miércoles, 23 de junio de 2010
Saffold Cardioviruses in Children, China | CDC EID
EID Journal Home > Volume 16, Number 7–July 2010
Volume 16, Number 7–July 2010
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Saffold Cardioviruses of 3 Lineages in Children with Respiratory Tract Infections, Beijing, China
Lili Ren, Richard Gonzalez, Zhengde Xie, Yan Xiao, Yongjun Li, Chunyan Liu, Lan Chen, Qingqing Yang, Guy Vernet, Gláucia Paranhos-Baccalà, Qi Jin, Kunling Shen, and Jianwei Wang
Author affiliations: State Key Laboratory for Molecular Virology and Genetic Engineering, Beijing, People's Republic of China (L. Ren, Q. Jin, J. Wang); Institute of Pathogen Biology, Beijing (L. Ren, R. Gonzalez, Y. Xiao, L. Chen, Q. Yang, Q. Jin, J. Wang); Fondation Mérieux, Lyon, France (R. Gonzalez, Y. Li, G. Vernet, G. Paranhos-Baccalà); and Beijing Children's Hospital, Beijing (Z. Xie, C. Liu, K. Shen)
Suggested citation for this article
Abstract
To clarify the potential for respiratory transmission of Saffold cardiovirus (SAFV) and characterize the pathogen, we analyzed respiratory specimens from 1,558 pediatric patients in Beijing. We detected SAFV in 7 (0.5%) patients and identified lineages 1–3. However, because 3 patients had co-infections, we could not definitively say SAFV caused disease.
Saffold cardiovirus (SAFV) is a new piconavirus, originally identified from fecal samples of a female infant with fever of unknown origin (1). SAFV has since been reported worldwide, and 8 lineages have been identified (1–6). Although serologic surveys have shown that SAFV-3 infection occurs early in life (7), the pathogenicity of SAFV is still unclear.
Because SAFVs are mainly detected in fecal samples, virus transmission is thought to occur by the fecal–oral route (1,3–7). However, 2 research groups also found SAFV-2 lineage in respiratory secretions (2,4). Thus, we investigated whether the respiratory tract route could be an additional transmission route and whether SAFV lineages other than SAFV-2 may also infect the respiratory tract. We identified and characterized 7 SAFV strains, which belonged to 3 distinct lineages, from respiratory samples of children with lower and upper respiratory tract infections (LRTIs and URTIs, respectively).
The Study
We assessed 2 cohorts. Cohort 1 comprised 1,032 children (617 boys and 415 girls) with acute LRTIs, hospitalized in Beijing Children's Hospital (BCH), from whom nasopharyngeal aspirates were collected from May 2007 through March 2009. The patients ranged in age from 2 weeks to 16 years (mean age 31.3 months, median 9 months). Cohort 2 comprised 506 BCH outpatient children (277 boys and 229 girls) with acute URTIs, from whom throat swabs were collected from May through August 2009. These patients ranged in age from 4 months to 16 years (mean age 46.7 months, median 37 months).
Virus nucleic acids in clinical samples were extracted by using the NucliSens easyMAG system (bioMérieux, Marcy-l'Etoile, France) according to the manufacturer's instructions. SAFV RNA was detected by nested reverse transcription–PCR (RT-PCR) by using primers selective for the 5´ untranslated region (UTR) (3). The viral protein (VP) 1 gene was amplified by using 3 pairs of primers as previously described (3,5,6). The full genomic sequences were obtained by a genome walking method (7). The 5´ and 3´ UTR sequences were determined by using the RACE System (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's protocol. After being cloned into the pGEM-T Easy vector (Promega, Madison, WI, USA), all PCR products were verified by sequencing. In addition, all screened specimens were tested for known respiratory viruses as previously described (8,9). Mycoplasma pneumoniae was detected by using the gelatin particle agglutination test kit (SERODIA-MYCO II, Fujirebio, Japan).
For phylogenetic analysis, we constructed neighbor-joining trees based on the distances of SAFV nucleotide or amino acid sequences by using MEGA 4.0 (10). We used SimPlot (version 3.5.1) to analyze possible recombination between viral genome sequences (11).
LLC-MK2 cells were used to isolate SAFV as previously described (12). Cells were collected either when cytopathic effects were observed or after 12 days postinoculation, and then they were tested for SAFV by RT-PCR.
We detected SAFV RNA in 4 (0.4%) of the 1,032 nasopharyngeal aspirates from patients with LRTIs and in 3 (0.6%) of the 506 throat swab specimens from outpatients with URTIs. The SAFV-positive patients (4 girls and 3 boys) were 5 months to 9 years of age (Table). SAFV infection did not appear to have a predominant time for occurrence: cases were detected in a range of months for the periods covered (August and December 2007, October and November 2008, and June 2009). All SAFV-positive patients exhibited symptoms of respiratory tract infection, such as coughing, gasping, sneezing, or fever. Of the 4 SAFV-positive patients with LRTIs, 2 had underlying illnesses, i.e., tuberculosis, hepatic dysfunction, or respiratory failure (Table). All SAFV-positive patients recovered within 7–11 days. No major differences were found in disease duration between patients who had underlying diseases and those who did not.
Co-infections with additional respiratory pathogens were detected for 3 of 7 SAFV-positive patients, all in the first cohort. These pathogens were respiratory syncytial virus (1 patient), enterovirus (1 patient), and M. pneumoniae (1 patient) (Table). A SAFV-3 strain was isolated from sample BCH1031. Starting at 5 days postinoculation, cytopathic effects were observed. Virus was not isolated from other SAFV-positive samples (data not shown).
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Saffold Cardioviruses in Children, China | CDC EID
Suggested Citation for this Article
Ren L, Gonzalez R, Xie Z, Xiao Y, Li Y, Liu C, et al. Saffold cardioviruses of 3 lineages in children with respiratory tract infections, Beijing, China. Emerg Infect Dis [serial on the Internet]. 2010 Jul [date cited]. Available from http://www.cdc.gov/EID/content/16/7/1158.htm
DOI: 10.3201/eid1607.091682
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