Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MYXOVIRUS INFECTIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1960

Isolation of an unidentified agent from the respiratory tract of chickens.

A relatively stable filterable virus, not previously described, which hemagglutinated red blood cells of chickens, was isolated from the tracheae of birds suffering from an unusually severe outbreak of infectious laryngotracheitis. The latter disease concealed the infection caused by the new hemagglutinating agent, which was shown to cause, by itself, a mild and transient illness in susceptible chickens. Preliminary studies indicate that the new agent may be a new entity of the myxovirus group.

Animals↗
PubMed1979

Fer de Lance virus (FDLV): a probable paramyxovirus isolated from a reptile.

A new virus has been isolated by inoculation of lung tissues of diseased snakes into snake embryos. Homogenates of infected embryo tissues caused c.p.e. in cell cultures incubated at 30 degrees C. The virus replicates in a wide variety of reptilian or mammalian cell types incubated at 30 degrees C, inducing either syncytium formation or minimal or no cytopathic changes. Efficient replication occurs in embryonated hens' eggs at 27 to 30 degrees C. The virus haemagglutinates guinea pig and chick erythrocytes; it possesses a neuraminidase similar to the receptor-destroying enzyme of Vibrio cholera. Electron microscopic observations of infected cells examined in thin section revealed pleomorphic viruses 146 to 321 nm in diam. resembling known myxoviruses. Internal nucleocapsid strands are 15 to 16 nm in diam.; nucleocapsid observed in negatively stained preparations measures 14 nm in diam. The virus was determined to possess a nucleoprotein core containing a 50S single-stranded unsegmented RNA genome. All characters of the virus are similar to those of the paramyxovirus group except that the nucleocapsid diam. is intermediate between that of paramyxoviruses and pneumoviruses. The virus is antigenically distinct from known myxoviruses and is unique among myxoviruses in its restriction to growth at temperature below 37 degrees C.

Animals↗
PubMed1973

Quantitative assessment of hemadsorption by myxoviruses: anti-immunoglobulin G hemadsorption-inhibition test.

A quantitative hemadsorption-inhibition test was developed to estimate myxovirus serum antibodies within 24 h by determining the serum dilution inhibiting hemadsorption in 50% of the infected cells. The test depends on the interactions of virus-infected cell monolayers with antiviral serum and of the resultant complexes with antiimmunoglobulin G serum. The incorporation of species-specific anti-immunoglobulin G serum into the test significantly increased sensitivity.

Animals↗
PubMed1970

Virological examination of bovine mammary lymph nodes.

Mammary lymph nodes from 42 Hereford cows culled for poor reproductive performance were examined for cytopathogenic virus and hemadsorption. No evidence of viral infection was detected using the methods employed. Serum from all the animals gave positive reactions to the hemagglutination-inhibition test for bovine myxovirus parainfluenza 3. Six of 12 had neutralizing antibody against bovine virus diarrhea virus, but none of the 12 had neutralizing antibodies against infectious bovine rhinotracheitis virus.

Animals↗
PubMed1993

[Combined viral-mycoplasma placentitis].

265 placentas were studied by means of light and fluorescent microscopy. 82 placentas showed combined infections induced by 2-5 agents (various viruses and mycoplasmas). Bacterial and fungal placentitis were excluded Manifestations depended on the infectious agents, their number and variants of their combination. Enhancement of vascular damage was observed in placentitis with participation of myxoviruses and herpes simplex virus. Enhancement of lymphoplasmacytic infiltration and sclerosis was typical for combined placentitis as well as alteration of antibody formation and interferon production. This reflects the gravity of the infection and its spread to the extra-placental membranes.

Antibody Formation↗
PubMed1979

[Otitis nigra: etiologic pathogenetic and clinical aspects (author's transl)].

The clinical picture of otitis nigra (idiopathic sero-hemmorrhagic otitis media) as independent clinical entity is shown, presenting 5 cases requiring mastoid surgery. Samples of mastoid mucosa were investigated by light- and electron-microscopy employing histochemical, immunofluorescent and virological techniques. Pathological changes of the small vessels in the subepithelial connective tissue with increased vascular permeability and extravasation of red blood cells and serum play a central role in the pathogenetic course of the disease. Disintegration of erythrocytes leads by catabolism of hemoglobin to formation of hemosiderin and ferretin, whereas by processing of phospholipids of the cell-membrane cholesterin cristals are deposited in the connective tissue. These cholesterin deposits in turn induce a foreign body reaction with formation of typical cholesterol granulomas. The mucosa shows secretory activity in intraepithelial secretory cells and glandlike structures in the subepithelial connective tissue. Neutral and acidic mucopolysaccharides are demonstrated in the secretory product. As possible cause for the vascular lesion that in turn sets off the pathomechanisme of otitis nigra a subclinical viral infection is discussed. This conjecture is supported by demonstration of virus-like inclusion bodies in macrophages and fibrocytes and of virus-like particles in antral smears. In addition myxoviruses of the parotitis-epidemica group could be identified in these smears by serological methods. Furthermore, the stimulation of the local immunological defense system, evidenced by the presence of numerous immunoglobulin-producing plasmacells in the tissue, is in concord with a viral infection. Therapy requires mastoidectomy in combination with posterior tympanotomy in order to eradicate completely the intractably diseased mastoid mucosa.

