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PubMedDate not supplied

[Myxovirus structural investigations by spin probe methods. II. Influence of rimantadine on the structure of viral and artificial lipid membranes].

The lipid membrane structure of two myxoviruses (influenza and Sendai viruses), red blood cells and liposomes (prepared from total lipids of Sendai virus) have been investigated in the presence of rimantadine by means of two spin probes C5 and C6--the iminoxyl derivatives of stearic acids. Rimantadine was shown to penetrate the lipid membranes of myxoviruses and red blood sells and change the structure of the lipid phase no less than 0.8 nm apart from the viral surface. In the depth of 2.2 nm the structure of these lipid membranes remains unchanged after addition of rimantadine. Rimantadine also displaces the phase transition points of cell and viral lipid membranes to lower temperatures. Rimantadine does not change the lipid bilayer structure of liposomes 0.8 nm apart from its surface. These finding allow to suggest that rimantadine affects the cell and viral lipoprotein membranes.

Adamantane↗
PubMedDate not supplied

[Suppression of the proteolytic activation of myxoviruses in infected chick embryos by using aprotinin].

The mandatory step in reproduction of myxoviruses (influenza viruses and paramyxoviruses) is proteolytic shearing of viral glycoproteins activating the infectivity of virions. Such activation of myxoviruses is realized by trypsin-like proteases of the host. This study demonstrated that proteolytic activation of virions could be inhibited by a physiological inhibitor of proteases, aprotinine. A single injection of aprotinine (preparations Gordox or Contrycal) into chick embryos infected with various influenza viruses (WSN/34, Udorn/72) and paramyxoviruses (Sendai/960, NDV/La Sota, NDV/Queensland) blocked shearing of viral glycoproteins, HA, FO, HNO as a result of which noninfectious virions with unsheared glycoproteins were predominantly synthesized. In aprotinine-treated embryos, multicycle virus infection was markedly decreased which led to the 10(4)-fold or greater reduction of the virus yield. The antiviral effect of protease inhibitors and possibilities of their practical use in viral diseases are discussed.

Animals↗
PubMed1977

[Correlation between structure and pathogenicity of myxoviruses (author's transl)].

Myxoviruses (ortho- and paramyxoviruses) possess on their surface two virus-specific glycoproteins, the functions of which are largely understood; These glycoproteins are synthesized on the rought endoplasmic reticulum, and during their transport to the plasma membrane on smooth intracellular membranes, they undergo modification through proteolytic cleavage. In this way, the orthomyxovirus hemagllutinin is converted from a high-molecular weight form (HA) into two smaller cleavage products (HA1 and HA2). With the paramyxoviruses, the glycoprotein F, which is responsible for fusion and hemolysis, is derived from proteolytic cleavage of a precursor, F0. Furthermore, with a few strains of avirulent NDV, a precursor of the hemagglutinin-neuraminidase complex, (HN0), has been identified which again, as a result of proteolysis, undergoes cleavage to HN. Whether cleavage takes place is as much dependent on the structure of the glycoprotein as on the host cell type. Proteolytic cleavage is indeed not necessary for virus particle production but is required for infectivity. Virus particles which possess the uncleaved glycoproteins may be activated by in vitro treatment with trypsin. As evidenced by experiments with orthomyxovirus recombinants, the glycoproteins alone do not determine the pathogenicity of the viruses. With paramyxoviruses, the pathogenic and apathogenic strains show clear differences in their host range spectrum which is directly related to the sensitivity of their glycoproteins twoard proteases. These observations provide an initial sketch for the molecular basis of infectivity and pathogenicity with myxoviruses.

Animals↗
PubMed1980

Levamisole reduces the thrombocytopenia associated with myxovirus vaccination.

Mature dogs were vaccinated with a myxovirus vaccine. At this time, half of the dogs were also given a subcutaneous injection of levamisole hydrochloride (2.2 mg/kg). Blood platelets were counted daily. The dogs that had received only the vaccine showed, after 48 hours, a 48% decrease in platelets. Levamisole reduced the thrombocytopenia associated with myxovirus vaccination. Levamisole could have a protective effect on platelets by preventing their aggregation induced by viral neuraminidase.

