Human coronavirus NL63 infection in Canada.
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ABSTRACT:
SUBMITTER: Bastien N
PROVIDER: S-EPMC7199484 | biostudies-literature | 2005 Feb
REPOSITORIES: biostudies-literature
Publications
Human coronavirus NL63 infection in Canada.
Bastien Nathalie N Anderson Kelly K Hart Laura L Van Caeseele Paul P Brandt Ken K Milley Doug D Hatchette Todd T Weiss Elise C EC Li Yan Y
The Journal of infectious diseases 20050104 4
The isolation of human coronavirus NL63 (HCoV-NL63) in The Netherlands raised questions about its contribution to respiratory illness. In this study, a total of 525 respiratory specimens, collected in Canada primarily during the winter months of 2001-2002, were tested for HCoV-NL63; 19 tested positive for HCoV-NL63, demonstrating virus activity during January-March 2002. Patients with HCoV-NL63 were 1 month-100 years old (median age, 37 years). The main clinical presentations were fever (15/19), ...[more]
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Project description:The human coronavirus NL63 (HCoV-NL63) was first identified in The Netherlands, and its circulation in France has not been investigated. We studied HCoV-NL63 infection in hospitalized children diagnosed with respiratory tract infections. From November 2002 to April 2003, we evaluated 300 respiratory specimens for HCoV-NL63. Of the 300 samples, 28 (9.3%) were positive for HCoV-NL63. The highest prevalence was found in February (18%). The main symptoms were fever (61%), rhinitis (39%), bronchiolitis (39%), digestive problems (33%), otitis (28%), pharyngitis (22%), and conjunctivitis (17%). A fragment of the spike protein gene was sequenced to determine the variety of circulating HCoV-NL63. Phylogenetic analysis indicated that strains with different genetic markers cocirculate in France.
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Project description:Even though coronavirus infection of humans is not normally associated with severe diseases, the identification of the coronavirus responsible for the outbreak of severe acute respiratory syndrome showed that highly pathogenic coronaviruses can enter the human population. Shortly thereafter, in Holland in 2004, another novel human coronavirus (HCoV-NL63) was isolated from a seven-month old infant suffering from respiratory symptoms. This virus has subsequently been identified in various countries, indicating a worldwide distribution. HCoV-NL63 has been shown to infect mainly children and the immunocommpromised, who presented with either mild upper respiratory symptoms (cough, fever and rhinorrhoea) or more serious lower respiratory tract involvement such as bronchiolitis and croup, which was observed mainly in younger children. In fact, HCoV-NL63 is the aetiological agent for up to 10% of all respiratory diseases. This review summarizes recent findings of human coronavirus HCoV-NL63 infections, including isolation and identification, phylogeny and taxonomy, genome structure and transcriptional regulation, transmission and pathogenesis, and detection and diagnosis.
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Project description:We establish a mouse model of HCoV-NL63 and compare outcomes with a model of rhinovirus (RV)-A1B. Transgenic mice expressing human ACE2 were infected intranasally with sham LLC-MK2 cell lysate, 100,000 TCID50 units HCoV-NL63, or 1,000,000 PFU RV-A1B. Lungs were assessed for host gene expression by next generation sequencing. RNAseq showed increases in IFN-α, IFN-β, IFN-λ and many IFN-stimulated genes (ISGs) in NL63-infected mice. In addition to ISGs, RV-A1B induced expression of IFN-γ, IL-1β, NLRP3, TLR2 and C-X-C chemokines. We established a mouse model of HCoV-NL63 replicative infection characterized by expression of ISGs but fewer pro-inflammatory genes compared to RV-A1B.
2024-08-25 | GSE254967 | GEO
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| S-EPMC1479111 | biostudies-literature
Project description:Human coronavirus (HCoV) NL63 was first described in 2004 and is associated with respiratory tract disease of varying severity. At the genetic and structural level, HCoV-NL63 is similar to other members of the Coronavirinae subfamily, especially human coronavirus 229E (HCoV-229E). Detailed analysis, however, reveals several unique features of the pathogen. The coronaviral nucleocapsid protein is abundantly present in infected cells. It is a multi-domain, multi-functional protein important for viral replication and a number of cellular processes. The aim of the present study was to characterize the HCoV-NL63 nucleocapsid protein. Biochemical analyses revealed that the protein shares characteristics with homologous proteins encoded in other coronaviral genomes, with the N-terminal domain responsible for nucleic acid binding and the C-terminal domain involved in protein oligomerization. Surprisingly, analysis of the subcellular localization of the N protein of HCoV-NL63 revealed that, differently than homologous proteins from other coronaviral species except for SARS-CoV, it is not present in the nucleus of infected or transfected cells. Furthermore, no significant alteration in cell cycle progression in cells expressing the protein was observed. This is in stark contrast with results obtained for other coronaviruses, except for the SARS-CoV.
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Project description:Although human coronavirus (HCoV)-NL63 was once considered a possible causative agent of Kawasaki disease based on RT-PCR analyses, subsequent studies could not confirm the result. In this study, this possibility was explored using serological tests. To evaluate the role of HCoV infection in patients with Kawasaki disease, immunofluorescence assays and virus neutralizing tests were performed. Paired serum samples were obtained from patients with Kawasaki disease who had not been treated with γ-globulin. HCoV-NL63 and two antigenically different isolates of HCoV-229E (ATCC-VR740 and a new isolate, Sendai-H) were examined as controls. Immunofluorescence assays detected no difference in HCoV-NL63 antibody positivity between the patients with Kawasaki disease and controls, whereas the rate of HCoV-229E antibody positivity was higher in the patients with Kawasaki disease than that in controls. The neutralizing tests revealed no difference in seropositivity between the acute and recovery phases of patients with Kawasaki disease for the two HCoV-229Es. However, the Kawasaki disease specimens obtained from patients in recovery phase displayed significantly higher positivity for Sendai-H, but not for ATCC-VR740, as compared to the controls. The serological test supported no involvement of HCoV-NL63 but suggested the possible involvement of HCoV-229E in the development of Kawasaki disease.