Adolescent↗
PubMed1990

Studies in the in vivo expression of the influenza resistance gene Mx by in-situ hybridisation.

The inbred laboratory mouse strain A2G carries a functional, interferon type 1 inducible gene, Mx which upon expression confers specific resistance to an otherwise lethal dose of influenza virus. We investigated in vivo Mx gene expression by performing Northern hybridisation and in-situ hybridisation on A2G (Mx+) and (CBA/J x C57)F1 (Mx-) mice that were induced either with human, natural interferon; human, recombinant interferon or double stranded poly(I):(C). All 3 inducers were able to stimulate Mx expression in all organs examined in the A2G strain. However, contrary to previous reports, Mx expression was confined to a small number of cell types; the main contributor was most probably mononuclear cells. Specialised cells such as hepatocyte, nephron, ovarian follicle and seminiferous tubules did not show detectable Mx level. There was also constitutive Mx expression in the epithelia of uterus and duodenum which suggested direct gene activation independent of blood-bourne interferon.

Animals↗
PubMed1995

Characterization of a rainbow trout Mx gene.

A full-length cDNA clone of a rainbow trout (Oncorhynchus mykiss) Mx gene was obtained using RACE (rapid amplification of cDNA ends) polymerase chain reaction (PCR) amplification of RNA extracted from poly (I).(C)-induced rainbow trout gonad cells (RTG-2). Mx was previously identified in rainbow trout by Staeheli et al. by hybridization with a partial perch genomic Mx probe to induced rainbow trout mRNA. The 2.5 kb rainbow trout cDNA clone contains an open reading frame of 1863 nt (nucleotides) encoding a 621 amino acid protein. The deduced rainbow trout Mx protein is 70.6 kD and contains the characteristic tripartite GTP binding motif common to all Mx protein. Southern blot analysis with the rainbow trout Mx probe demonstrated the presence of Mx homologous genes in four other salmonid fish species, including chinook, coho, and kokanee salmon and brook trout. Poly (I).(C) treatment of both RTG-2 and chinook salmon cells (CHSE-214) induced two transcripts whose appearance was observed first at 24 h and as long as 72 h after treatment. Infection of rainbow trout with the salmonid rhabdovirus, IHNV (infectious hematopoietic necrosis virus), also induced the synthesis of Mx mRNA. A comparison of the rainbow trout Mx protein with other reported Mx proteins indicates that the piscine Mx is highly homologous to the mammalian Mx proteins.

Amino Acid Sequence↗
PubMed2006

Association of SARS susceptibility with single nucleic acid polymorphisms of OAS1 and MxA genes: a case-control study.

BACKGROUND: Host genetic factors may play a role in susceptibility and resistance to SARS associated coronavirus (SARS-CoV) infection. The study was carried out to investigate the association between the genetic polymorphisms of 2',5'-oligoadenylate synthetase 1 (OAS1) gene as well as myxovirus resistance 1 (MxA) gene and susceptibility to SARS in Chinese Han population. METHODS: A hospital-based case-control study was conducted. A collective of 66 SARS cases and 64 close contact uninfected controls were enrolled in this study. End point real time polymerase chain reaction (PCR) and PCR-based Restriction Fragment Length Polymorphism (RFLP) analysis were used to detect the single nucleic polymorphisms (SNPs) in OAS1 and MxA genes. Information on other factors associated with SARS infection was collected using a pre-tested questionnaire. Univariate and multivariate logistic analyses were conducted. RESULTS: One polymorphism in the 3'-untranslated region (3'-UTR) of the OAS1 gene was associated with SARS infection. Compared to AA genotype, AG and GG genotypes were found associated with a protective effect on SARS infection with ORs (95% CI) of 0.42 (0.20-0.89) and 0.30 (0.09-0.97), respectively. Also, a GT genotype at position 88 in the MxA gene promoter was associated with increased susceptibility to SARS infection compared to a GG genotype (OR = 3.06, 95% CI: 1.25-7.50). The associations of AG genotype in OAS1 and GT genotype in MxA remained significant in multivariate analyses after adjusting for SARS protective measures (OR = 0.38, 95% CI: 0.14-0.98 and OR = 3.22, 95% CI: 1.13-9.18, respectively). CONCLUSION: SNPs in the OAS1 3'-UTR and MxA promoter region appear associated with host susceptibility to SARS in Chinese Han population.

