Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ocular viral infections are a major cause of loss of vision and their effective control by applications of chemical compounds has been extensively investigated. To achieve such a control, better understanding of virus-host-drug interactions become a necessity. Two models, hamster and rabbit cornea, were selected for assays of protection afforded by tilorone dihydrochloride against herpes simplex (HSV) and vesicular stomatitis viruses (VSV). To obtain basic biologic comparison between viral interference and interferon-induction by tilorone, the hamster cornea system was first studied to produce a mutual viral interference by double infection. Furthermore, its effect against ascending herpetic ocular infection into encephalitis was evaluated in the rabbit. This compound was reported to have promising results in improving manifestations such as corneal ulceration, uveitis and conjunctivitis.
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PMID:The mode of inhibition of herpes simplex and vesicular stomatitis ocular viral infections in the rabbit and hamster by an interferon inducer tilorone dihydrochloride. 16 23

The pathogenicity of infection produced following intracerebral (i.c.) inoculation of wild-type vesicular stomatitis virus (VSV) or temperature-sensitive (ts) mutants of VSV was compared. ts mutants used were ts 31 (VSV complementation group II) and ts 41 (VSV complementation group IV). The i.c. injection of wild-type VSV in weanling Swiss mice produced a rapidly fatal encephalitis with death of mice in 2 to 3 days. Histopathologically, such mice exhibited minimal changes of encephalitis on light microscopy. In contrast to the highly virulent, rapidly fatal central nervous system (CNS) infection seen after i.c. inoculation of wild-type VSV, infection with ts 31 VSV produced a more slowly progressive CNS infection characterized by hind limb paralysis and death 6 to 9 days after infection. Histopathologically, CNS infection with ts 31 is associated with previously unreported extensive spongiform changes in the gray matter of the spinal cord. The inoculation of ts 41 i.c., on the other hand, did not result in either clinical illness or histopathological changes in the spinal cords or brains of infected mice. The absence of clinical and histopathological lesions following i.c. infection of ts 41 VSV suggests that the capacity to alter the pathogenesis of VSV CNS infection may be a function of only certain ts mutants of VSV.
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PMID:Comparison of central nervous system disease produced by wild-type and temperature-sensitive mutants of vesicular stomatitis virus. 17 53

Vaccination of animals may have both positive and negative effects on human health. The negative consequences largely occur with live vaccines. The protection provided by vaccination to animals is taken advantage of for human health in the most diverse ways, both directly and indirectly. Typical examples are vaccination of dogs and cats against against rabies and inoculation against diseases of cattle, horses and dogs in which reoviruses of serotypes 1, 2 and 3 are involved. An important contribution to the protection of human health is also provided by vaccination with inactivated pathogens against leptospirosis and salmonellosis, against stomatitis vesicularis and American equine encephalitis and in developing countries against brucellosis.
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PMID:[Vaccinations of animals and human health (author's transl)]. 19 46

3-Deazaguanine (ICN 4221), 3-deazaguanosine (ICN 4793), and 3-deazaguanylic acid (ICN 5412) represent a new class of synthetic guanine analogs having antiviral activity. In vitro, nine ribonucleic acid and seven deoxyribonucleic acid viruses were inhibited, including influenza, parainfluenza, rhino-, vesicular stomatitis, adeno-, herpes-, cytomegalo-, vaccinia, pseudorabies, and myxoma viruses. They were effective orally against influenza types A and B and parainfluenza type 1 (Sendai) virus infections in mice, with a therapeutic index of 16 against the latter two viruses. The course of herpes encephalitis was altered only when the drugs were applied directly into the brain. In addition, these drugs were effective inhibitors of Friend leukemia virus-induced splenomegaly in mice; treatment also produced extensions of life in these animals.
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PMID:Antiviral activity of 3-deazaguanine, 3-deazaguanosine, and 3-deazaguanylic acid. 19 46

