title: Diffuse alveolar lesion in BALB/c mice induced with human reovirus BYD1 strain and its potential relation with SARS.
abstract: The objective of this study was to investigate the pathogenicity and associated lesions of a new reovirus (ReoV) isolated from patients with Severe Acute Respiratory Syndrome (SARS) in China. Twenty-five four-week-old BALB/c female mice inoculated intranasally with either ReoV (strain BYD1) alone, or ReoV combined with SARS-CoV (strain BJF) displayed ejecting fur and loss of body weight compared with control animals. ReoV and SARS-CoV were isolated from most postmortem tissues. The histopathological features of ReoV infected animals consisted of diffuse alveolar damage, with scattered hemorrhage, hyaline membrane formation and interstitial pneumonia. A typical type II pneumocyte hyperplasia and fibrogranulomatous tissue formation in the alveolar septae were observed both in the animals inoculated simultaneously with these two viruses and in the animals inoculated firstly with SARS-CoV, followed by ReoV. The animals inoculated firstly with ReoV, followed with SARS-CoV displayed scattered hemorrhage in the alveolar septa. Furthermore, other lesions in above two combination groups included depletion of lymphocytes in the germinal center of lymph nodes in the lung hilus and the spleen, hemorrhagic necrosis in white pulp of spleen, hydroid degeneration, and fatty degeneration in the liver and kidney. Mice induced with SARS-CoV alone did not display clinical signs, characteristically hyaline membrane formation, hemorrhage and early pulmonary fibrosis in lung tissue. This study demonstrated that the newly isolated ReoV might be a virulent pathogen for BALB/c mice. Mice infected firstly with SARS-CoV, followed with ReoV developed a typical diffuse alveolar lesion.
authors.affiliation: Laboratory Animal Institute, College of Veterinary Medicine, China Agricultural University, Beijing, PR China.
authors.forename: Cheng
authors.initials: C
authors.lastname: He
authors.forename: Qi
authors.initials: Q
authors.lastname: Yang
authors.forename: Ming
authors.initials: M
authors.lastname: Lei
authors.forename: Wanyong
authors.initials: W
authors.lastname: Pang
authors.forename: Jianmin
authors.initials: J
authors.lastname: Yang
authors.forename: Hong
authors.initials: H
authors.lastname: Zhu
authors.forename: Qing
authors.initials: Q
authors.lastname: Duan
mesh_terms: D000818:Animals; D017934:Coronavirus / Q000302:isolation & purification; D005260:Female; D006470:Hemorrhage / Q000378:metabolism / Q000473:pathology / Q000821:virology; D006801:Humans; D006818:Hyalin / Q000378:metabolism / Q000821:virology; D008171:Lung Diseases / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D017563:Lung Diseases, Interstitial / Q000378:metabolism / Q000473:pathology / Q000821:virology; D008198:Lymph Nodes / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D030102:Orthoreovirus, Mammalian / Q000302:isolation & purification / Q000472:pathogenicity*; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D012088:Reoviridae Infections / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D045169:Severe Acute Respiratory Syndrome / Q000473:pathology*