scholarly journals Virus-induced diabetes mellitus. XX. Polyendocrinopathy and autoimmunity.

1981 ◽  
Vol 153 (6) ◽  
pp. 1457-1473 ◽  
Author(s):  
T Onodera ◽  
A Toniolo ◽  
U R Ray ◽  
A B Jenson ◽  
R A Knazek ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Gene Segment ◽  
Inflammatory Cells ◽  
S1 Gene ◽  
Virus Particles ◽  
Viral Antigens ◽  
Reovirus Type ◽  
Type 3 ◽  
Runting Syndrome

Mice infected with reovirus type 1 developed transient diabetes and a runting syndrome. The diabetes was characterized by hyperglycemia, abnormal glucose tolerance tests, and hypoinsulinemia. Inflammatory cells and viral antigens were found in the islets of Langerhans, and virus particles were seen in alpha, beta, and delta cells. The runting syndrome consisted of retarded growth, oily hair, alopecia, and steatorrhea. Inflammatory cells and viral antigens were found in the anterior, but not posterior pituitary. Electron microscopy revealed virus particles in growth hormone (GH)-producing cells and radioimmunoassay showed that the concentration of GH in the blood was decreased. Examination of sera from infected mice revealed autoantibodies that, by immunofluorescence, reacted with cytoplasmic antigens in the islets of Langerhans, anterior pituitary, and gastric mucosa of uninfected mice. Absorption studies and enzyme-linked immunosorbent assays designed to identify the reactive antigens showed that some of the autoantibodies were directed against insulin and others against GH. Reovirus type 3, in contrast to reovirus type 1, did not induce autoantibodies to GH. By use of recombinant viruses, the segment of the reovirus genome responsible for the induction of autoantibodies to GH was identified. Virus containing the S1 gene segment from reovirus type 1, which codes for the sigma 1 polypeptide (i.e., hemagglutinin), infected cells in the anterior pituitary and induced autoantibodies to GH, whereas virus containing the S1 gene segment from reovirus type 3 failed to infect cells in the anterior pituitary and did not induce autoantibodies to GH. We conclude that reovirus type 1 infection can lead to polyendocrinopathy and autoimmunity and that the S1 gene segment is required for the induction of autoantibodies to GH.

Reovirus type 1 and type 3 differ in their binding to isolated intestinal epithelial cells

1988 ◽  
Vol 5 (1) ◽  
pp. 29-40 ◽  
Author(s):  
David B. Weiner ◽  
Karen Girard ◽  
William V. Williams ◽  
Thomas McPhillips ◽  
Donald H. Rubin
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Reovirus Type ◽  
Type 3

Murine Infection with Reovirus Type 3 and the Runting Syndrome

Nature ◽  
1963 ◽  
Vol 199 (4900) ◽  
pp. 1309-1310 ◽  
Author(s):  
N. F. STANLEY ◽  
P. J. LEAK
Keyword(s):  
Reovirus Type ◽  
Type 3 ◽  
Runting Syndrome

scholarly journals An assessment of morphological and pathological changes in paravertebral muscle degeneration using imaging and histological analysis: a cross-sectional study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ding-Chao Zhu ◽  
Jia-Hao Lin ◽  
Jia-Jing Xu ◽  
Qiang Guo ◽  
Yi-Han Wang ◽  
...  
Keyword(s):  
Histological Analysis ◽  
Inflammatory Cells ◽  
Fatty Degeneration ◽  
High Signal ◽  
Pathological Changes ◽  
Paravertebral Muscle ◽  
Inflammatory Edema ◽  
Type 3

Abstract Background The high signal of paravertebral muscle (PVM) on T2-weighted image (T2WI) is usually considered to be fatty degeneration. However, it is difficult to distinguish inflammatory edema from fatty degeneration on T2WI. The purpose of this study was to identify different types of PVM high signal in patients with low back pain (LBP) through magnetic resonance imaging (MRI) and histology. Methods Seventy patients with LBP underwent MRI. The signal change of multifidus both on T2WI and fat suppression image (FSI) was quantified by Image J. Furthermore, 25 of the 70 patients underwent surgery for degenerative lumbar disease and their multifidus were obtained during the operation. Histological analysis of the samples was performed by HE staining. Result Three types of PVM signal changes were identified from the MRI. Type 1 (n = 36) indicated fatty degeneration characterized by a high signal on T2WI and low signal on FSI. High signal on both T2WI and FSI, signifying type 2 meant inflammatory edema (n = 9). Type 3 (n = 25) showed high signal on T2WI and partial signal suppression on FSI, which meant a combination of fatty degeneration and inflammatory edema. Histological results were consistent with MRI. Among the 25 patients who underwent surgery, type 1 (n = 14) showed adipocytes infiltration, type 2 (n = 3) showed inflammatory cells infiltration and type 3 (n = 8) showed adipocytes and inflammatory cells infiltration. Conclusion From our results, there are three types of pathological changes in patients with PVM degeneration, which may help to decide on targeted treatments for LBP.

