Human rhinovirus group C infection in children with lower respiratory tract infection.
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ABSTRACT:
SUBMITTER: Xiang Z
PROVIDER: S-EPMC2609892 | biostudies-literature | 2008 Oct
REPOSITORIES: biostudies-literature
Publications
Human rhinovirus group C infection in children with lower respiratory tract infection.
Xiang Zichun Z Gonzalez Richard R Xie Zhengde Z Xiao Yan Y Chen Lan L Li Yongjun Y Liu Chunyan C Hu Yinghui Y Yao Yuan Y Qian Suyun S Geng Rong R Vernet Guy G Paranhos-Baccalà Gláucia G Shen Kunling K Jin Qi Q Wang Jianwei J
Emerging infectious diseases 20081001 10
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Project description:ObjectiveTo determine the prevalence of human rhinoviruses (HRV) infections in children with lower respiratory disease in Thailand and monitor the association between species of HRV and clinical presentation in hospitalized paediatric patients.MethodTwo hundred and eighty-nine nasopharyngeal (NP) suction specimens were collected from hospitalized paediatric patients admitted to King Chulalongkorn Memorial Hospital, Thailand during February 2006-2007. Nucleic acids were extracted from each sample with subsequent amplification of VP4/2 by semi-nested RT-PCR for HRV detection. Other viral respiratory pathogens were also detected by PCR, RT-PCR or real time PCR. Nucleotide sequences of the VP4 region were used for genotyping and phylogenetic tree construction.ResultIn total, 87 of 289 specimens were positive for HRV indicating an annual prevalence of 30%. Wheezing or asthma exacerbation was the most common clinical presentation observed in infected patients. Sequence analysis and phylogenetic tree showed that 29 (33%) and 8 (9%) specimens belonged to HRV-A and HRV-B, respectively. Most of the HRV positive samples were HRV-C (58%). Moreover, species C was predominantly found in the paediatric population of Thailand in raining season (p<0.05). The frequency of co-infection of HRV-C with other respiratory viral pathogens was approximately 40%.ConclusionHRV-C represents the predominant species and is one of the etiologic agents in acute lower respiratory tract infection, causes of wheezing and asthma exacerbation in infants and young children in Thailand.
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Project description:Analysis of transcriptional profiles in whole blood from children < 2 years of age (and healthy matched controls) with RSV, rhinovirus and influenza infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity and that RSV infection induces a distinct host response compared with influenza and rhinovirus infection Total RNA extracted from whole blood (lysed in Tempus tubes) drawn from individual pediatric patients with acute RSV, influenza and Rhinovirus lower respiratory tract infection. A total of 241 samples are analyzed: 135 with acute RSV LRTI, 30 with Rhinovirus LRTI, 16 with influenza LRTI, 39 age-sex matched healthy controls and 21 samples obtained one month after the acute hospitalization in children with RSV. Samples GSM1226237-GSM1226272, which were hybridized to Platform GPL10558, were normalized separately from the other Samples in this Series, which were hybridized to Platform GPL6884. 'GSE38900_non-normalized_GSM1226237-GSM1226272.txt.gz' includes the non-normalized data for Samples GSM1226237-GSM1226272; 'GSE38900_non-normalized.txt.gz' includes the non-normalized data for the other Samples.
2013-11-12 | E-GEOD-38900 | biostudies-arrayexpress
Project description:Analysis of transcriptional profiles in whole blood from children < 2 years of age (and healthy matched controls) with RSV, rhinovirus and influenza infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity and that RSV infection induces a distinct host response compared with influenza and rhinovirus infection
2013-11-12 | GSE38900 | GEO
Project description:Recently, HRV-C was identified as a new species of HRV, but its spectrum of clinical disease is still not clear. The purpose of this study was to investigate the molecular epidemiology of HRVs in children with acute lower respiratory tract infections (LRTIs). A total of 54 HRV-positive samples that were negative for other respiratory viruses were sequenced. HRV-A was detected in 33, HRV-B in 4, and HRV-C in 17 of these samples. All HRV-C-positive patients showed favorable clinical outcomes. We confirmed the presence of HRV-C in children with LRTIs, but its association with clinical severity is not clear.