Animals↗
PubMed1990

Nuclear myxovirus-resistance protein Mx is a minor histocompatibility antigen.

Minor histocompatibility antigens (MiHAgs) cause slow-to-rapid organ transplant rejection by immunocompetent hosts and mild-to-severe graft-versus-host reactions in immunosuppressed hosts. MiHAgs are allelic forms of major histocompatibility complex (MHC) class I-restricted self-antigens recognized by cytotoxic T cells and usually are defined immunogenetically. Although structurally not identified as yet, it is assumed that MiHAgs are internal cell antigens that are processed and then presented by MHC class I proteins similar to viral antigens. To define a MiHAg both molecularly and functionally, we took advantage of the allelic difference of the structurally characterized intracellular myxovirus-resistance protein (Mx) and investigated its antigenicity. Skin grafts from congenic Mx+ mice carrying the functional Mx1 gene were rejected by mice lacking a functional Mx1 gene (Mx- mice). In parallel, cytotoxic MHC class I-restricted effector T cells specific for Mx protein and the H-2Kk antigen (but not for several other allelic H-2 antigens) were strongly induced in Mx- mice immunized with spleen cells from interferon-treated Mx+ mice. These data show that allelic forms of cell internal proteins presented by MHC class I may act as MiHAgs.

Alleles↗
PubMed2004

Differential transcriptional expresión of the polymorphic myxovirus resistance protein A in response to interferon-alpha treatment.

Levels of myxovirus resistance protein A (MxA) mRNA were studied for a single nucleotide polymorphism in the promoter region at nucleotide position -88 of the gene to identify individual-specific responses to interferon (IFN)-alpha2 that might predict responsiveness to IFN-alpha therapy. We quantified MxA expression by reverse transcription and real-time polymerase chain reaction in peripheral blood mononuclear cells (PBMC) in vitro, induced by IFN-alpha2, from 22 healthy donors, in relation with G/T polymorphism located in the promoter of the MxA. MxA mRNA was significantly upregulated in all subjects (mean of 53-fold) in response to IFN-alpha2 in vitro (P < 0.01). Comparison of the inducibility of MxA mRNA expression in relation with G/T polymorphism showed a 4.26-fold higher induction of MxA mRNA levels in PBMC from carriers of the mutant allele (GT or TT) than homozygotes with the wild-type allele (GG) (P < 0.001). We propose that expression of the IFN-inducible MxA is affected by a single nucleotide polymorphism in the MxA promoter which can identify an individual response to IFN-alpha2.

Adult↗
PubMed1963

MYXOVIRUSES ASSOCIATED WITH ACUTE LARYNGOTRACHEOBRONCHITIS IN TORONTO, 1962-63.

Between November 1962 and March 1963, myxoviruses were isolated from 95 of 224 children (40.5%), most of whom were aged less than three years, who were admitted to The Hospital for Sick Children, Toronto, with acute laryngotracheobronchitis (tracheitis or croup). Viral isolates included 87 strains of Parainfluenza-1, five of Parainfluenza-3, and three of Influenza A2. An epidemic of Influenza A2 afflicted Toronto during March 1963, at which time this virus was isolated from tracheitis patients.Myxoviruses were isolated from nasopharyngeal secretions of 285 of 794 tracheitis patients between November 1960 and March 1963. Parainfluenza-1 virus was the dominant serotype, being found in 241 (30.0%) of subjects. Three peaks of Parainfluenza-1 virus isolations were observed in December 1960, March 1962 and November 1962, and this serotype has been isolated during all months except June and July. Although most of the 28 Parainfluenza-3 virus infections occurred between November and February, this strain has also been isolated during summer. Strains of Influenza A2 and Influenza B viruses have been isolated from tracheitis patients during epidemics of influenza in Toronto due to these agents.

Antibodies↗
PubMed1981

Functions of surface glycoproteins of myxoviruses and paramyxoviruses and their inhibition.