Wild type Eastern equine encephalitis virus (E) was compared with a mutant (Em) derived from it. The latter was tested as an attenuated vaccine in mice. They differed in the following properties: Em formed smaller plaques on chick embryo (CE) cell monolayers and, unlike E, did not plaque on mouse embryo (ME) monolayers. Futher, Em had a longer latent period and attained a lower peak titer than E after infection of CE cells, was more senssitive than E to chick interferon, and was less virulent for mice (SC and IP routes) and hamsters (IP route) than E. Both viruses were similar in several other properties tested. The mutant was found to induce a gradient in the specificity of protection in mice against challenge by selected viruses after a single subcutaneous injection of living virus. The protection was best against autologous (Em) challenge, was next best against challenge by the virulent parent (E) virus, but was not demonstrable against cross challenge by Venezuelan encephalitis (V) virus. Conventional hemagglutination-inhibiting (HI), complement-fixing (F), and neutralizing (N) antibodies could not be detected in Em-immunized mice even when fresh monkey or guinea pig serum was included in Ntests to provide complement and/or accessory factor(s). However, N antibodies were detected in protected mice by an indirect antiglobulin test. Passive protection by serum or ascites fluids (a.f.) was characterized by a lower but otherwise similar protection gradient like that found after active immunization with virus as described above. Interferon was not detected in the a.f. used for passive protection, nor was heterologous interference evident in Em immunized mice challenged 18 days later with vaccinia or vesicular stomatitis virus. Immunized mice that survived autologous (Em) challenge showed broadened protection against a second challenge by parent E virus, and cross protection against V virus. This typical protection was associated with the presence of HI and conventional N antibodies, except for V which showed no detectable neutralizing antibodies by either a standard or antiglobulin technique.
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PMID:An attenuated variant of Eastern encephalitis virus: biological properties and protection induced in mice. 111 39

During 1988 and 1989, a serologic survey of wildlife was conducted in northeastern Mexico to determine the presence, prevalence, and distribution of arboviruses and other selected disease agents. Eighty mammal specimens were tested. Antibodies to vesicular stomatitis-Indiana, Venezuelan equine encephalitis-Mena II, Rio Grande virus, and vesicular stomatitis-New Jersey were detected predominantly in small mammals. Deer and mouflon (Ovis musimon) had antibodies to bluetongue and epizootic hemorrhagic disease. Two species had serologic evidence of recent exposure to Francisella tularensis. A white-tailed deer (Odocoileus virginianus) had antibodies to Anaplasma marginale. All specimens tested for antibodies against Yersinia pestis and Brucella abortus were negative. Sera from 315 birds were tested for antibody against five equine encephalitis viruses and six avian pathogens. During 1988, antibodies to Venezuelan equine encephalitis-Mena II, Venezuelan equine encephalitis-TC83, St. Louis encephalitis, eastern equine encephalitis, and western equine encephalitis were detected in birds of several species. Antibodies to Pasteurella multocida and Newcastle disease virus were also detected. Birds from five species presented antibodies to Mycoplasma meleagridis. Specimens tested for M. gallisepticum, M. synoviae, and Chlamydia psittaci were negative. To the best of our knowledge, this survey represents the first serologic evidence of bluetongue, Cache Valley virus, epizootic hemorrhagic disease, Jamestown Canyon virus, vesicular stomatitis-Indiana, vesicular stomatitis-New Jersey, Rio Grande virus, and tularemia reported among wildlife in Mexico.
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PMID:Serologic survey for selected arboviruses and other potential pathogens in wildlife from Mexico. 151 76

Hundreds of striped dolphins (Stenella coeruleoalba) died along the Spanish Mediterranean coast during the second half of 1990. We necropsied 58 dolphins. Partial collapse of the lungs with patchy atelectasis, subcutaneous edema, icterus, and stomatitis were the most prominent gross morphologic changes. Histologically, a bronchiolo-interstitial pneumonia was the most frequent lesion (72% of the animals). It was characterized by hyperplasia of alveolar epithelial type II cells and formation of multinucleate syncytia in alveolar and bronchiolar lumina. Other prominent lesions were encephalitis (69%), lymphoid depletion, and formation of multinucleate syncytia in the cortex of lymph nodes. The distribution of morbillivirus antigen was investigated in 23 well-preserved dolphins using a monoclonal antibody against the hemagglutinin glycoprotein of phocine distemper virus. Positive immunostaining was found in brain (77%), in lung (70%), and in mesenteric (61%), mediastinal (47%), and prescapular (45%) lymph nodes. Phocine distemper virus antigen was demonstrated less frequently in trachea, stomach, biliary epithelium, intestine, kidney, and mammary gland. Necrotizing-hemorrhagic pneumonia and encephalitis due to Aspergillus fumigatus were seen in three dolphins, whereas two animals had lesions of toxoplasmosis. Changes in our dolphins were similar to those caused by distemper in seals and porpoises. The origin of the dolphin virus and the relationships among dolphin, seal, and porpoise morbilli viruses are unknown.
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PMID:Pathologic and immunocytochemical studies of morbillivirus infection in striped dolphins (Stenella coeruleoalba). 155 61

