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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Co-infection of cells with vesicular stomatitis viruses of the Indiana and New Jersey serotypes results in interference. Using specifically-labelled immunofluorescent antibodies, it was demonstrated that within any one co-infected cell, one virus serotype replicated to the relative exclusion of the other serotype. This result was further substantiated by an examination of the virus serotypes released by infectious centres co-infected with both viruses. Dominance of one serotype over the other was shown to be a function of the relative multiplicity of the two viruses. Superinfection by the second serotype at a higher multiplicity resulted in dominance by the second virus during the early period (up to 1-5 h) post-infection. After this time, the minority virus was able to overcome this dominance. Dominance of the majority virus was also abolished by u.v; inactivation. Cell protein synthesis appeared to be less affected in cells infected with both serotypes than when infection was with a single serotype.
J Gen Virol 1977 Apr
PMID:Heterotypic exclusion between vesicular stomatitis viruses of the New Jersey and Indiana serotypes. 19 45

The effect of interferon on the synthesis of the RNA species and proteins of vesicular stomatitis virus has been studied in two cell types. Virus protein synthesis is inhibited by interferon despite the apparent presence of near normal amounts of virus RNA with sedimentation values characteristic of virus messenger RNA. The synthesis of those virus RNA species which are completely dependent on virus protein synthesis is preferentially inhibited in interferon-treated cells. These results are most consistent with a model of interferon action postulating a primary effect on translation of virus messenger RNA.
J Gen Virol 1977 May
PMID:Effects of interferon on vesicular stomatitis virus transcription and translation. 19 9

The distribution pattern of actin-containing structures in BHK21 cells and the changes which they undergo upon infection with Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV) were studied by means of immunofluorescence. Double labelling with antibodies conjugated with fluorescein (for actin) and rhodamine (for virus antigens) has shown that the progressive cytopathic effects after virus infection are accompanied by extensive alterations of the structures demonstrable by antiactin antibodies. In NDV-infected BHK21 cells the number of actin filaments increases, some zones which contain virus antigens apparently being in close association with the actin structures. By contrast, infection with VSV results in a strong reduction of actin-containing fibres. The results indicate that in the genesis of morphologically detectable alterations of a cell after virus infection--the 'cytopathic changes'--alterations of those structural elements are involved which are also probably responsible for maintenance of cell shape and motility.
J Gen Virol 1977 Nov
PMID:Alterations of actin-containing structures in BHK21 cells infected with Newcastle disease virus and vesicular stomatitis virus. 20 Jul 6

The individual structural polypeptides of vesicular stomatitis virus have been examined by tryptic peptide analysis of 35S-methionine preparations labelled in vivo and 125I-preparations labelled in vitro. Isolates of the two classical serotypes of the virus (Indiana and New Jersey) and of a sub-type of the Indiana serotype, Brazil virus, were compared. The study showed that the major internal proteins of all three viruses gave similar maps, whereas the surface glycoproteins gave distinct maps that had very few spots in common. The map of the glycoprotein of Brazil virus, which has been shown previously to be more closely related serologically to Indiana virus than to New Jersey virus, did not show any greater similarity to the Indiana virus than to the New Jersey virus glycoprotein. On the other hand, peptide maps of the nucleoprotein and matrix protein showed Indiana and Brazil viruses to be more closely related to each other than to New Jersey virus.
J Gen Virol 1978 Feb
PMID:Tryptic peptide analysis of the structural proteins of vesicular stomatitis virus. 20 55

Transcription of vesicular stomatitis virus (VSV) in Vero cells was confined to the synthesis of parentally-derived mRNA (primary transcription) by the use of cycloheximide and/or a ts mutant, G41(IV), at a non-permissive temperature (40 degrees C). More transcripts accumulated in the presence of cycloheximide than in its absence. This so-called "cycloheximide effect" results from higher rates of virus transcription sustained for longer periods of time. The rate of VSV transcription initially increases linearly for 1 to 2 h after injection. Interferon reduces this rate (congruent to fourfold with 50 units/ml interferon) irrespective of the presence or absence of cycloheximide. The VSV mRNA transcripts synthesized in mock- or interferon-treated cells were equal in size and had an equivalent half-life of 17 h at 40 degrees C. It seems likely that once transcription is initiated in interferon-treated cells, it is completed successfully. Since interferon reduces the rate of early VSV primary transcript synthesis to below that achieved in the presence of cycloheximide, we conclude that interferon has an effect on transcription beyond that attributable solely to protein synthesis inhibition. We postulate that interferon decreases the probabiltiy of initiating virus transcription. Virus mRNA escaping this facet of interferon action may then encounter other facets such as post-transcriptional modification and/or inhibition of translation. However, the mandatory sequence of primary transcription leads to primary translation for negative-strand viruses like VSV dictates that the overall inhibitory effect of interferon on translation would derive in part from this prior inhibition of transcription. Thus, to apply the term "primary effect" to one particular facet of interferon action may not always be meaningful.
J Gen Virol 1978 Mar
PMID:Interferon action III. The rate of primary transcription of vesicular stomatitis virus is inhibited by interferon action. 20 29

