scholarly journals Virus-induced diabetes mellitus. XVIII. Inhibition by a nondiabetogenic variant of encephalomyocarditis virus.

1980 ◽  
Vol 152 (4) ◽  
pp. 878-892 ◽  
Author(s):  
J W Yoon ◽  
P R McClintock ◽  
T Onodera ◽  
A L Notkins
Keyword(s):  
Infectious Virus ◽  
Islet Cells ◽  
Encephalomyocarditis Virus ◽  
The Other ◽  
Male Mice ◽  
Virus Antibody ◽  
Viral Antigens ◽  
Emc Virus ◽  
Plaque Purification ◽  
Infection Experiments

Plaque purification of the M variant of encephalomyocarditis (EMC) virus resulted in the isolation of two stable variants: one diabetogenic and designated D and the other nondiabetogenic and designated B. When the D variant was inoculated into SJL/J male mice, hypoinsulinemia and hyperglycemia developed in > 90% of the animals. In contrast, none of the mice inoculated with the B variant developed diabetes. Histologic examination of pancreata from mice infected with the D variant revealed insulitis and necrosis of beta cells, whereas islets from mice infected with the B variant showed little, if any, change. When islets were assayed for infectious virus, approximately 10 times more virus was recovered from animals inoculated with the D as compared with the B variant. Moreover, approximately 60% of islet cells from mice infected with the D variant contained viral antigens when stained with fluorescein-labeled anti-EMC virus antibody, whereas < 5% of islet cells from animals infected with the B variant contained viral antigens. Co-infection experiments showed that the induction of diabetes by the D variant was inhibited by the B variant. When the B and D variants were mixed together at B:D ratios of 1, 9, and 99, diabetes developed in 60, 11, and 0% of the mice, respectively. Tissue-culture experiments revealed that the B variant induced considerably more interferon than the D variant, and studies in animals showed that interferon appeared earlier and in greater amounts in the circulation of mice infected with the B as compared with the D variant. These studies suggest that the induction of interferon by the B variant is, at least in part, responsible for the inhibition of diabetes by the D variant.

scholarly journals Serologic, Virologic, and Histopathologic Observations of Encephalomyocarditis Virus Infection in Mummified and Stillborn Pigs

1989 ◽  
Vol 1 (2) ◽  
pp. 101-104 ◽  
Author(s):  
Hyun S. Kim ◽  
Han S. Joo ◽  
Martin E. Bergeland
Keyword(s):  
United States ◽  
Virus Infection ◽  
Neutralizing Antibody ◽  
The United States ◽  
Encephalomyocarditis Virus ◽  
Virus Antibody ◽  
Tissue Samples ◽  
Swine Farms ◽  
Emc Virus ◽  
Antibody Titers

Stillborn and mummified swine fetuses from swine farms experiencing reproductive problems were investigated for evidence of infection with encephalomyocarditis (EMC) virus by fetal serology, virus isolation, and histopathologic examination. Fetal sera or thoracic fluids of 478 abnormal fetuses collected during January through December 1987 were tested for the presence of antibody specific to EMC virus. Of 478 samples tested, 175 (36.6%) had EMC virus serum neutralizing antibody titers of 1:64 or greater. The samples positive for EMC virus antibody were obtained from 38 swine farms located in 9 states in the United States. In addition to serologic observations, tissue samples of some abnormal fetuses were examined for the presence of virus and histopathologic lesions. The EMC virus was isolated in 1 case from the fetuses of an aborted litter. The isolate was serologically identical to a reference EMC virus. Nonsuppurative encephalitis and myocarditis were observed in the fetal samples collected from 2 different herds. Thoracic fluid of 1 stillborn pig with lesions was positive for EMC virus antibody at a titer of 1:512. We suggest that a widespread reproductive problem recently experienced in several major swine-producing areas of the United States may have been caused by EMC virus infection.

scholarly journals Encephalomyocarditis (EMC) virus-induced testicular lesion in BALB/c mice

1994 ◽  
Vol 28 (4) ◽  
pp. 330-334 ◽  
Author(s):  
M. Shigesato ◽  
K. Hirasawa ◽  
M. Takeda ◽  
K. Doi
Keyword(s):  
Virus Titre ◽  
Male Mice ◽  
Inflammatory Infiltration ◽  
Emc Virus ◽  
Testicular Lesions ◽  
Almost All ◽  
Germinal Cells ◽  
Old Mice

