For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
49
views
35
references
 Top references
cited by
78
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      192
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Molecular modeling, organ culture and reverse genetics for a newly identified human rhinovirus C

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A recently recognized human rhinovirus species C (HRV-C) is associated with up to half of HRV infections in young children. We for the first time propagated two HRV-C isolates ex vivo in organ culture of nasal epithelial cells, sequenced a new C15 isolate, and developed the first reverse genetics system for HRV-C. Using contact points for the known HRV receptors, intercellular adhesion molecule 1 (ICAM-1) and low density lipoprotein receptor (LDLR), inter- and intraspecies footprint analysis predicted a unique cell attachment site for HRV-Cs. Antibodies directed to binding sites for HRV-A and -B failed to inhibit HRV-C attachment, consistent with the alternative receptor footprint. HRV-A and -B infected HeLa and WisL cells, but HRV-C did not. However, HRV-C RNA synthesized in vitro and transfected into both cell types resulted in cytopathic effect and recovery of functional virus, indicating that the viral attachment mechanism is a primary distinguishing feature of HRV-C.

          Related collections

          Most cited references35

          • Record: found
          • Abstract: found
          • Article: not found

          Wheezing rhinovirus illnesses in early life predict asthma development in high-risk children.

          Daniel J. Jackson, Ronald Gangnon, Michael D C Evans … (2008)
          Virus-induced wheezing episodes in infancy often precede the development of asthma. Whether infections with specific viral pathogens confer differential future asthma risk is incompletely understood. To define the relationship between specific viral illnesses and early childhood asthma development. A total of 259 children were followed prospectively from birth to 6 years of age. The etiology and timing of specific viral wheezing respiratory illnesses during early childhood were assessed using nasal lavage, culture, and multiplex reverse transcriptase-polymerase chain reaction. The relationships of these virus-specific wheezing illnesses and other risk factors to the development of asthma were analyzed. Viral etiologies were identified in 90% of wheezing illnesses. From birth to age 3 years, wheezing with respiratory syncytial virus (RSV) (odds ratio [OR], 2.6), rhinovirus (RV) (OR, 9.8), or both RV and RSV (OR , 10) was associated with increased asthma risk at age 6 years. In Year 1, both RV wheezing (OR, 2.8) and aeroallergen sensitization (OR, 3.6) independently increased asthma risk at age 6 years. By age 3 years, wheezing with RV (OR, 25.6) was more strongly associated with asthma at age 6 years than aeroallergen sensitization (OR, 3.4). Nearly 90% (26 of 30) of children who wheezed with RV in Year 3 had asthma at 6 years of age. Among outpatient viral wheezing illnesses in infancy and early childhood, those caused by RV infections are the most significant predictors of the subsequent development of asthma at age 6 years in a high-risk birth cohort.
          Article 0 comments Cited 428 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Sequencing and analyses of all known human rhinovirus genomes reveal structure and evolution.

            Ann Palmenberg, David Spiro, Ryan Kuzmickas … (2009)
            Infection by human rhinovirus (HRV) is a major cause of upper and lower respiratory tract disease worldwide and displays considerable phenotypic variation. We examined diversity by completing the genome sequences for all known serotypes (n = 99). Superimposition of capsid crystal structure and optimal-energy RNA configurations established alignments and phylogeny. These revealed conserved motifs; clade-specific diversity, including a potential newly identified species (HRV-D); mutations in field isolates; and recombination. In analogy with poliovirus, a hypervariable 5' untranslated region tract may affect virulence. A configuration consistent with nonscanning internal ribosome entry was found in all HRVs and may account for rapid translation. The data density from complete sequences of the reference HRVs provided high resolution for this degree of modeling and serves as a platform for full genome-based epidemiologic studies and antiviral or vaccine development.
            Article 0 comments Cited 180 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Association between human rhinovirus C and severity of acute asthma in children.

