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Wang J.,Chongqing Medical University | Wang J.,Ministry of Education Key Laboratory of Child Development and Disorders | Wang J.,Key Laboratory of Pediatrics in Chongqing CSTC2009CA5002 | Huang Y.,Chongqing Medical University | And 4 more authors.
Tuberculosis | Year: 2011

In vitro and in animal studies have suggested an important role for the Mycobacterium tuberculosis PE-PGRS33 protein in the pathogenesis of TB. A significant level of PE-PGRS33 gene DNA polymorphism among clinical isolates from adult tuberculosis (TB) patients and its association with clinical and epidemiological phenotypes of the disease has been found. To better understand the role of PE-PGRS33 protein in the pathogenesis pediatric TB, we investigated DNA polymorphism of the PE-PGRS33 gene among 101 of pediatric TB patients' isolates and assessed the relationship between the PE-PGRS33 sequence variation and clinical characteristics of TB. Twelve different PE-PGRS33 sequence variations representing 12 different alleles were observed among the 101 M. tuberculosis clinical isolates investigated. Of these 101 isolates, 62(59.41%) had PE-PGRS33 alleles that would result in a change in the amino acid sequence of the PE-PGRS33 protein. The degree of DNA polymorphism within individual M. tuberculosis isolates from pediatric TB patients was remarkably lower than that previously found in M. tuberculosis isolates from adults TB patients. The frequency distribution of isolates having PE-PGRS33 gene sequence variations was similar between Beijing and non-Beijing families of the pathogen. Patients having TB meningitis and negative PPD skin test results appeared to be more likely to be infected by isolates having a mutant type of the PE-PGRS33 gene than patients who had no TB meningitis (OR 2.54, 95% CI [1.11-5.84]) and patients who had positive PPD-skin test results (OR 4.26, 95% CI [1.14-12.86]), respectively. This study provides new insight into the molecular pathogenesis of pediatric TB. © 2011 Elsevier Ltd. All rights reserved.

Xu L.-J.,Chongqing Medical University | Xu L.-J.,Key Laboratory of Child Development and Disorders | Xu L.-J.,Key Laboratory of Pediatrics in Chongqing CSTC2009CA5002 | Xu L.-J.,Cooperation Technology | And 7 more authors.
Virology Journal | Year: 2013

Background: Japanese encephalitis virus (JEV) is one of the major causative agents of viral encephalitis in East Asia, Southeast Asia and Australia. However, no clinical JEV strain has yet been isolated from JE patients in Chongqing, China. In this study, we report the genomic analysis of a new JEV strain, CQ11-66, isolated from a pediatric patient in Chongqing, China. Findings. Virus isolation was carried out in BHK-21 cells. Nested PCR was used to detect and isolate the JEV strain, and computer analysis of phylogenetic relationships, nucleic acid homology studies and deduction of the amino acid sequence were conducted using ClustalX (1.8) and Mega5 software. The JEV strain CQ11-66 was isolated from patient cerebrospinal fluid. The sequenced genome of CQ11-66 was 10,863 nucleotides in length, whereas other strains, such as SX09S-01, contain 10,965 nucleotides. Sequence comparison of the CQ11-66 polyprotein open reading frame (ORF) with those of 21 other JEV strains revealed that the nucleotide sequence divergence ranged from 1.68% to 18.46%. Sequence analysis of the full-length CQ11-66 E gene sequence with those of 30 other JEV isolates also identified nucleotide divergence, ranging from 1.69% to 18.74%. Phylogenetic analyses indicated that the CQ11-66 strain belonged to genotype III. Conclusions: JEV genotype III still circulates in Chongqing and it is therefore important for active surveillance of JEV genotype III to be conducted in the pediatric population. © 2013 Xu et al.; licensee BioMed Central Ltd.