Characteristics of encephalomyocarditis (EMC) virus-induced testicular lesions were investigated in 4- and 8-week-old BALB/c male mice after intraperitoneal (i.p.) and intratesticular (left) (i.t.) inoculation of the D variant of EMC virus (EMC-D). Apart from variation in severity and incidence, the histopathological nature of the resultant testicular lesion was similar in all infected mice, and was characterized by degeneration and necrosis of germinal cells and spermatogonia with inflammatory infiltration. Almost all the inoculated left testes of the i.t. group developed marked lesions. In general, the virus titre in the testis and incidence of testicular lesions were higher in 4-week-old mice than in 8-week-old mice. In addition, testicular lesions developed earlier and with a higher incidence in the PBS-inoculated right testis of the i.t. group than in either testis of the i.p. group of the same age.

P–060 Dose- dependent mitigation of lead acetate toxicity in males on embryo development in female mice

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
P Dolati ◽  
M J Zamiri ◽  
A Akhlaghi ◽  
Z Jahromi
Keyword(s):  
Adverse Effects ◽  
Embryonic Development ◽  
Embryo Development ◽  
Lead Acetate ◽  
Endocrine System ◽  
Cell Number ◽  
The Other ◽  
Control Group ◽  
Male Mice ◽  
Female Mice

Abstract Study question Does quercetin (75 or 100 mg/kg BW/day) co-administration with lead acetate to male mice affects embryonic development in female mice? Summary answer The low-dose quercetin (75 mg/kg BW/day) ameliorated the adverse effects of lead acetate on mouse embryogenesis. What is known already Lead causes male infertility by impacting on endocrine system and spermatogenesis, and may exert undesirable effects on the offspring. The currently approved treatment for lead poisoning is the use of chelating agents, which form an insoluble complex with lead and shield it from biological targets; thus, reducing its toxicity. One of the main mechanisms of lead-induced toxicity is oxidative stress, and it has been reported that natural antioxidants can reduce the heavy metals toxicity. The aim of the present study was to examine the protective effects of quercetin on the toxicity induced by lead acetate on the embryogenesis in mice. Study design, size, duration Sexually mature (eight-week-old) NMRI male mice (n = 24) were randomly divided into four groups (n = 6 per group) receiving (i) distilled water (control group); (ii) lead acetate (150 mg/kg BW/day) dissolved in deionized water (LA); (iii) lead acetate (150 mg/kg BW/day) + quercetin (75 mg/kg BW/day) (LQ75); (IV) lead acetate (150 mg/kg BW/day) + quercetin (100 mg/kg BW/day) (LQ100). Treatments were applied daily as oral gavages for one cycle of the seminiferous epithelium (35 days). Participants/materials, setting, methods At the end of treatment administration, the males were joined with super-ovulated females, and the retrieved zygotes were cultured for evaluation of the embryo development (at 2-cell, 4-cell, 8-cell, and blastocyst stages), and blastocyst cell number using differential staining (propidium iodide and bisbenzimide). After incubation of capacitated sperm with oocytes, an ultraviolet light microscope was used following 3 min incubation with 25 µg⁄mL bisbenzamide solution for fertilization assessment. Main results and the role of chance Lead acetate (LA) treatment of male mice decreased the 2-cell stage compared with the control group (P > 0.05). There was no difference between control and LQ75, and between LA and LQ100. The other stages of embryonic development were not significantly affected by the treatment. Overall, early embryonic development in the control and LQ75 mice were better than LQ100 and LA mice. The number of cells in the trophectoderm and inner-cell mass were not affected by treatments. However, the total blastocyst cell number in the control was higher than in the other groups; there was no significant difference between LQ100, LQ75 and LA groups. Fertilization rate was not affected by the treatments (P < 0.05). Quercetin acts as a potent antioxidant at low doses, but at high doses exerts a pro-oxidant action. According to previous reports, higher concentrations of quercetin increased apoptosis and necrosis while decreasing the activities of the antioxidant enzymes. Also, it has been suggested that quercetin might disrupt the endocrine system and interfere with Sertoli cell function and sperm motility. Limitations, reasons for caution A limitation of this study is narrow dose selection; more studies are needed to determine the effective dose of quercetin in ameliorating the lead toxicity. There are also side effects of lead-quercetin chelates such as metal redistribution, essential metal loss, accumulation and persistency in intracellular sites, and peroxidation. Wider implications of the findings: Lead administration adversely impacted on the embryogenesis; on the other hand, paternal quercetin co-administration somewhat ameliorated the adverse effects of lead on mice embryogenesis. Trial registration number Not applicable

scholarly journals Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. I. Rapid evolution of encephalomyocarditis virus infection.

