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)

We studied a pronounced Arias-Stella reaction in an incomplete abortion curettage specimen; the gestational age was 8 weeks by size. The majority of cells in this reaction showed ground glass, eosinophilic nuclear "inclusions" simulating herpetic Cowdry type B nuclear inclusions. This was coupled with a history of herpetic stomatitis of the patient and her husband 2 weeks prior to the curettage, raising the question of viremia and transplacental herpetic endometrial infection. Immunoperoxidase staining using the PAP technique directed against Herpes simplex virus types 1 and 2 was negative. Ultrastructural analysis elucidated the true nature of the nuclear "inclusions" as pseudonuclear inclusions consisting of invaginations of cytoplasm within the nuclei. Viral particles were not found. We are unaware of any similar report, and present this case to suggest the possible differential diagnosis between herpetic endometritis with associated cytologic atypia and the Arias-Stella reaction.
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PMID:Arias-Stella reaction with prominent nuclear pseudoinclusions simulating herpetic endometritis. 628 66

The increased use of serotype 2 Marek's disease virus (MDV) and serotype 3 turkey herpesvirus (HVT) as components of effective bivalent vaccines against Marek's disease (MD) prompted studies on the possible interactions of these two viruses in vitro and in vivo. The replication of the SB-1 strain of MDV was compared with replication of the FC126/2 strain of HVT in chickens and cell cultures infected with one or both viruses. Replication of MDV was reduced in the presence of HVT in both in vitro and in vivo systems. MDV plaque counts in dually infected chicken embryo fibroblast cultures inoculated with tissue-culture-propagated viruses were reduced by up to 91%; however, no inhibition was noted when inocula consisted of virus-infected buffy-coat cells. Plaque formation by MDV in chicken embryo fibroblast cultures was inhibited by virus-free conditioned medium from HVT-infected cultures. This conditioned medium also inhibited growth of vesicular stomatitis virus in a standard interferon assay. In chickens inoculated with both MDV and HVT, MDV viremia titers were lower and the dose required to infect 50% of susceptible chickens was increased 13-fold compared with chickens inoculated with MDV alone. In spite of these findings, there was no evidence that high concentrations of HVT interfered with either the ability of MDV to induce protective synergism in vivo or the protective efficacy of bivalent vaccines. No reciprocal inhibitory effects of MDV on the replication of HVT in vivo or in vitro were noted.
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PMID:Partial inhibition by turkey herpesvirus of serotype 2 Marek's disease virus plaque formation and in vivo infectivity. 770 14

Sentinel feral swine (Sus scrofa) on Ossabaw Island, Georgia (USA), were serologically monitored for antibodies to vesicular stomatitis New Jersey serotype (VSNJ) virus from 17 April to 27 August 1990. Seroconversions to VSNJ virus were detected in 24% of swine island-wide. Differences in the incidence of seroconversion were detected between swine sampled in the Pleistocene and Holocene formations of the island suggesting that the presence of virus is forest type dependent. Based on the consistency in onset and spatial distribution of seroconversions with data from 1981 to 1985, this is a very stable host-parasite system. Sequential virus isolation attempts from nasal swabs, tonsil swabs, and blood were made on a subsample of 54 sentinel swine from 9 May to 4 July 1990. The VSNJ virus was isolated from five swine from 16 May to 20 June. Vesicular lesions were detected on only two of these animals. Although infections in these feral swine were short-lived (< 7 days) and were followed by a strong neutralizing antibody response, VSNJ virus was detected in a single group of swine for a period exceeding 1 month. From these data, it appears that feral swine could provide a source of virus to feeding arthropods for extended periods of time. The failure to detect a viremia in these animals, however, indicates that a source other than blood may be required for transmission to occur.
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PMID:Feral swine as a potential amplifying host for vesicular stomatitis virus New Jersey serotype on Ossabaw Island, Georgia. 839 41

We have determined the partial nucleotide sequences of the polymerase genes of the fish rhabdoviruses, spring viremia of carp virus (SVCV) and infectious hematopoietic necrosis virus (IHNV). At this point we have deduced the amino acid sequences and analysed the first 1,400 amino acids comprising two thirds of the polymerase genes of SVCV and IHNV. We have compared sequence similarities of SVCV and IHNV polymerases with other rhabdovirus and paramyxovirus polymerases. The SVCV polymerase showed the closest relationship with the vesicular stomatitis virus polymerases and also shared significant sequence identity with the polymerase of rabies virus. Other rhabdovirus and paramyxovirus polymerases showed lower sequences identities with the SVCV polymerase. The IHNV polymerase shared a relatively low amino acid sequence identity with the rabies virus polymerase, and similar low identities with other rhabdovirus and paramyxovirus polymerases. Several domains of various lengths were conserved in the virus polymerases included in this study. These domains were less conserved in the IHNV polymerase than in the SVCV polymerase, and some of the domains present in the other polymerases were not identified in the IHNV. These preliminary results indicate that SVCV is closely related to mammalian vesiculoviruses and that IHNV may be only distantly related to mammalian lyssa and vesiculotype rhabdoviruses.
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PMID:Comparison of the polymerases (L genes) of spring viremia of carp virus and infectious hematopoietic necrosis virus. 858 Oct 12