Two glycoproteins, HN and F, are present on the surface of paramyxoviruses. HN has receptor-binding amd neuraminidase activities. F is involved in viral penetration, cell fusion and haemolysis and is activated by proteolytic cleavage by a host enzyme into two disulphide-bonded subunits (f1 and F2). The ability of the virus to initiate infection and undergo multiple cycle replication depends on the presence of an activating protease in the host; thus cleavage of F is a major determinant of pathogenesis. The new N-terminus generated on F1 by cleavage is involved in biological activity, and the amino acid sequence of this region of F1 by cleavage is involved in biological activity, and the amino acid sequence of this region of F1 is hydrophobic and highly conserved among para-myxoviruses. In an attempt to design specific inhibitors, oligopeptides and analogous to this region were synthesized and found to be highly active, specific inhibitors of viral penetration, cell fusion and haemolysis. Inhibition is amino-acid-sequence-specific and affected by peptide length, steric configuration and addition of groups to the n-terminal and C-terminal amino acids. Replication of influenza virus was also specifically inhibited by oligopeptides resembling the N-terminus of the HA2 polypeptide. Like that of F1 protein the N-terminus of HA2 is generated by a proteolytic cleavage that activates infectivity. These results have provided information on the action of proteins in viral penetration and membrane fusion and they suggest a possible new approach to chemical inhibition of viral replication. Studies with specific antibodies to each of the paramyxovirus glycoproteins have shown that antibodies to the F protein are essential for effective prevention of the spread of infection. Antibodies to the HN protein, although capable of neutralizing released virus, do not prevent spread to adjacent cells through membrane fusion mediated by the F protein. These findings have implications for the design of effective vaccines against paramyxoviruses and also provided additional insight into the mechanisms involved in the atypical and severe infections observed in individuals who received inactivated paramyxovirus vaccines and were later infected.

Amino Acid Sequence↗
PubMed1983

Myxoviruses do not induce non-specific alterations in membrane permeability early on in infection.

The permeability characteristics of cells infected with myxoviruses have been studied by measuring the concentrative uptake of nutrients, the concentration of intracellular K+, and the maintenance of the Na+ gradient across the plasma membrane. Cells either show no change at all (Sendai virus-infected BHK cells and measles virus-infected Vero cells) or they show a decreased ability to concentrate nutrients, while intracellular K+ and the Na+ gradient remain unchanged (Sendai and influenza virus-infected L-1210 cells, measles virus-infected lymphocytes and mumps virus-infected L-41 cells). In no case, therefore, was a change observed that resembles the non-specific increase in membrane permeability induced by haemolytic paramyxoviruses (35, 42) or the non-specific membrane leakiness postulated to take place in infected cells (8, 9). A preliminary account of some of these findings has been presented (39).

Animals↗
PubMed1976

A possible mechanism for the action of some myxoviruses.

The redox properties of some myxoviruses [Fowl plaque virus strain Rostock (FPV), New Castle Disease virus strain Italy (NDV), B/Hong Kong, A/Port Chalmers, A/Victoria, A/Scotland, and A/Fort Dir) and electron microscopic studies as well as by the determination of the hemagglutination (HA) titer (antigen efficiency). The results have shown that viruses decrease the spin concentration of Cu2+ by acting as a reducing species (electron donor) which will result in the inactivation (oxidation) of the virus. Addition of an oxidizing substance, such as H2O2, to a virus suspension also leads to an oxidation of the viruses, and, thus, to their inability to reduce Cu2+. This result is confirmed by the decrease of the HA titer of viruses with increasing Cu2+ concentrations. H2O2 could not be applied for the HA titer test since it interacts with the erythrocytes of the chicken blood used for this determination. Therefore, another oxidizing substance (oxidized glutathione, GSS) was selected which exhibited a slightly less pronounced effect than Cu2+. Since reduced glutathione (GSH) exerts a similar but less pronounced effect than GSS, it might be concluded that viruses have a redox system of their own and act as reducing or oxidizing substance depending on the biological receptor system. Electron microscopic studies confirm this hypothesis. As can be seen by the electron micrographs, increasing concentrations of either Cu2+, GSS, H2O2, KMnO4, or GSH will, finally, result in a complete destruction of the virus. Because of structural similarities it might be assumed that other types of viruses behave very similarly.