1976 ◽  
Vol 144 (5) ◽  
pp. 1305-1315 ◽  
Author(s):  
I Gresser ◽  
M G Tovey ◽  
M E Bandu ◽  
C Maury ◽  
D Brouty-Boyé
Keyword(s):  
Virus Infection ◽  
High Titer ◽  
Rapid Evolution ◽  
Human Leukocyte ◽  
Central Nervous System Disease ◽  
Virus Multiplication ◽  
Encephalomyocarditis Virus ◽  
Visceral Organs ◽  
Emc Virus

The role of interferon in the pathogenesis of encephalomyocarditis (EMC) virus infection was determined by treating mice with potent, partially purified sheep anti-mouse interferon globulin. In control mice, EMC virus was present in low titers in various visceral organs but attained high titers in the brain towards the 4th to 5th day, at which time mice died with signs of central nervous system disease. In mice treated with anti-mouse interferon globulin, virus was present in high titer in visceral organs 24--36 h after viral inoculation and virtually all mice were dead by 45 h. This rapid evolution of EMC virus infection was not observed in mice treated with the globulin fraction prepared from a normal sheep, from a sheep exhibiting a low anti-mouse interferon-neutralizing titer, nor from a sheep having a high titer of antibody to human leukocyte interferon. The experimental results indicated that anti-interferon globulin neutralized the interferon liberated by virus-infected cells, thus permitting extensive virus multiplication in several visceral organs. We conclude that interferon is an important early component of host resistance to this virus infection.

scholarly journals ANTIBODY RESPONSE OF PATIENTS WITH POLIOMYELITIS TO VIRUS RECOVERED FROM THEIR OWN ALIMENTARY TRACT

1949 ◽  
Vol 90 (4) ◽  
pp. 349-372 ◽  
Author(s):  
Alex J. Steigman ◽  
Albert B. Sabin
Keyword(s):  
Single Dose ◽  
Antibody Response ◽  
Acute Phase ◽  
Alimentary Tract ◽  
High Titer ◽  
The Other ◽  
Minimal Amount ◽  
Virus Antibody ◽  
Serum Dilution

Of 20 strains of virus recovered from 40 patients with poliomyelitis only 9 possessed a titer of 10–3 or more, permitting significant quantitative neutralization tests in monkeys. Seven of the 9 high titer strains were derived from patients whose illness was ultimately paralytic, and tests with their undiluted sera indicated that the acute phase as well as the 3 month convalescent specimens neutralized maximum amounts of the patient's own virus. However when varying dilutions of the sera were tested against a single dose of virus, it was found that the antibody was present in lowest concentration early after onset and progressively increased in titer over a period of weeks during convalescence. The 2 remaining high titer strains were recovered from patients with a non-paralytic illness, and in both of these the acute phase sera were without significant amounts of antibody for their own virus. Antibody was demonstrable at 14, 28, and 92 days after onset in one of these patients, while the other had none at 1 month and only a minimal amount at 3 and 8 months. Tests with the Lansing virus on the same sera, clearly established the specificity of the antibody response to the strain of virus recovered from each patient under investigation. Five of the 9 patients, whose sera were studied with both viruses, had no antibody for the Lansing virus during the acute phase and none 3 months later. Two had antibody during the acute phase but serum dilution tests showed no increase in titer in the 3 month convalescent specimen. In 2 others, who were without antibody for the Lansing virus during the acute phase but had it at 3 months after onset, it was possible to show that this antibody appeared later than 1 month after the illness and that the virus recovered from these patients during their illness was not antigenically of the Lansing type.

scholarly journals IX.— The life-history and cytology of synchytrium endobioticum (schilb.), perc., the cause of wart disease in potato