The nucleotide sequences of the glycoprotein genes and all of the internal gene junctions of the fish pathogenic rhabdoviruses spring viremia of carp virus (SVCV) and hirame rhabdovirus (HIRRV) have been determined from cDNA clones generated from viral genomic RNA. The SVCV glycoprotein gene sequence is 1588 nucleotides (nt) long and encodes a 509 amino acid (aa) protein. The HIRRV glycoprotein gene sequence comprises 1612 nt, coding for a 508 aa protein. In sequence comparisons of 15 rhabdovirus glycoproteins, the SVCV glycoprotein gene showed the highest amino acid sequence identity (31.2-33.2%) with vesicular stomatitis New Jersey virus (VSNJV), Chandipura virus (CHPV) and vesicular stomatitis Indiana virus (VSIV). The HIRRV glycoprotein gene showed a very high amino acid sequence identity (74.3%) with the glycoprotein gene of another fish pathogenic rhabdovirus, infectious hematopoietic necrosis virus (IHNV), but no significant similarity with glycoproteins of VSIV or rabies virus (RABV). In phylogenetic analyses SVCV was grouped consistently with VSIV, VSNJV and CHPV in the Vesiculovirus genus of Rhabdoviridae. The fish rhabdoviruses HIRRV, IHNV and viral hemorrhagic septicemia virus (VHSV) showed close relationships with each other, but only very distant relationships with mammalian rhabdoviruses. The gene junctions are highly conserved between SVCV and VSIV, well conserved between IHNV and HIRRV, but not conserved between HIRRV/IHNV and RABV. Based on the combined results we suggest that the fish lyssa-type rhabdoviruses HIRRV, IHNV and VHSV may be grouped in their own genus within the family Rhabdoviridae. Aquarhabdovirus has been proposed for the name of this new genus.
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PMID:The glycoprotein genes and gene junctions of the fish rhabdoviruses spring viremia of carp virus and hirame rhabdovirus: analysis of relationships with other rhabdoviruses. 880 75

An enzootic focus of vesicular stomatitis virus New Jersey serotype (VSV-NJ) exists on Ossabaw Island, Georgia. Many questions regarding the epizootiology of this virus at this focus still exist, but evidence suggests that the vector for this virus is a phlebotomine sand fly (Lutzomyia shannoni), with feral swine serving as a potential source of virus for the sand fly and for other swine via contact transmission. We conducted 2 experimental trials in domestic swine using VSV-NJ isolated from a sand fly from Ossabaw Island to determine if route of inoculation or immunosuppression via steroid administration affected the development of disease, viremia, viral shedding, or the neutralizing antibody response. In a third trial, we studied the potential for contact transmission among swine using this isolate. Virus isolations were made from nasal cavity or palatine tonsil of the soft palate, and VSV-NJ neutralizing antibodies developed when pigs were inoculated intradermally in the apex of the snout, ear, or coronary band, intravenously, intranasally, or via scarification of the apex of the snout or coronary band. Vesicles developed only in pigs inoculated in the apex of the snout or coronary band, and these vesicles were at the site of inoculation. Steroid treatment did not potentiate the development of secondary vesicles and did not prolong the period of virus shedding from VSV-NJ-infected swine. Contact transmission, as determined by shedding of virus from the tonsil of the soft palate and the development of VSV-NJ neutralizing antibodies, occurred in pigs in contact with animals inoculated in the apex of the snout but not in contact animals exposed to pigs inoculated intradermally in the coronary band or intranasally. These trials show that contact transmission can occur and VSV-NJ can be shed without the development of clinical disease (i.e., vesicle formation). Viremia was never detected in any of the experimental pigs, suggesting that swine may not be a good amplifying host for VSV-NJ.
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PMID:Experimental vesicular stomatitis in swine: effects of route of inoculation and steroid treatment. 921 Dec 31

