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)

Synovial cell lines were established from patients with rheumatoid arthritis (RA) and from normal human embryos. High levels of hyaluronic acid (HA) were produced by some RA cell lines, some of which were partially or completely resistant to infection with Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and rubella virus (RV). Normal fetal synovial cells lines were susceptible to NDV, VSV, and RV. Infection with virus became possible after treatment of RA cells with hyaluronidase to depolymerize HA, and HA prevented infection of normal synovial cells with VSV. These results provide evidence that HA and not chronic or latent viral infection is responsible for the lack of susceptibility of RA synovial cells to certain viruses.
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PMID:Rubella and rheumatoid arthritis: hyaluronic acid and susceptibility of cultured rheumatoid synovial cells to viruses. 16 79

In accordance with the system of viral species, viral disorders of the oral mucosa may be classified with regard to their intensity of affection. There are but few viral infections exclusively affecting the oral mucosa like e.g. 1. Glossitis papulosa of Michelson, representing a special form of vaccinia inoculata, 2. Gingivo-stomatitis herpetica and 3. warts of the mucosa or condyloma-like papillomas of the oral mucosa including oral papillomatosis, that, itself shows morphological and clinical similarities to laryngeal papilloma. A second group of disorders mainly affecting the oral mucosa includes the "Aphthoid of Pospischill and Feyrter", Zahorsky's herpangina and other viral infections by the Coxsackie group, like vesicular stomatitis. The 3rd group represents viral infections of other organs in which affection of the oral mucosa is a prerogative, e.g. smallpox, varicella, foot-and-mouth disease and pharyngo-conjunctival fever. A 4th group includes those viral infections of the organs in which co-affection of oral mucosa occurs frequently or once in a while (at occasions). Here, we find eczema vaccinatum, herpes zoster, herpes simplex of the oral mucosa mostly on the hard palate, eczema herpeticatum, post-herpetic Erythema exsudativum multiforme, Mononucleosis infectiosa Pfeiffer, viral flu, German measles, parotitis epidemica, rubeola and ECHO-exanthema. A 5th and last group is made up by viral infections of other organs, in which affection of the oral mucosa hardly occurs at all. This group contains paravaccinal Ecthyma contagiosum, poliomyelitis, viral infection of the city of Marburg and some Arbovirus infections. Relatively few viral disorders never co-exist with lesions on the oral mucosa like e.g. Virus-hepatitis or some viral encephalitides. Groups 1 and 2, most important of all, are presented in detail regarding clinics, diagnostics, differential-diagnosis and therapy. The disorders within the other 3 groups are discussed only regarding their importance in the field of ENT-related symptoms of the oral mucosa. A number of pictures and tables completes important clinical details and give further hints to their differential-diagnosis.
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PMID:[Virus diseases of the mouth mucosa]. 83 Jan 6

We developed enzyme linked immunosorbent assay (ELISA) for the detection of rubella virus antigen, using two monoclonal antibodies, MC-7 and MC-22. The double antibody sandwich ELISA method was carefully standardized and found to be sensitive enough to detect as small as 2.5 ng protein of rubella virus. The infective titers by the double antibody sandwich ELISA closely related to those judged by interference of vesicular stomatitis virus in RK-13 cells. The method is simple, sensitive, and readily applicable to the detection of rubella virus.
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PMID:Double antibody sandwich ELISA for the detection of rubella virus antigen. 133 82

Chick embryo otocyst organ cultures were subjected to live vesicular stomatitis virus and rubella virus preparations, to interferon (IFN), and to a combination of both virus and IFN, and compared to control untreated otocysts. We observed morphologic and microscopic changes suggestive of individual cell death and delayed organ differentiation in the virus-treated groups, along with an appreciable decrease in size of the otocyst. Low-dose IFN treatment prior to virus inoculation appeared to partially prevent these effects. The addition of IFN alone did not seem to affect the differentiation process. Time-lapse videophotography further confirmed the above findings. This study suggests that the peripheral component of congenital deafness associated with viral infections is likely to be an effect of the virus itself, and not of the IFN. Interferon provides a partial protective effect against the insult from the virus in vitro and does not seem to be toxic to the developing otocyst.
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PMID:Effect of viruses and interferon on chick embryo otocyst cultures. 172 Sep 34

Presistent infections with rubella virus were established in baby hamster kidney, BSC-1, HeLa, RK-13, rabbit embryo chondrocyte, and Vero cell lines. All of the cultures except Vero continually produced rubella virus and interferon to which the virus was sensitive. Concurrently, only the Vero cells did not display interference against superinfection with Newcastle disease and vesicular stomatitis viruses. The addition of 1,000 U of exogenous interferon to the cultures cured only the rabbit embryo and Vero cells of the persistent infection. That the interferon is not required for the initiation and maintenance of rubella viral persistence in vitro is implied by the following. (1) Vero cells were persistently infected in the absence of interferon; (2) actinomycin D or cortisone inhibited interferon synthesis but not the rubella viral infection; and (3) cells continuously cultured in the presence of cortisone maintained a viral persistence without interferon synthesis. On the other hand, interferon seems to be responsible for the viral interference; Vero cells infected with rubella virus and cultures inoculated with rubella virus in the presence of actinomycin D or cortisone did not display interference against Newcastle disease or vesicular stomatitis viruses.
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PMID:Role of interferon in six cell lines persistently infected with rubella virus. 421 83

