Human rhinovirus group C in hospitalized children, Singapore.
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ABSTRACT:
SUBMITTER: Tan BH
PROVIDER: S-EPMC2815983 | biostudies-literature | 2009 Aug
REPOSITORIES: biostudies-literature
Publications
Human rhinovirus group C in hospitalized children, Singapore.
Tan Boon Huan BH Loo Liat Hui LH Lim Elizabeth Ai-Sim EA Kheng Seah Shirley Lay SL Lin Raymond T P RT Tee Nancy W S NW Sugrue Richard J RJ
Emerging infectious diseases 20090801 8
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Project description: Not available
| S-EPMC2609892 | biostudies-literature
Project description:BackgroundThe clinical impact of common human coronavirus (cHCoV) remains unclear. We studied the clinical manifestations of pediatric cHCoV infections and the possible modifying effects of codetected human rhinovirus (RV) and respiratory syncytial virus (RSV).MethodsWe used data from an 11-year-long prospective study of hospitalized children with community-acquired respiratory tract infections. Nasopharyngeal aspirates were analyzed with real-time polymerase chain reaction assay for cHCoV OC43, NL63, HKU1 and 229E, and 15 other respiratory viruses. We assessed disease severity based on the clinical factors hospitalization length, oxygen requirement, other respiratory support and supplementary fluids.ResultscHCoV was detected in 341 (8%) of 4312 children. Among 104 children with single cHCoV detections, 58 (56%) had lower respiratory tract infection (LRTI) and 20 (19%) developed severe disease. The proportion with severe disease was lower among single cHCoV detections compared with single RSV detections (338 of 870; 39%), but similar to single RV detections (136 of 987; 14%). Compared with single cHCoV, codetected cHCoV-RSV was more often associated with LRTI (86 of 89; 97%) and severe disease (adjusted odds ratio, 3.3; 95% confidence interval: 1.6-6.7). LRTI was more frequent in codetected cHCoV-RV (52 of 68; 76%) than single cHCoV, but the risk of severe disease was lower (adjusted odds ratios, 0.3; 95% confidence interval: 0.1-1.0).ConclusionscHCoV was associated with severe LRTI in hospitalized children. Viral codetections were present in two-thirds. Codetections of cHCoV-RV were associated with lower proportions of severe disease, suggesting a modifying effect of RV on HCoV.
| S-EPMC8826606 | biostudies-literature
Project description:Human Rhinovirus (HRV) classification is an evolving process. New genotypes have been described within HRV-A and HRV-C species, but only one has been accepted related to HRV-B. From 2003 to 2010, a total of 3987 nasopharyngeal aspirate samples were taken from pediatric patients admitted to the Severo Ochoa Hospital in Madrid (Spain). After viral analysis, 949 (23.8%) tested positive to HRV. A random selection of 397 (42%) positive samples showed that 39 (9.8%) were HRV-B. The sequencing of partial VP4/VP2 coding region revealed the spread of 13 of 25 defined HRV-B serotypes and three putative new genotypes. Such results remark the high diversity of HRV-B.
| S-EPMC5855153 | biostudies-literature
Project description:Despite great advances in describing Bordetella pertussis infection, the role of the host microbiota in pertussis pathogenesis remains unexplored. Indeed, the microbiota plays important role in defending against bacterial and viral respiratory infections. We investigated the nasopharyngeal microbiota in infants infected by B. pertussis (Bp), Rhinovirus (Rv) and simultaneously by both infectious agents (Bp + Rv). We demonstrated a specific nasopharyngeal microbiome profiles for Bp group, compared to Rv and Bp + Rv groups, and a reduction of microbial richness during coinfection compared to the single infections. The comparison amongst the three groups showed the increase of Alcaligenaceae and Achromobacter in Bp and Moraxellaceae and Moraxella in Rv group. Furthermore, correlation analysis between patients' features and nasopharyngeal microbiota profile highlighted a link between delivery and feeding modality, antibiotic administration and B. pertussis infection. A model classification demonstrated a microbiota fingerprinting specific of Bp and Rv infections. In conclusion, external factors since the first moments of life contribute to the alteration of nasopharyngeal microbiota, indeed increasing the susceptibility of the host to the pathogens' infections. When the infection is triggered, the presence of infectious agents modifies the microbiota favoring the overgrowth of commensal bacteria that turn in pathobionts, hence contributing to the disease severity.
| S-EPMC8613181 | biostudies-literature
Project description:Four hundred specimens were collected from pediatric patients hospitalized in Singapore; 21 of these specimens tested positive for human metapneumovirus (HMPV), with the A2 genotype predominating. A 5% infection rate was estimated, suggesting that HMPV is a significant cause of morbidity among the pediatric population of Singapore.
| S-EPMC2857288 | biostudies-literature
Project description:Here, the coding-complete genome of a human rhinovirus (HRV) belonging to the HRV-A clade was determined from a pool containing nine nasopharyngeal secretion specimens from hospitalized neonates. PCR screening indicated that this HRV variant was present in a cohort of 45 hospitalized neonates, with a positivity rate of 11.1% (5/45 patients).
