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Human bocavirus infection in young children with acute respiratory tract infection in Lanzhou, China

✍ Scribed by Li-shu Zheng; Xin-hui Yuan; Zhi-ping Xie; Yu Jin; Han-chun Gao; Jing-rong Song; Rong-fang Zhang; Zi-qian Xu; Yun-de Hou; Zhao-jun Duan


Publisher
John Wiley and Sons
Year
2010
Tongue
English
Weight
96 KB
Volume
82
Category
Article
ISSN
0146-6615

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✦ Synopsis


Abstract

Human bocavirus (HBoV) is a recognized human parvovirus associated with acute respiratory tract infection. However, HBoV has yet to be established as a causative agent of respiratory disease. In this study, the epidemiological and virological characteristics of HBoV infection were studied in children with acute respiratory tract infection in China. In total, 406 children younger than 14 years of age with acute respiratory tract infection were included in this prospective 1‐year study. HBoV was detected in 29 (7.1%) of the 406 children. No clear seasonal fluctuation was observed in infection rates of HBoV. Of the 29 children infected with HBoV, 16 (55.2%) were coinfected with other respiratory viruses, most commonly respiratory syncytial virus (RSV). Viral coinfection with HBoV did not affect the severity of the respiratory disease (P = 0.291). The number of HBoV genome copies ranged from 5.80 × 10^2^ to 9.72 × 10^8^ copies/ml in nasopharyngeal aspirates among HBoV‐positive specimens by real‐time PCR, and neither coinfection nor the severity of disease correlated with the viral load (P = 0.148, P = 0.354, respectively). The most common clinical features were cough and acute upper respiratory infection, and acute bronchopneumonia. Additionally, the NP‐1 gene of HBoV showed minimal sequence variation. These data suggest that HBoV is frequent in young children with acute respiratory tract infection in Lanzhou, China, and RSV is the most common coinfecting virus. There was no apparent association between the viral load of HBoV and coinfection or disease severity. The NP‐1 gene was highly conserved in HBoV. J. Med. Virol. 82:282–288, 2010. Β© 2009 Wiley‐Liss, Inc.


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