              F Vang, Tu Le, V Lee … (2011)
              A new and potentially more pathogenic group of human rhinovirus (HRV), group C (HRVC), has recently been discovered. We hypothesised that HRVC would be present in children with acute asthma and cause more severe attacks than other viruses or HRV groups. Children with acute asthma (n = 128; age 2-16 yrs) were recruited on presentation to an emergency department. Asthma exacerbation severity was assessed, and respiratory viruses and HRV strains were identified in a nasal aspirate. The majority of the children studied had moderate-to-severe asthma (85.2%) and 98.9% were admitted to hospital. HRV was detected in 87.5% and other respiratory viruses in 14.8% of children, most of whom also had HRV. HRVC was present in the majority of children with acute asthma (59.4%) and associated with more severe asthma. Children with HRVC (n = 76) had higher asthma severity scores than children whose HRV infection was HRVA or HRVB only (n = 34; p = 0.018), and all other children (n = 50; p = 0.016). Of the 19 children with a non-HRV virus, 13 had HRV co-infections, seven of these being HRVC. HRVC accounts for the majority of asthma attacks in children presenting to hospital and causes more severe attacks than previously known HRV groups and other viruses.
              Article 0 comments Cited 156 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9502015
                Journal ID (pubmed-jr-id): 8791
                Journal ID (nlm-ta): Nat Med
                Title: Nature medicine
                ISSN (Print): 1078-8956
                ISSN (Electronic): 1546-170X
                Publication date Nihms-submitted: 2 December 2010
                Publication date (Electronic): 10 April 2011
                Publication date (Print): May 2011
                Publication date PMC-release: 1 November 2011
                Volume: 17
                Issue: 5
                Pages: 627-632
                Affiliations
                [1 ]Department of Pediatrics, University of Wisconsin School of Medicine and Public Health , Madison, WI, USA.
                [2 ]Institute for Molecular Virology, University of Wisconsin-Madison, Madison, WI, USA.
                [3 ]Cardiopulmonary Genomics Program, University of Maryland School of Medicine, Baltimore, MD, USA.
                [4 ]Laboratory of Genetics, University of Wisconsin-Madison, Madison, WI, USA.
                [5 ]Department of Surgery, University of Wisconsin School of Medicine and Public Health , Madison, WI, USA.
                [6 ]Department of Medicine, University of Wisconsin School of Medicine and Public Health , Madison, WI, USA.
                Author notes

                AUTHOR CONTRIBUTIONS

                Y.A.B. designed and performed experiments, analyzed data and was the principal author of the paper; A.C.P. performed sequence alignments, statistical receptor footprint analysis and contributed to writing; W.-M.L. performed partial sequencing of clinical isolates, constructed pW10-2R, designed antiviral compound experiments and provided purified HRVs; J.A.R. determined complete genome sequence of HRV-C15; S.P.A. assisted with virus inhibition experiments; X.S. designed and assisted with in situ hybridization experiments; T.R.P. assisted with establishment of the sinus organ culture; N.N.J. and S.B.L. analyzed data and contributed to writing; J.E.G. designed the project, analyzed data and contributed to writing.

                [* ]Corresponding author: Yury A Bochkov, K4/945 CSC #9988 600 Highland Ave, Madison, WI 53792-9988 Fax: (608) 265-2207 Phone: (608) 263-8553 yabochkov@ 123456wisc.edu
                Article
                Manuscript ID: nihpa255768
                DOI: 10.1038/nm.2358
                PMC ID: 3089712
                PubMed ID: 21483405
                SO-VID: 54de0d2f-9dc5-4ce5-998d-97b7eb0137ee
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Award ID: U19 AI070503-05 ||AI
                Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Award ID: R01 HL091490-02 ||HL
                Funded by: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID
                Funded by: National Heart, Lung, and Blood Institute : NHLBI
                Award ID: R01 HL080412-04 ||HL
                Categories
                Subject: Article

                ScienceOpen disciplines: Medicine
                Data availability:
                ScienceOpen disciplines: Medicine

                Comments

                Comment on this article

                scite_

                Similar content192

                See all similar

                Cited by75

                See all cited by

                Most referenced authors623

                See all reference authors