| S-EPMC8050964 | biostudies-literature
Project description:Recent developments in molecular diagnostic tools have led to the easy and rapid detection of a large number of rhinovirus (HRV) strains. However, the lack of clinical and epidemiological data hampers the interpretation of these diagnostic findings. From October 2009 to January 2011, we conducted a prospective study in hospitalized children from whom samples were taken for the detection of respiratory viruses. Clinical, epidemiological and microbiological data from 644 patients with 904 disease episodes were collected. When HRV tested positive, strains were further characterized by sequencing the VP4/VP2 region of the HRV genome. HRV was the single respiratory virus detected in 254 disease episodes (28%). Overall, 99 different serotypes were detected (47% HRV-A, 12% HRV-B, 39% HRV-C). Patients with HRV had more underlying pulmonary illness compared with patients with no virus (p 0.01), or patients with another respiratory virus besides HRV (p 0.007). Furthermore, cough, shortness of breath and a need for oxygen were significantly more present in patients with HRV infection. Particularly, patients with HRV-B required extra oxygen. No respiratory symptom, except for oxygen need, was predictive of the presence of HRV. In 22% of HRV-positive disease episodes, HRV infection was hospital acquired. Phylogenetic analysis revealed several clusters of HRV; in more than 25% of these clusters epidemiological information was suggestive of transmission within specific wards. In conclusion, the detection of HRV may help in explaining respiratory illness, particular in patients with pulmonary co-morbidities. Identifying HRV provides opportunities for timely implementation of infection control measures to prevent intra-hospital transmission.
| S-EPMC7129489 | biostudies-literature
Project description:BACKGROUND:Human rhinoviruses (HRVs) are among the most common causes of community-acquired pneumonia (CAP) in children. However, the differential roles of the three HRV species HRV-A, HRV-B, and HRV-C in pediatric CAP are not fully understood. OBJECTIVE:To determine the distribution of HRV species and their roles in children hospitalized with CAP in Beijing, China. STUDY DESIGN:Nasopharyngeal aspirates were collected between April 2007 and March 2008 from 554 children with a primary diagnosis of CAP. HRVs in the clinical samples were detected by RT-PCR and by sequencing. Infections with other respiratory viruses were identified by PCR. RESULTS:HRVs were detected in 99 patients (17.87%). Among these patients, 51.52% tested positive for HRV-A, 38.38% for HRV-C, and 10.10% for HRV-B. HRVs were detected throughout the study period. The monthly distribution of HRV infections varied with HRV species. Median age, gender, symptoms, severity, and duration of hospitalization for single HRV-C infections were similar to those observed for single HRV-A infections. Co-infections with other respiratory viruses were detected in 57.58% of the HRV-positive children. HRV/RSV dual infections were correlated with a higher frequency of shortness of breath (HRV-A group, P(2 tail)= 0.01; HRV-C group, P(2 tail) = 0.015) and lower median ages (HRV-A group, P(2 tail) = 0.049; HRV-C group, P(2 tail) = 0.009). CONCLUSION:Our study shows that HRV-C strains circulate at a prevalence intermediate between HRV-A and HRV-B. The severity of clinical manifestations for HRV-C is comparable to that for HRV-A in children with CAP. These findings point to an important role of both HRV-A and HRV-C in pediatric CAP.
| S-EPMC7185749 | biostudies-literature
Project description:Major- and minor-group rhinoviruses enter their host by binding to the cell surface molecules ICAM-1 and LDL-R, respectively, which are present on both macrophages and epithelial cells. Although epithelial cells are the primary site of productive HRV infection, previous studies have implicated macrophages in establishing the cytokine dysregulation that occurs during rhinovirus-induced asthma exacerbations. Even though major- and minor-group rhinoviruses are nearly genetically identical, these viruses do not replicate with equal success in monocyte-lineage cell lines. In human primary macrophages, differential mitochondrial activity and signaling pathway activation was observed between major- and minor-group rhinovirus upon initial HRV binding, indicating discordant receptor-dependent response to these rhinovirus types. As well, variances in phosphorylation of kinases (p38, JNK, ERK5) and transcription factors (ATF-2, CREB, CEBP-alpha) were observed between the major- and minor- group HRV treatments. The difference between major- and minor- group HRV activation of signaling pathways was confirmed through RNA-sequencing and observation of differential production of the asthma-relevant cytokines CCL20, CCL2, and IL-10. This is the first report of genetically similar viruses eliciting dissimilar cytokine release, transcription factor phosphorylation, and MAPK activation from macrophages. These results suggest that receptor dependence plays a role in establishing the inflammatory microenvironment initiated in part by monocytic-lineage cells in the human airway upon exposure to rhinovirus.
2014-03-14 | GSE55271 | GEO
Project description:Backgroundhuman rhinovirus (HRV) is a major cause of influenza-like illness (ILI) in adults and children. Differences in disease severity by HRV species have been described among hospitalized patients with underlying illness. Less is known about the clinical and virologic characteristics of HRV infection among otherwise healthy populations, particularly adults.Objectivesto characterize molecular epidemiology of HRV and association between HRV species and clinical presentation and viral shedding.Study designobservational, prospective, facility-based study of ILI was conducted from February 2010 to April 2012. Collection of nasopharyngeal specimens, patient symptoms, and clinical information occurred on days 0, 3, 7, and 28. Patients recorded symptom severity daily for the first 7 days of illness in a symptom diary. HRV was identified by RT-PCR and genotyped for species determination. Cases who were co-infected with other viral respiratory pathogens were excluded from the analysis. We evaluated the associations between HRV species, clinical severity, and patterns of viral shedding.Resultseighty-four HRV cases were identified and their isolates genotyped. Of these, 62 (74%) were >18 years. Fifty-four were HRV-A, 11HRV-B, and 19HRV-C. HRV-C infection was more common among children than adults (59% vs. 10%, P<0.001). Among adults, HRV-A was associated with higher severity of upper respiratory symptoms compared to HRV-B (P=0.02), but no such association was found in children. In addition, adults shed HRV-A significantly longer than HRV-C (P trend=0.01).Conclusionsamong otherwise healthy adults with HRV infection, we observed species-specific differences in respiratory symptom severity and duration of viral shedding.
| S-EPMC4347877 | biostudies-literature