Various studies were done during a spontaneous outbreak of stomatitis-rhinitis-complex (mouth rot) in a collection of Mediterranean land tortoises (21 Testudo hermanni, Hermann's tortoises, and three Testudo graeca, spur-thighed tortoises) in southern Germany. These studies were intended to help diagnose the causative agent, establish a possible diagnostic method in vivo and provide information on the efficacy of aciclovir and ganciclovir against chelonian herpesviruses. Thirteen T. hermanni and no T. graeca died within a period of 6 weeks following the introduction of one apparently healthy T. graeca. Two of the dead Testudo hermanni were submitted for post-mortem examination. In addition, blood samples from 11 of the 12 tortoises still surviving at the beginning of this study were cultured for virus content and for the presence of neutralizing antibodies to chelonian herpesviruses and swabs from conjunctiva, pharynx and cloaca were cultured for the presence of viruses. Herpesviruses were isolated from tissues of the two dead Testudo hermanni (tongue, intestine, trachea, lung, spleen, heart and brain). Peripheral leukocytes from one of 11 blood samples were positive for herpesvirus isolation, indicating viremia in at least one animal. Nine of 11 pharyngeal swabs but none of the conjunctival and cloacal swabs yielded herpesviruses. Circulating neutralizing antibodies were present in two of two tested T. graeca, but absent in all of the nine samples from T. hermanni. Aciclovir and ganciclovir were effective when tested in vitro against one of the herpesvirus isolates.
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PMID:Herpesviruses in tortoises: investigations into virus isolation and the treatment of viral stomatitis in Testudo hermanni and T. graeca. 932 27

Vesicular stomatitis is an economically important arboviral disease of livestock. Viremia is absent in infected mammalian hosts, and the mechanism by which insects become infected with the causative agents, vesicular stomatitis viruses, remains unknown. Because infected and noninfected insects potentially feed on the same host in nature, infected and noninfected black flies were allowed to feed on the same host. Viremia was not detected in the host after infection by a black fly bite, but because noninfected black flies acquired the virus while co-feeding on the same host with infected black flies, it is concluded that a viremic host is not necessary for an insect to be infected with the virus. Thus co-feeding is a mechanism of infection for an insect-transmitted virus.
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PMID:Transmission of vesicular stomatitis virus from infected to noninfected black flies co-feeding on nonviremic deer mice. 1064 50

The matrix (M) protein of vesicular stomatitis virus inhibits both nuclear import and export. Here, we demonstrate that this inhibitory property is conserved between the M proteins from two other vesiculoviruses, chandipura virus and spring viremia carp virus. All three M proteins completely block nuclear transport of spliced mRNA, small nuclear RNAs, and small nuclear ribonucleoproteins and slow the nuclear transport of many other cargoes. In all cases where transport was merely slowed by the M proteins, the chandipura virus M protein had the strongest inhibitory activity. When expressed in transfected HeLa cells, active M proteins displayed prominent association with the nuclear rim. Moreover, mutation of a conserved methionine abolished both the inhibitory activity and efficient targeting of the M proteins to the nuclear rim. We propose that all of the vesiculoviral M proteins associate with the same nuclear target, which is likely to be a component of the nuclear pore complex.
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PMID:Multiple vesiculoviral matrix proteins inhibit both nuclear export and import. 1144 72

The pathogenesis of vesicular stomatitis virus (VSV) infection has not been investigated previously in native New World rodents that may have a role in the epidemiology of the disease. In the present study, 45 juvenile and 80 adult deer mice (Peromyscus maniculatus) were inoculated intranasally with VSV New Jersey serotype (VSV-NJ) and examined sequentially over a 7-day period. Virus was detected by means of immunohistochemistry and in situ hybridization in all tissues containing histologic lesions. Viral antigen and mRNA were observed initially in olfactory epithelium neurons, followed by olfactory bulbs and more caudal olfactory pathways in the brain. Virus also was detected throughout the ventricular system in the brain and central canal of the spinal cord. These results support both viral retrograde transneuronal transport and viral spread within the ventricular system. Other tissues containing viral antigen included airway epithelium and macrophages in the lungs, cardiac myocytes, and macrophages in cervical lymph nodes. In a second experiment, 15 adult, 20 juvenile, and 16 nestling deer mice were inoculated intradermally with VSV-NJ. Adults were refractory to infection by this route; however, nestlings and juveniles developed disseminated central nervous system infections. Viral antigen also was detected in cardiac myocytes and lymph node macrophages in these animals. Viremia was detected by virus isolation in 35/72 (49%) intranasally inoculated juvenile and adult mice and in 17/36 (47%) intradermally inoculated nestlings and juveniles from day 1 to day 3 postinoculation. The documentation of viremia in these animals suggests that they may have a role in the epidemiology of vector-borne vesicular stomatitis.
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PMID:Pathogenesis of experimental vesicular stomatitis virus (New Jersey serotype) infection in the deer mouse (Peromyscus maniculatus). 1146 73


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