scholarly journals Identification of astrovirus serotypes from children treated at the Hospitals for Sick Children, London 1981–93

1994 ◽  
Vol 113 (1) ◽  
pp. 153-159 ◽  
Author(s):  
J. Noel ◽  
D. Cubitt
Keyword(s):  
Immune Deficiency ◽  
Aqueous Suspension ◽  
Deficiency Disease ◽  
Severe Combined Immune Deficiency ◽  
Virus Particles ◽  
Combined Immune Deficiency ◽  
Sick Children ◽  
Type 3

SUMMARYAn enzyme immunoassay (EIA) for astrovirus type 1 together with immune electronmicroscopy (IBM) was used to type a collection of 162 astroviruses obtained from 1981–93 from children with diarrhoea. The EIA was found to be specific for astrovirus type 1. Astrovirus types 2–4 were typed by IEM.Astrovirus type 1 was the prevalent serotype 107/125 (86%), followed by type 3 (8%), type 4 (6%) and type 2 (1 %). Six samples containing astrovirus could not be typed or detected by EIA because they were coated with coproantibodies; 11 others were not identified. Virus particles could no longer be detected in 15/162 (9%) samples following storage for≥2 years.Selected samples containing astrovirus types 1–4 were passaged in CaCO2cells and their identity confirmed by one or both assays. One sample was shown to have remained viable for 10 years when stored as an aqueous suspension at −20 °C.Two patients with severe combined immune deficiency disease (SCID) were shown to be excreting astrovirus type 1 for 32 and 102 days respectively. One child was simultaneously shedding rotavirus and the other child was excreting adenovirus.

The S1 Gene From Reovirus Type 1 is Required for Immunosuppression

1985 ◽  
Vol 152 (3) ◽  
pp. 640-643 ◽  
Author(s):  
C. Garzelli ◽  
T. Onodera ◽  
U. R. Ray ◽  
A. L. Notkins
Keyword(s):  
S1 Gene ◽  
Reovirus Type

Structure-activity studies on open-chain analogues of nucleosides: Inhibition of S-adenosyl-L-homocysteine hydrolase and antiviral activity 2. Acid open-chain analogues

1985 ◽  
Vol 50 (1) ◽  
pp. 262-279 ◽  
Author(s):  
Antonín Holý ◽  
Ivan Votruba ◽  
Erik De Clercq
Keyword(s):  
Antiviral Activity ◽  
Antiviral Agents ◽  
Inhibitory Effects ◽  
Open Chain ◽  
Reovirus Type ◽  
Vesicular Stomatitis ◽  
Hydroxybutanoic Acid ◽  
Type 3 ◽  
Derivatives Of

Over 50 ω-carboxyalkyl derivatives of adenine and other purine bases were examined for their inhibitory effects on rat liver S-adenosyl-L-homocysteine hydrolase and their antiviral activity. To be an inhibitor of SAH-hydrolase the analogue must contain an adenine base substituted at the position 9 by an ω-carboxyalkyl (C3-C5) chain bearing at least one hydroxyl function. The absolute configuration at the side-chain is decisive for the dihydroxy and trihydroxy compounds, but less important for the monohydroxyalkanoic acids. D-Eritadenine (1a) and 3-(adenin-9-yl)-2-hydroxypropanoic acids (12a) are the most potent SAH-hydrolase inhibitors and the only compounds possessing an antiviral activity (against vesicular stomatitis, parainfluenza type 3, reovirus type 1, and vaccinia virus). All these compounds effect a rapid irreversible inactivation of SAH-hydrolase. The esters of 1a and 12a exhibit little, if any inhibitory activity toward the enzyme; they are, however, much more potent antiviral agents than the parent compounds 1a and 12a, most probably acting as prodrugs of the latter. 2-Amino-D-eritadenine, (2R,3R)-5-(adenin-9-yl)-2,3-dihydroxypentanoic acid, 9-(dicarboxymethyl)adenine, 4-(adenin-9-yl)-2-hydroxybutanoic acid, 3-(8-bromoadenin-9-yl)-2-hydroxypropanoic acid and O-carboxymethyl derivatives of 9-(2,3-dihydroxypropyl)- and 9-(2,3,4-trihydroxybutyl)adenine are described as novel compounds.