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Project description:In 2004, the novel respiratory human coronavirus NL63 (HCoV-NL63) was identified, and subsequent research revealed that the virus has spread worldwide. HCoV-229E is a close relative of HCoV-NL63, and infection with either virus can lead to the hospitalization of young children, immunocompromised persons, and the elderly. Children infected with HCoV-NL63 often develop croup, with obstruction of the airway. In this study we investigated at which age children are confronted for the first time with an HCoV-NL63 infection and, thus, at which age they seroconvert to HCoV-NL63 positivity. We designed a recombinant HCoV-229E and a recombinant HCoV-NL63 nucleocapsid protein enzyme-linked immunosorbent assay and performed a seroepidemiology survey on longitudinal and cross-sectional serum samples. The longitudinal serum samples were collected from 13 newborns, and data for those newborns were available from multiple time points spanning a period of at least 18 months. For the cross-sectional survey we tested serum samples of 139 children, including newborns to children 16 years of age. In examinations of the longitudinal serum samples we observed that all of the children had maternal anti-NL63 and anti-229E antibodies at birth that disappeared within 3 months. Seven of the 13 children became HCoV-NL63 seropositive during follow-up, whereas only 2 became HCoV-229E seropositive. The serology data of the cross-sectional serum samples revealed that 75% and 65% of the children in the age group 2.5 to 3.5 years were HCoV-NL63 and HCoV-229E seropositive, respectively. We conclude that on average, HCoV-NL63 and HCoV-229E seroconversion occurs before children reach the age of 3.5 years.
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Project description:Coronaviruses are responsible for upper and lower respiratory tract infections in humans. It is estimated that 1 to 10% of the population suffers annually from cold-like symptoms related to infection with human coronavirus NL63 (HCoV-NL63), an alphacoronavirus. The nucleocapsid (N) protein, the major structural component of the capsid, facilitates RNA packing, links the capsid to the envelope, and is also involved in multiple other processes, including viral replication and evasion of the immune system. Although the role of N protein in viral replication is relatively well described, no structural data are currently available regarding the N proteins of alphacoronaviruses. Moreover, our understanding of the mechanisms of RNA binding and nucleocapsid formation remains incomplete. In this study, we solved the crystal structures of the N- and C-terminal domains (NTD, residues 10 to 140, and CTD, residues 221 to 340, respectively) of the N protein of HCoV-NL63, both at a 1.5-Å resolution. Based on our structure of NTD solved here, we proposed and experimentally evaluated a model of RNA binding. The structure of the CTD reveals the mode of N protein dimerization. Overall, this study expands our understanding of the initial steps of N protein-nucleic acid interaction and may facilitate future efforts to control the associated infections.IMPORTANCE Coronaviruses are responsible for the common cold and other respiratory tract infections in humans. According to multiple studies, 1 to 10% of the population is infected each year with HCoV-NL63. Viruses are relatively simple organisms composed of a few proteins and the nucleic acids that carry the information determining their composition. The nucleocapsid (N) protein studied in this work protects the nucleic acid from the environmental factors during virus transmission. This study investigated the structural arrangement of N protein, explaining the first steps of its interaction with nucleic acid at the initial stages of virus structure assembly. The results expand our understanding of coronavirus physiology and may facilitate future efforts to control the associated infections.
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Project description:BackgroundHuman coronavirus NL63 (HCoV-NL63) is a recently discovered human coronavirus found to cause respiratory illness in children and adults that is distinct from the severe acute respiratory syndrome (SARS) coronavirus and human coronaviruses 229E (HCoV-229E) and OC43 (HCoV-OC43).MethodsWe investigated the role that HCoV-NL63, HCoV-OC43, and HCoV-229E played in children hospitalized with fever and acute respiratory symptoms in Hong Kong during the period from August 2001 through August 2002.ResultsCoronavirus infections were detected in 26 (4.4%) of 587 children studied; 15 (2.6%) were positive for HCoV-NL63, 9 (1.5%) were positive for HCoV-OC43, and 2 (0.3%) were positive for HCoV-229E. In addition to causing upper respiratory disease, we found that HCoV-NL63 can present as croup, asthma exacerbation, febrile seizures, and high fever. The mean age (+/- standard deviation [SD]) of the infected children was 30.7 +/- 19.8 months (range, 6-57 months). The mean maximum temperature (+/- SD) for the 12 children who were febrile was 39.3 degrees C +/- 0.9 degrees C, and the mean total duration of fever (+/- SD) for all children was 2.6 +/- 1.2 days (range, 1-5 days). HCoV-NL63 infections were noted in the spring and summer months of 2002, whereas HCoV-OC43 infection mainly occurred in the fall and winter months of 2001. HCoV-NL63 viruses appeared to cluster into 2 evolutionary lineages, and viruses from both lineages cocirculated in the same season.ConclusionsHCoV-NL63 is a significant pathogen that contributes to the hospitalization of children, and it was estimated to have caused 224 hospital admissions per 100,000 population aged < or = 6 years each year in Hong Kong.
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