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Project description:OBJECTIVE:This study was performed to further identify the previously uncharacterized human coronavirus 229E (hCoV-229E) and human coronavirus OC43 (hCoV-OC43) in Thailand by using the RT-PCR technique. In addition, we performed this study in order to delineate the prevalence, the potential clinical impacts and evaluation of the genetic characterization of this pathogen in young children who presented with acute lower respiratory tract infections (ALRI). METHODS:We obtained nasopharyngeal secretions (NPs) from 226 children <5 years of age who were either attending the outpatient department or hospitalized with ALRI from March 2002 to July 2003. All clinical, laboratory, RT-PCR, direct sequencing and phylogenetic analysis data were collected and analyzed. RESULTS:Of the 226 NPs samples from infants and young children presented with ALRI, 8 (3.54%) were positive for hCoV-229E, 2 (0.88%) were positive for hCoV-OC43, and 1 (0.44%) had co-infection. The following clinical presentations were noted: fever (100%), rhinitis (44%), acute bronchiolitis (44%), viral pneumonia (33%), viral pneumonia triggering asthma exacerbation (11%) as well as viral pneumonia causing BPD exacerbation (11%). All positive samples were subjected to direct sequencing. The amino acid sequences had 82-99% similarity to previous sequences stored in the GenBank database. CONCLUSION:The molecular technique we applied to detect human coronavirus appears justified as a valuable diagnostic approach to elucidate the prevalence, cause and clinical implications of ALRI among infants and young children.
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Project description:The clinical profile of human rhinovirus (HRV) with regard to lower respiratory infections remains unclear. We analyzed the clinical features and cytokine responses of HRV isolates in children with respiratory infections. Quantitative analysis and genotyping of the HRV-positive samples from 601 nasopharyngeal aspirates (NPAs) were performed using VP4/VP2 sequencing. To compare T-helper1 (Th1) type (IFN-γ, TNF-α) and Th2 type (IL-4, IL-10) cytokine responses between HRV-A, B and C, the levels of the four cytokines were measured. The HRV-positive children had shorter fever duration (P = 0.018), and higher frequencies of chest retraction (P = 0.002) and wheezing (P = 0.022) than did the HRV-negative group. HRV-A was identified in 55 cases (58.5%), HRV-B in 8 (8.5%), and HRV-C in 31 (33.0%). There were no significant differences in the clinical data or NPA cytokines levels between patients with HRV-A and HRV-C infections. HRV is an important pathogen of the lower respiratory tract in young children. HRV-A and HRV-C are the dominant species that cause respiratory difficulty in young children.
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Project description:The 17q21 asthma susceptibility locus includes asthma risk alleles associated with decreased sphingolipid synthesis, likely resulting from increased expression of ORMDL3. ORMDL3 inhibits serine-palmitoyl transferase (SPT), the rate-limiting enzyme of de novo sphingolipid synthesis. There is evidence that decreased sphingolipid synthesis is critical to asthma pathogenesis. Children with asthma and 17q21 asthma risk alleles display decreased sphingolipid synthesis in blood cells. Reduced SPT activity results in airway hyperreactivity, a hallmark feature of asthma. 17q21 asthma risk alleles are also linked to childhood infections with human rhinovirus (RV). This study evaluates the interaction of RV with the de novo sphingolipid synthesis pathway, and the alterative effects of concurrent SPT inhibition in SPT-deficient mice and human airway epithelial cells. In mice, RV infection shifted lung sphingolipid synthesis gene expression to a pattern that resembles genetic SPT deficiency, including decreased expression of Sptssa, a small SPT subunit. This pattern was pronounced in lung epithelial cellular adhesion molecule (EpCAM+) cells and reproduced in human bronchial epithelial cells. RV did not affect Sptssa expression in lung CD45+ immune cells. RV increased sphingolipids unique to the de novo synthesis pathway in mouse lung and human airway epithelial cells. Interestingly, these de novo sphingolipid species were reduced in the blood of RV-infected wild-type mice. RV exacerbated SPT deficiency-associated airway hyperreactivity. Airway inflammation was similar in RV-infected wild-type and SPT-deficient mice. This study reveals the effects of RV infection on the de novo sphingolipid synthesis pathway, elucidating a potential mechanistic link between 17q21 asthma risk alleles and rhinoviral infection.
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