BALB/c mice and congenic H-2Ld-deficient BALB/c-H-2dm2 (dm2) mice were experimentally infected intranasally with isolates of vesicular stomatitis virus (VSV). The survival of infected hosts, viral replication in lungs and brains, and histopathologic in the two mouse strains were compared. In both strains of mice, mortality occurred during the period 7 to 10 days postinfection. However, dm2 mice were relatively resistant to lethal infections. Viral replication occurred at low levels in the lungs of both strains and did not evoke significant pathologic changes. In contrast, viral replication in the brains was much greater; in the BALB/c strain, this was accompanied by more frequent and more severe pathologic changes. In general, mice surviving at day 10 had effectively cleared virus from central nervous system but not respiratory sites. Evidence is presented that viral replication occurs first in the nasal cavity and is transmitted both to the lungs and to the olfactory bulb where focal cytopathology occurs. Virus enters the ventricles, causing encephalitis; necrosis occurs around the ventricles and in the lumbosacral region of the spinal cord. Necrotic lesions were accompanied by mononuclear infiltration. Mice immunized with virus of the same serotype or with a vaccinia virus hybrid encoding the VSV glycoprotein were protected from lethal infection; in contrast, mice immunized with heterotypic virus were susceptible to challenge.
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PMID:Murine infection by vesicular stomatitis virus: initial characterization of the H-2d system. 165 14

In this study, we investigated the effect of a lentivirus-induced interferon (LV-IFN) on the interaction of caprine arthritis-encephalitis virus and its host cell, the monocyte-macrophage. LV-IFN was produced in culture supernatant 48 h after adding fresh goat lymphocytes to caprine arthritis-encephalitis virus-infected goat macrophages. The culture supernatant contained IFN activity at a titer of 1:360 as assayed by inhibition of vesicular stomatitis virus-induced lysis of fibroblasts. LV-IFN inhibited in vitro monocyte proliferation and maturation of monocytes to macrophages. Nevertheless, treated monocytes produced prostaglandin E2, a cytokine generally produced by activated macrophages. By inhibiting the maturation of monocytes to the more permissive macrophage, LV-IFN indirectly downregulated virus replication. The cytokine also had a direct inhibitory effect on virus gene expression in already mature macrophages. In these cells, LV-IFN blocked the viral life cycle at the level of transcription. Finally, LV-IFN blocked fusion between infected macrophages and highly permissive goat synovial membrane cells. By restricting macrophage maturation, viral replication, and cell fusion, LV-IFN may downregulate the net rate of virus replication in vivo. These functions may contribute to the persistence of the virus in the host by reducing the expression of the viral genome.
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PMID:Lentivirus-induced interferon inhibits maturation and proliferation of monocytes and restricts the replication of caprine arthritis-encephalitis virus. 247 Sep 18

Interleukin 6 (IL6) was found to be produced in the central nervous system (CNS) of ICR+/+ mice infected with lymphocytic choriomeningitis virus (LCMV) or with vesicular stomatitis virus (VSV). When infecting athymic ICR nu/nu mice which cannot develop T cell-mediated meningitis after LCMV infection, no significant synthesis of IL6 was detected in the CNS. IL6 was found, however, to be produced intrathecally in ICR nu/nu mice infected with VSV, which causes a T cell-independent acute encephalitis. This suggested that IL6 may also originate from cells not belonging to the T cell compartment. Indeed, in vitro assays showed that both virus-infected microglial cells and astrocytes secreted IL6. In astrocytes, the infection resulted in the induction of the 1.3-kb messenger RNA IL6. Besides its effect on the development of B cell immunity in the brain, IL6 may be involved in repair mechanisms initiated in the course of viral-induced tissue damage. As shown here, IL6 induced an increase of the secretion of a neurotrophic factor, nerve growth factor by astrocytes. Thus, the intrathecal synthesis of IL6 may be part of the host response to infection favoring immune-mediated elimination of the infectious agent as well as trophic support for neurons.
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PMID:On the cellular source and function of interleukin 6 produced in the central nervous system in viral diseases. 254 84


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