Vero cells, a line of African green monkey kidney cells, failed to produce interferon when infected with Newcastle disease, Sendai, Sindbis, and rubella viruses, although the cells were sensitive to interferon. Further, infection of Vero cells with rubella virus did not result in interference with the replication of echovirus 11, Newcastle disease virus, or vesicular stomatitis virus, even in cultures where virtually every cell was infected with rubella virus. Under the same conditions, BSC-1 cells and other cells of primate origin produced interferon and showed rubella virus interference. The results indicate that the presence of rubella virus in the cell does not in itself exclude multiplication of other viruses and that rubella virus interference appears to be linked to the capability of the cell to produce interferon.
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PMID:Defectiveness of interferon production and of rubella virus interference in a line of African green monkey kidney cells (Vero). 430 13

A series of 19 different primary and serial tissue cultures were investigated for their sensitivity to virulent or attenuated rubella virus (RV). Primary guinea pig tissues, a serial passage of baby hamster kidney, and primary human amnion were comparable to African green monkey kidney tissue cultures in their sensitivity. In general, primary human tissues were relatively insusceptible to the Gilchrist strain of RV. RV interfered with the growth of vesicular stomatitis virus. Based on this finding, it was possible to develop an assay method in guinea pig tissue cultures by using VSV as the challenge virus. This system appeared to be comparable in sensitivity to the use of primary monkey kidney tissue cultures for the detection of small amounts of RV and offers the advantages of economy, rapidity, and safety.
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PMID:Comparative sensitivity of tissue cultures to rubella virus: use of guinea pig cells for virus titration. 497 43

Spontaneous rubella carrier cultures derived from tissues of infants with congenital rubella were studied in an attempt to elucidate a possible mechanism for viral persistence observed in these infants. Chronically infected cells were found to have a reduced growth rate and the cultures appeared to have a shortened life span. The rubella carrier state was not dependent on serum inhibitors or rubella antibodies. Virtually every cell in the carrier population was found to be producing virus. The carrier cultures could not be cured by rubella antibodies. The rubella-infected cells were resistant to superinfection with vesicular stomatitis virus and herpes simplex virus but were susceptible to infection with echovirus 11. The replication of vesicular stomatitis virus was apparently blocked at an intracellular site, for the virus readily adsorbed to the chronically infected cells and entered into an eclipse phase; however no infectious virus developed. No evidence of interferon production by these cells could be obtained. It is postulated that clones of rubella-infected cells in vivo, with properties similar to those in carrier cultures developed in vitro from tissues of in utero infected infants, might explain the observed viral persistence noted in congenital rubella.
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PMID:Rubella virus carrier cultures derived from congenitally infected infants. 593 14

A persistent infection of the human MCF-7 cell line (MCF-7RV) was established with the DBS strain of rubella virus at a low multiplicity of infections. Fluorescent antibody staining revealed that 100% of the cells were positive for rubella antigens. The infected cells were refractory to superinfection with vesicular stomatitis virus (VSV) but were susceptible to herpes simplex virus type 2 (HSV-2). No interferon could be detected in infected cell culture fluid, and continuous passage in the presence of antibody did not lead to a decrease in the percentage of infected cells. Virus production in the persistently infected cells represented a 5- to 10-fold increase over primary infection. Plaque assays at 30 and 39 degree C of the virus produced at 37 degree C revealed the presence of temperature-sensitive (ts) mutants. If MCF-7RV cells were maintained at 30 degree C, significant increases in virus production were observed, leading to cytopathic effect and destruction of the monolayer. If maintained at 39 degree C, MCF-7RV cells produced less virus and demonstrated normal morphology. These data suggest that the naturally selected population of ts mutants being produced by these cells represents the mechanism by which persistence is maintained.
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PMID:Characteristics of a persistent rubella infection in a human cell line. 616 85

Autoreactive T cells specific for myelin basic protein (MBP), a major component of central nervous system (CNS) protein, are frequently found in blood and cerebrospinal fluid of patients with postinfectious encephalomyelitis. This autoimmune syndrome is a CNS complication after infections with a number of different enveloped viruses, e.g. mumps, measles, rubella, influenza and varicella. However, the pathophysiological mechanism leading to this breaking of natural self tolerance in the course of viral infection remains an enigma. A long-lasting hypothesis has suggested that incorporation of cellular (self) proteins into the envelope of budding viruses might be a possible mechanism leading to autosensitization. In a model study we demonstrate here that vesicular stomatitis virus (VSV), grown in myelin protein-expressing cell cultures, is highly efficient in triggering T cell responses to MBP in vitro and can prime autoreactive T cell immune responses in vivo. On the basis of these findings, we suggest that incorporation of CNS membrane components into the viral envelope and subsequent priming of self-reactive immune responses might be the common pathogenic mechanism underlying the postinfectious encephalomyelitis syndrome.
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PMID:Autoimmunity caused by host cell protein-containing viruses. 753 Dec 73


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