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      Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections†

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          Abstract

          The pathogenesis of severe acute respiratory syndrome (SARS) is poorly understood and cytokine dysregulation has been suggested as one relevant mechanism to be explored. We compared the cytokine profile in Caco2 cells after infection of SARS coronavirus (SARS‐CoV) with other respiratory viruses including respiratory syncytial virus (RSV), influenza A virus (FluAV), and human parainfluenza virus type 2 (hPIV2). Interferon (IFN) system (production and response) was not suppressed by SARS‐CoV infection. Therefore, SARS‐CoV replication was suppressed by pretreatment with IFN. SARS‐CoV and RSV induced high levels of IL‐6 and RANTES compared with FluAV and hPIV2. Induction level of suppressor of cytokine signaling‐3 (SOCS3) by SARS‐CoV was significantly lower than that by RSV in spite of the significant production of IL‐6. Toll‐like receptors 4 and 9, which correlate with the induction of inflammatory response, were upregulated by SARS‐CoV infection. Collectively, overinduction of inflammatory cytokine and dysregulation of cytokine signaling may contribute to the immunopathology associated with “severe” inflammation in SARS. J. Med. Virol. 78:417–424, 2006. © 2006 Wiley‐Liss, Inc.

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          Most cited references32

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          Recognition of single-stranded RNA viruses by Toll-like receptor 7.

          Viral infection of mammalian host results in the activation of innate immune responses. Toll-like receptors (TLRs) have been shown to mediate the recognition of many types of pathogens, including viruses. The genomes of viruses possess unique characteristics that are not found in mammalian genomes, such as high CpG content and double-stranded RNA. These genomic nucleic acids serve as molecular signatures associated with viral infections. Here we show that TLR7 recognizes the single-stranded RNA viruses, vesicular stomatitis virus and influenza virus. The recognition of these viruses by plasmacytoid dendritic cells and B cells through TLR7 results in their activation of costimulatory molecules and production of cytokines. Moreover, this recognition required intact endocytic pathways. Mice deficient in either the TLR7 or the TLR adaptor protein MyD88 demonstrated reduced responses to in vivo infection with vesicular stomatitis virus. These results demonstrate microbial ligand recognition by TLR7 and provide insights into the pathways used by the innate immune cells in the recognition of viral pathogens.
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            Enteric involvement of severe acute respiratory syndrome-associated coronavirus infection 1

            Background & Aims: Severe acute respiratory syndrome (SARS) is a recently emerged infection from a novel coronavirus (CoV). Apart from fever and respiratory complications, gastrointestinal symptoms are frequently observed in patients with SARS but the significance remains undetermined. Herein, we describe the clinical, pathologic, and virologic features of the intestinal involvement of this new viral infection. Methods: A retrospective analysis of the gastrointestinal symptoms and other clinical parameters of the first 138 patients with confirmed SARS admitted for a major outbreak in Hong Kong in March 2003 was performed. Intestinal specimens were obtained by colonoscopy or postmortem examination to detect the presence of coronavirus by electron microscopy, virus culture, and reverse-transcription polymerase chain reaction. Results: Among these 138 patients with SARS, 28 (20.3%) presented with watery diarrhea and up to 38.4% of patients had symptoms of diarrhea during the course of illness. Diarrhea was more frequently observed during the first week of illness. The mean number of days with diarrhea was 3.7 ± 2.7, and most diarrhea was self-limiting. Intestinal biopsy specimens obtained by colonoscopy or autopsy showed minimal architectural disruption but the presence of active viral replication within both the small and large intestine. Coronavirus was also isolated by culture from these specimens, and SARS-CoV RNA can be detected in the stool of patients for more than 10 weeks after symptom onset. Conclusions: Diarrhea is a common presenting symptom of SARS. The intestinal tropism of the SARS-CoV has major implications on clinical presentation and viral transmission.
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              Respiratory syncytial virus bronchiolitis in infancy is an important risk factor for asthma and allergy at age 7.

              We previously reported an increased risk for bronchial obstructive disease and allergic sensitization up to age 3 in 47 children hospitalized with a respiratory syncytial virus (RSV) bronchiolitis in infancy compared with 93 matched control subjects recruited during infancy. The aims of the present study were to evaluate the occurrences of bronchial obstructive disease and allergic sensitization in these children at age 7(1)/ (2). All 140 children reported for the follow-up, which included physical examination, skin prick tests, and serum IgE tests for common food and inhaled allergens. The cumulative prevalence of asthma was 30% in the RSV group and 3% in the control group (p < 0.001), and the cumulative prevalence of "any wheezing" was 68% and 34%, respectively (p < 0.001). Asthma during the year prior to follow-up was seen in 23% of the RSV children and 2% in the control subjects (p < 0.001). Allergic sensitization was found in 41% of the RSV children and 22% of the control subjects (p = 0.039). Multivariate evaluation of possible risk factors for asthma and sensitization using a stepwise logistic statistical procedure for all 140 children showed that RSV bronchiolitis had the highest independent risk ratio for asthma (OR: 12.7, 95% CI 3.4 to 47.1) and a significantly elevated independent risk ratio for allergic sensitization (OR: 2.4, 95% CI 1.1 to 5.5). In conclusion, RSV bronchiolitis in infancy severe enough to cause hospitalization was highly associatied with the development of asthma and allergic sensitization up to age 7(1)/ (2). The results support the theory that the RSV influences the mechanisms involved in the development of asthma and allergy in children.
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                Author and article information

                Contributors
                fujii@sapmed.ac.jp
                Journal
                J Med Virol
                J. Med. Virol
                10.1002/(ISSN)1096-9071
                JMV
                Journal of Medical Virology
                Wiley Subscription Services, Inc., A Wiley Company (Hoboken )
                0146-6615
                1096-9071
                15 February 2006
                April 2006
                : 78
                : 4 ( doiID: 10.1002/jmv.v78:4 )
                : 417-424
                Affiliations
                [ 1 ]Department of Microbiology, Sapporo Medical University School of Medicine, Chuo‐ku, Sapporo, Hokkaido, Japan
                [ 2 ]Laboratory of Public Health, Department of Environmental Veterinary Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan
                [ 3 ]Department of Pediatrics, Sapporo Medical University School of Medicine, Hokkaido, Japan
                Author notes
                [*] [* ]Department of Microbiology, Sapporo Medical University School of Medicine, South‐1, West‐17, Chuo‐ku, Sapporo 060‐8556, Hokkaido, Japan.===
                Article
                JMV20556
                10.1002/jmv.20556
                7166776
                16482545
                62097afb-6950-4472-8788-c76f59787f6c
                Copyright © 2006 Wiley‐Liss, Inc.

                This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.

                History
                : 12 December 2005
                Page count
                Figures: 5, Tables: 2, References: 51, Pages: 8, Words: 1531
                Categories
                Research Article
                Article
                Custom metadata
                2.0
                April 2006
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.0 mode:remove_FC converted:15.04.2020

                Microbiology & Virology
                sars‐cov,socs3,cytokine,il‐6,ifn,tlr
                Microbiology & Virology
                sars‐cov, socs3, cytokine, il‐6, ifn, tlr

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