Ren Z.,Chongqing Medical University | Ren Z.,Key Laboratory of Pediatrics in Chongqing CSTC2009CA5002 | Kong Y.,Chongqing Medical University | Kong Y.,Key Laboratory of Pediatrics in Chongqing CSTC2009CA5002 | And 6 more authors.
BMC Infectious Diseases | Year: 2013

Background: Enteric viruses are a major cause of diarrhea in children, especially those <5 years old. Identifying the viral agents is critical to the development of effective preventive measures. This study aimed to determine the prevalence of common enteric viruses in children <5 years old presented with diarrhea to the Children's Hospital of Chongqing Medical University.Methods: Five hundred fecal samples were collected between August and November 2010 from children <5 years of age who presented with acute diarrhea at the Children's Hospital of Chongqing Medical University. All samples were tested for rotaviruses A, B, and C, noroviruses GI and GII, adenovirus, sapovirus, and astrovirus using enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction (RT-PCR), or PCR. Partial sequences of norovirus, sapovirus, adenovirus, and astrovirus were phylogenetically analyzed to determine the genotype.Results: Enteric viruses were detected in 302 of the 500 children who presented with acute diarrhea (277/477; 58.07%) and persistent diarrhea (5/23; 21.74%). In 277 samples from children with acute diarrhea in whom at least one viral agent was found, rotavirus A was the most frequent virus identified (132 cases; 27.67%), followed by norovirus GII in 130 cases (27.25%), adenovirus in 30 cases (6.29%), sapovirus in 9 cases (1.89%) and astrovirus in one case (0.21%). Twenty-two of the norovirus GII-positive cases were randomly selected for genotyping. GII/4 was the predominant strain, followed by GII/6, GII/2, GII/3, and GII/7. Sapovirus was classified into four genotypes: GI/1 was predominant, followed by GI/2, GII/1, and GIV. The predominant adenovirus was type 41. Mixed infections were found in 25 cases, all of which presented with acute diarrhea (25/477; 5.24%). Viruses were positive in 5/23 (21.74%) cases with persistent diarrhea. Neither rotavirus B, rotavirus C, nor norovirus GI were found in any of the samples.Conclusions: Enteric viruses are a major cause of diarrhea in children <5 years old in Chongqing. Rotavirus A is the most common etiological agent, follow by norovirus. © 2013 Ren et al.; licensee BioMed Central Ltd.

Zhou L.,Chongqing International Science And Technology Coop Center For Child Development And Disorders | Zhou L.,Key Laboratory of Pediatrics in Chongqing CSTC2009CA5002 | Xiao Q.,Chongqing International Science And Technology Coop Center For Child Development And Disorders | Xiao Q.,Key Laboratory of Pediatrics in Chongqing CSTC2009CA5002 | And 6 more authors.
Journal of Medical Virology | Year: 2015

The impact of dynamic respiratory syncytial virus (RSV) load on the clinical severity of hospitalized infants with bronchiolitis has not been clarified. Nasopharyngeal aspirates were obtained from 60 infants who were diagnosed with bronchiolitis within 96hr of wheezing onset upon admission and on days 3, 5, and 7 in the hospital, and 17 respiratory viruses were detected. The RSV load was quantified by real-time qPCR for RSV subtypes A and B at different time points. Scoring criteria were used to evaluate the degree of severity. A total of 40 infants were determined to be RSV-positive, nine were identified as RSV subtype A (RSVA), and 31 were RSV subtype B (RSVB). The peak RSV load was observed upon admission, and the RSV load decreased significantly over time; in addition, this decrease began to have significant differences on day 5. There was a positive correlation between the RSV load and the clinical score (r2=0.121 and P<0.001). According to the clinical scores, the infants in the severe group tended to have higher RSV loads than those in the moderate and mild groups. Multivariate logistic regression models revealed that the viral load on day 3 was independently associated with the degree of severity. This study elucidated that a higher mean RSV load was associated with a more severe disease and a longer duration of hospitalization and symptoms. This study also clarified RSV replication in infants and provides a theoretical basis for specifying an anti-RSV therapy strategy. © 2015 Wiley Periodicals, Inc..

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