scholarly journals Development of a reverse transcription loop mediated isothermal amplification assay for the detection of Mouse reovirus type 3 in laboratory mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Taofeng Lu ◽  
Lingyun Tao ◽  
Haibo Yu ◽  
Hui Zhang ◽  
Yanjun Wu ◽  
...  
Keyword(s):  
Reverse Transcription ◽  
Lamp Assay ◽  
Isothermal Amplification ◽  
Laboratory Mice ◽  
Blood Samples ◽  
S1 Gene ◽  
Loop Mediated Isothermal Amplification ◽  
Reovirus Type ◽  
One Step ◽  
Type 3

AbstractMouse reovirus type 3 (Reo-3) infection is a viral disease that is harmful for laboratory mice. No rapid and accurate detection methods are currently available for this infection. In this study, we describe a rapid, simple, closed-tube, one step, reverse transcription-loop-mediated isothermal amplification (RT-LAMP) assay for Reo-3 and compare our assay with indirect enzyme-linked immunosorbent assay (ELISA). Three sets of RT-LAMP primers were designed by sequence analysis of a specific conserved sequence of the Reo-3 S1 gene. Using RS2 primer set, the RT-LAMP assay required 60 min at 65 °C to amplify the S1 gene in one step by using Reo-3 RNA template and had no cross-reactivity with the other related pathogens, such as Sendai virus (SV), pneumonia virus of mice (PVM), mouse hepatitis virus (MHV), Ectromelia virus (Ect), minute virus of mice (MVM), P. pneumotropica, B. bronchiseptica, K. pneumonia and P. aeruginosa. in our LAMP reaction system. The limit of detection (LOD) of our RT-LAMP assay is 4 fg/μL. The established RT-LAMP assay enabled visual detection when fluorescence detection reagents were added, and was demonstrated to be effective and efficient. We tested 30 clinical blood samples and five artificial positive samples from SPF mice, the concordance between the two methods for blood samples was 100% compared with indirect ELISA and RT-PCR. Considering its performance, specificity, sensitivity, and repeatability, the developed RT-LAMP could be a valuable tool to supply a more effective Reo-3 detection method in laboratory animal quality monitoring.

scholarly journals Noncanonical Cell Death Induction by Reassortant Reovirus

2020 ◽  
Vol 94 (22) ◽  
Author(s):  
Roxana M. Rodríguez Stewart ◽  
Vishnu Raghuram ◽  
Jameson T. L. Berry ◽  
Gaurav N. Joshi ◽  
Bernardo A. Mainou
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Host Cell ◽  
Caspase 3 ◽  
Gene Segment ◽  
Oncolytic Viruses ◽  
Viral Gene ◽  
Genetic Composition ◽  
Type 3

ABSTRACT Triple-negative breast cancer (TNBC) constitutes 10 to 15% of all breast cancer and is associated with worse prognosis than other subtypes of breast cancer. Current therapies are limited to cytotoxic chemotherapy, radiation, and surgery, leaving a need for targeted therapeutics to improve outcomes for TNBC patients. Mammalian orthoreovirus (reovirus) is a nonenveloped, segmented, double-stranded RNA virus in the Reoviridae family. Reovirus preferentially kills transformed cells and is in clinical trials to assess its efficacy against several types of cancer. We previously engineered a reassortant reovirus, r2Reovirus, that infects TNBC cells more efficiently and induces cell death with faster kinetics than parental reoviruses. In this study, we sought to understand the mechanisms by which r2Reovirus induces cell death in TNBC cells. We show that r2Reovirus infection of TNBC cells of a mesenchymal stem-like (MSL) lineage downregulates the mitogen-activated protein kinase/extracellular signal-related kinase pathway and induces nonconventional cell death that is caspase-dependent but caspase 3-independent. Infection of different MSL lineage TNBC cells with r2Reovirus results in caspase 3-dependent cell death. We map the enhanced oncolytic properties of r2Reovirus in TNBC to epistatic interactions between the type 3 Dearing M2 gene segment and type 1 Lang genes. These findings suggest that the genetic composition of the host cell impacts the mechanism of reovirus-induced cell death in TNBC. Together, our data show that understanding host and virus determinants of cell death can identify novel properties and interactions between host and viral gene products that can be exploited for the development of improved viral oncolytics. IMPORTANCE TNBC is unresponsive to hormone therapies, leaving patients afflicted with this disease with limited treatment options. We previously engineered an oncolytic reovirus (r2Reovirus) with enhanced infective and cytotoxic properties in TNBC cells. However, how r2Reovirus promotes TNBC cell death is not known. In this study, we show that reassortant r2Reovirus can promote nonconventional caspase-dependent but caspase 3-independent cell death and that the mechanism of cell death depends on the genetic composition of the host cell. We also map the enhanced oncolytic properties of r2Reovirus in TNBC to interactions between a type 3 M2 gene segment and type 1 genes. Our data show that understanding the interplay between the host cell environment and the genetic composition of oncolytic viruses is crucial for the development of efficacious viral oncolytics.

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