2',5'-Oligoadenylate Synthetase↗
PubMed2005

JC virus induces altered patterns of cellular gene expression: interferon-inducible genes as major transcriptional targets.

Human polyomavirus JC (JCV) infects 80% of the population worldwide. Primary infection, typically occurring during childhood, is asymptomatic in immunocompetent individuals and results in lifelong latency and persistent infection. However, among the severely immunocompromised, JCV may cause a fatal demyelinating disease, progressive multifocal leukoencephalopathy (PML). Virus-host interactions influencing persistence and pathogenicity are not well understood, although significant regulation of JCV activity is thought to occur at the level of transcription. Regulation of the JCV early and late promoters during the lytic cycle is a complex event that requires participation of both viral and cellular factors. We have used cDNA microarray technology to analyze global alterations in gene expression in JCV-permissive primary human fetal glial cells (PHFG). Expression of more than 400 cellular genes was altered, including many that influence cell proliferation, cell communication and interferon (IFN)-mediated host defense responses. Genes in the latter category included signal transducer and activator of transcription 1 (STAT1), interferon stimulating gene 56 (ISG56), myxovirus resistance 1 (MxA), 2'5'-oligoadenylate synthetase (OAS), and cig5. The expression of these genes was further confirmed in JCV-infected PHFG cells and the human glioblastoma cell line U87MG to ensure the specificity of JCV in inducing this strong antiviral response. Results obtained by real-time RT-PCR and Western blot analyses supported the microarray data and provide temporal information related to virus-induced changes in the IFN response pathway. Our data indicate that the induction of an antiviral response may be one of the cellular factors regulating/controlling JCV replication in immunocompetent hosts and therefore constraining the development of PML.

Cell Line↗
PubMed1975

Kinetics of neutralization of two strains of Myxovirus Parainfluenza 3 in the presence of complement and anti-gammaglobulin-serum.

Using the kinetics of neutralization, it was established that two strains of Myxovirus Parainfluenza 3 of cattle and sheep origin which are immunologicaly identical have a different sensitivity to early neutralizing antibodies of reconvalescent calf sera. Complement-dependent neutralizing antibodies, supplied by adding 5% guinea pig serum to the calf serum, appear earlier than the usual neutralizing antibodies. Goat anti-cattle gammaglobulin serum decreases the neutralizing activity of early reconvalescent serum and release some of the neutralizing virus from the virus-antibody complex. It is believed that the lability of the virus-antibody complex depends not only on the activity of the antibody, but also on some properties of the strains. The addition of complement stabilizes this complex. The previous addition of adenovirus antigen to bivalent cattle serum against Myxovirus Parainfluenza 3 and cattle adenovirus, decreases the complement-dependent neutralizing antibody of the serum against Myxovirus Parainfluenza 3. It is suggested that this is the possible mechanism for the mutual activation of mixed virus infections.

Animals↗
PubMed1994

Regulation of interferon-alpha-inducible cellular genes in human immunodeficiency virus-infected monocytes.

Cellular mechanisms that control susceptibility to opportunistic infection in human immunodeficiency virus (HIV)-infected individuals remain poorly understood. HIV may induce certain cellular genes that restrict HIV replication and protect cells against other superinfecting viral pathogens. Indeed, HIV-infected monocytes resist infection by vesicular stomatitis virus (VSV). HIV-induced VSV interference in monocytes increases with time after HIV infection. Such interference was evident 6 h after HIV infection and reached maximal levels at 14 days. Monocytotropic but not T cell-tropic HIV strains elicited these effects, signaling a requirement for viral entry and/or replication. Viral interference was independent of interferon (IFN) and was unaffected by addition of neutralizing IFN-alpha and -beta antibodies. The well-described IFN-alpha-inducible antiviral pathways were examined to determine their relationship to the cellular mechanism(s) underlying VSV interference. HIV and IFN-alpha both induced the expression of 2-5A synthetase and Mx gene. In contrast, the guanylate-binding protein (GBP), 6-16, and 9-27 cellular genes were up-regulated by IFN-alpha but not HIV. MxA was detected in HIV-infected monocytes but not in uninfected monocytes. The association between Mx expression and resistance to VSV, coupled with previously described anti-VSV activities by human MxA, suggested that Mx may be an effector molecule for the HIV-induced anti-VSV activities. These results, taken together, suggest that HIV can induce antiviral cellular gene expression, independent of IFN.

2',5'-Oligoadenylate Synthetase↗