The replication of human cytomegalovirus (CMV) and herpes simplex virus (HSV) was studied in three human embryo cell lines (CMV-Mj-HEL-I, CMV-Mj-HEL-2, and CMV-Mj-HEL-2,T-I) transformed in vitro by human CMV. Growth studies revealed that these cells were completely resistant to infection by CMV strains ADI69 and Mj and partially resistant to HSV types I and 2. Neither virus DNA nor virus proteins were synthesized in the transformed cells infected with CMV AD169. The HSV production in CMV-transformed human embryo lung (HEL) cells was delayed when compared to the virus production in normal HEL cells and spread of HSV c.p.e. was slower in the transformed cells. The treatment of normal HEL cells with a crude extract of CMV-transformed HEL cells also resulted in inhibition of the spread of c.p.e. of HSV types I and 2. The inhibitory effect was not due to interferon since vesicular stomatitis virus replication was not affected and several experiments showed that it was not due to mycoplasma. The presence of virus inhibitor molecules in CMV-transformed cells absent in normal HEL cells is postulated.
J Gen Virol 1978 Aug
PMID:Replication of herpesviruses in human cells transformed by cytomegalovirus. 21 Nov 87

The rate of development of interferon-induced virus resistance in a mixture of two human cell types (U and WISH) is determined by the cell type (WISH) in the mixture which responds first. This phenomenon has been shown with two types of interferon assay procedure, and with both vesicular stomatitis virus and Sindbis virus. The transfer of virus resistance from one human cell (WISH) to another (U) (homospecific transfer) is much more efficient than the transfer from mouse L cells to WISH cells (heterospecific transfer), as shown by a much lower ratio of donor to recipient cells required for maximum transfer as well as a more rapid transfer. Thus, virus protection afforded by the interferon system is amplified more efficiently in mixtures of different human cells than in mixtures of mouse and human cells. These results suggest that, in a mixed population of cells such as occurs in vivo, more slowly responding cells might be influenced by cells which respond more rapidly to interferon. A defensive role is suggested for this mechanism which amplifies protection due to interferon.
J Gen Virol 1978 Nov
PMID:Efficient transfer of interferon-induced virus resistance between human cells. 21 20

The effect of interferons on vesicular stomatitis virus (VSV) primary transcription, amplified RNA synthesis [i.e. the sum of primary transcription RNA replication (leading to [ - ] RNA) and secondary transcription (leading to [ + ] RNA) and virus protein synthesis were studied. In a human cell line, both human and simian interferons inhibited the initiation of primary transcription and amplified RNA synthesis. In contrast, in a simian cell line tested similarly, the initiation of these activities was not affected, though they decreased as the infection progressed. Nevertheless, virus protein synthesis was completely inhibited. These results demonstrate that the action of interferon on virus transcription and/or translation may depend more on the host cell than on the particular interferon used.
J Gen Virol 1978 Nov
PMID:Effect of interferon on transcription and translation of vesicular stomatitis virus in human and simian cell cultures. 21 23

Super-infection of Pichinde virus-infected cells with vesicular stomatitis virus (VSV) resulted in the production of pseudotype virus which was not neutralized by antiserum to VSV but which was neutralized by antiserum to Pichinde virus. Analysis of pseudotype virus production in relation to the kinetics of replication of Pichinde virus demonstrated that pseudotype virus production occurred when super-infection with VSV was initiated 8 h or more after infecting the cells with Pichinde virus. The quantities of pseudotype virus produced correlated with the quantities of Pichinde virus antigen detected on the surface of the cells both during acute infection and in cells chronically infected with Pichinde virus. The observations indicate that pseudotype of VSV and Pichinde virus are readily formed and that the formation of pseudotype virus may be used to examine the Pichinde virus antigens expressed on the surface of infected cells.
J Gen Virol 1979 Jan
PMID:Pseudotypes of vesicular stomatitis virus and Pichinde virus. 21 5

Sera from 67 patients treated for renal diseases were assayed by as many as three different tests for activities against Mason-Pfizer virus (M-P V) antigens. Firstly, in patients studied before kidney transplantation, neutralizing activity against syncytium-forming units of M-P V was found in 50% of 24 cases of chronic glomerulonephritis but in only 10% of 20 cases with other diseases (P less than 0.01). These proportions were higher after treatments accompanying transplantation since, of the 19 patients without antibodies before graft, 53% showed a sero-conversion after this treatment. The incidence of M-P V antibodies did not correlate with the number of transfusions received by the patients. Neither did these antibodies correlate with the presence of antibodies to antigens associated with baboon endogenous virus or simian sarcoma virus; antibodies to the latter two viruses were found in 6 to 21% of the sera, with no specific distribution among the sera. Secondly, pseudotypes of vesicular stomatitis virus with M-P V antigens in their envelope were prepared; they were inactivated by 90% of the sera which neutralized M-P V syncytium forming units and by none of the negative sera. Thirdly, specific complement-dependent cytotoxic antibodies to HeLa cells producing M-P V were also found in 61% of the sera with neutralizing activity to M-P V and only in 12% of the sera which did not neutralize M-P V. Absorption experiments indicated that the serum activities against M-P V associated antigens were not due to anticellular antibodies directed against normal constituents of human cells. However, no evidence has been provided that the M-P V associated antigens reacting with the human sera were virus coded.
J Gen Virol 1978 Dec
PMID:Neutralization of Mason-Pfizer virus by sera from patients treated for renal disease. 21 51


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