induce lung injury exists. The present study further investigates the induction of lung injury by B19V-VP1u and HBoV-VP1u in naïve Balb/c mice following subcutaneous injection of PBS, recombinant B19V-VP1u or HBoV-VP1u. The experimental results reveal significantly increased activity, protein expression and ratio of matrix metalloproteinase-9 (MMP-9) to MMP-2 in Balb/c mice that received B19V-VP1u or HBoV-VP1u compared to those that received PBS. Significantly higher levels of inflammatory cytokines, including IL-6 and IL-1β, and greater lymphocyte infiltration in lung tissue sections were detected in mice that received B19V-VP1u or HBoV-VP1u. Additionally, significantly increased levels of phosphorylated p65 (NF-κB) and MAPK signaling proteins were observed in lung tissue of mice that received B19V-VP1u or HBoV-VP1u compared to those of mice that received PBS. These findings demonstrate for the first time that B19V-VP1u and HBoV-VP1u proteins induce lung inflammatory reactions through p65 (NF-κB) and MAPK signaling.
ISSN:1932-6203