1921 ◽  
Vol 210 (372-381) ◽  
pp. 409-478 ◽  
Keyword(s):  
Life History ◽  
Host Cell ◽  
The Other ◽  
Short Paper ◽  
Winter Dormancy ◽  
Wart Disease ◽  
Linnean Society ◽  
Synchytrium Endobioticum ◽  
Infection Experiments

Wart disease of the potato was first reported from Hungary in 1896 by Schilberszky (43), who gave a brief description of the summer and the resting sporangia, named the organism Chrysophlyctis endobiotica , and included it in the Chytridinece . He saw the discharge of the zoospores from the summer-sporangia, and he put forward the view that the zoospores were responsible for the further distribution of the organism through the tumour by the ability which he believed they possessed of boring their way through the walls of the host cell into the adjoining cells. The fungus probably existed in England many years before Schilberszky’s paper was written, but its presence in this country was not generally recognised. In 1902 Potter (36) published a short paper on the organism. He there showed that resting sporangia, which had been kept dry during the winter, were able to cause the infection of tubers the next season. The distribution of the organism through the tumour he attributed,to its division, when in a condition which he describes as plasmodial, and to the passage of the segments so produced through the walls into the adjacent cells. For several years after Potter’s publication appeared few facts were added to the existing knowledge of the disease, but in 1907 Borthwick (4) reported that leaves could be attacked as well as tubers. In the following year, Salmon (42) carried out a series of infection experiments, from the results of which he concluded that resting sporangia, after exposure for I f hours to a temperature ranging from — 5° C. to — 6° C., could dispense with the winter dormancy and germinate at once. Shortly afterwards two notes appeared, one from the pen of Johnson (16) and the other from that of Weiss (49). Both succeeded in obtaining the germination of the resting sporangium, and, in addition, Johnson found that the zoospores liberated exhibited the usual characteristics of the Chytridian zoospore, while Weiss remarked upon the rapidity with which they became amoeboid. In December of the same year Masses (31), when exhibiting specimens of diseased tubers at a meeting of the Linnean Society, expressed the opinion that the organism belonged to the genus Synchytrium ; but he based his statement upon the so-called epidermal nature of the parasite and upon the supposed presence of an enveloping membrane round the protruding contents of the germinating resting sporangium, both of which suppositions have since been shown to be incorrect.

scholarly journals Kidney Complications in EMC Virus-induced Diabetes in Conventional DBA/2 Male Mice

1990 ◽  
Vol 39 (1) ◽  
pp. 113-116 ◽  
Author(s):  
Kazuhiro SHICHINOHE ◽  
Masumi SHIMIZU ◽  
Masamichi ISHIZAKI ◽  
Mitsuo ASAKAWA
Keyword(s):  
Male Mice ◽  
Emc Virus

scholarly journals Toxicity of silver nanoparticles on Endometrial Receptivity in Female Mice

2021 ◽  
Author(s):  
marziyeh ajdary ◽  
Sahar Eghbali ◽  
Vahid Pirhajati Mahabadi ◽  
Fariborz Keyhanfar ◽  
Rajender S Varma
Keyword(s):  
Silver Nanoparticles ◽  
Endometrial Receptivity ◽  
Endometrial Tissue ◽  
The Other ◽  
Male Mice ◽  
Uterine Tissue ◽  
Blood Samples ◽  
Female Mice ◽  
Molecular Tests ◽  
Major Increase

Nanoparticles (NPs) have many toxic effects on fertility and can prevent successful implantation by affecting the maternal uterine tissue. Herein, by deploying thirty female NMRI mice, the effect of silver nanoparticles on the endometrium and implantation has been investigated. Using spherical silver nanoparticles of a diameter of 18-30 nm at doses of 2 and 4 mg/kg, mice in both groups were treated. Then, female mice mated with male mice. Endometrial tissue was extracted 4.5 days later. On the fourth day of pregnancy, the mice were anesthetized and blood samples were taken from the heart; furthermore, endometrial tissue was isolated and used for molecular tests, ICP, and examination of pinopods. The results revealed that the levels of IL6 and IL1β and the accumulation of nanoparticles in endometrial tissue in the group receiving nanoparticles at a dose of 4 mg/kg had a major increase relative to the other two groups (p<0.05); group receiving a dose of 4 mg/kg, exhibited a decrease in pinopods and microvillus compared to the other two groups. According to the results, NPs can reach the endometrium, suggesting that caution should be exercised due to serious exposure to nanoparticles throughout pregnancy.

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