Copper↗
PubMed1983

The role of neutral glycolipids and phospholipids in myxovirus-induced membrane fusion.

Myxoviruses (influenza virus and paramyxovirus) enter host cells by two successive steps consisting of attachment and fusion between viral and cellular membranes. The initial attachment is known to occur through specific binding of the viruses with the neuraminic acid-containing receptors of cellular membranes. Evidence is presented here that, in the following step of membrane fusion, neutral glycolipids terminating in galactose and certain phospholipids (primarily lecithin and sphingomyelin) interact with the viral envelopes and that this interaction may be fundamental to the fusion process.

Animals↗
PubMed1969

Incorporation of branched-chain fatty acids into myxoviruses.

The incorporation of free fatty acids into myxoviruses was shown, using branched-chain fatty acids as molecular markers. The presence of isostearic or phytanic acid was detected by gas-liquid chromatography in the phospholipid fraction of the A(0)/PR8/34 strain of influenza virus. Uptake of free fatty acids into the virus varied from 8 to 11 per cent and was accompanied by a shift in the fatty acid profile. Infected allantoic fluids from eggs treated with branched-chain acids possessed higher hemagglutinin activity when compared to fluids infected under normal conditions. Attempts to detect branched-chain acids in Sendai virus were unsuccessful. Shifts in acyl chain composition persisted after three passages of modified viruses in the absence of branched-chain acids. Force-area curves at an air-water interface revealed the cross-sectional area of branched-chain acids to be greater than their straight-chain homologs. It is suggested that hydrophobic interactions can alter the configuration of envelope proteins. Such changes may have an important role in the selection of fragments of influenza viral genome and can conceivably alter viral genotype.

Chromatography, Gas↗
PubMed1956

Association of a new type of cytopathogenic myxovirus with infantile croup.

Viruses producing an unusual "sponge-like" cytopathogenic change in monkey kidney tissue culture were isolated from the pharyngeal swabs of 2 of 12 infants with croup. The infants from whom the viruses were isolated and 3 additional patients developed significant increases in neutralizing or hemagglutination-inhibition and complement-fixing or all 3 varieties of antibody during convalescence. The isolated agents appeared to be similar antigenically. Fluid from infected monkey kidney tissue culture agglutinated chick erythrocytes and in lower titer human "O" red cells. Hemagglutination occurred best at 4 degrees C. and pH 8.0. Agglutination was reversed at 37 degrees C. but resuspension and sedimentation of red cells at 4 degrees C. resulted in a restitution of positive patterns. In addition, the virus was capable of partially removing receptors from the erythrocyte surface, but only when large quantities of virus were incubated with red cells for 24 hours at 37 degrees C. and small doses of hemagglutinin used to test the treated cells. RDE removed both the erythrocyte receptors and the inhibitor for hemagglutinin present in certain normal sera. Low level multiplication occurred at a slow rate in the amniotic cavity of the fertile hen' egg. Gradocol membrane filtration yielded a size of 90 to 135 mmicro. The virus was stable at -70 degrees C. but infectivity was lost after treatment with 20 per cent ether for 15 hours. The properties of the isolated viruses were consistent with those required for classification in the myxovirus group. No antigenic relationship with influenza A, A', B, and C, Newcastle or Sendai viruses was found. The viruses were distinct from mumps virus but the existence of a common antigen was suggested. The high incidence of infection with this new virus in one group of croup patients suggests that it may be at least one of the etiologic agents of this clinical syndrome, but more extensive control studies will be necessary to establish a specific etiologic association. For the present the group will be referred to as CA viruses; i.e., croup-associated viruses.

Antigens↗
PubMed1978

Inborn resistance of mice to myxoviruses: macrophages express phenotype in vitro.

A strain of avian influenza A virus was adapted to grow in mouse peritoneal macrophages in vitro. The adapted strain, called M-TUR, induced a marked cytopathic effect in macrophages from susceptible mice. Mice homozygous (A2G) or heterozygous (F1 hybrids between A2G and several susceptible strains) for the gene Mx, shown previously to induce a high level of resistance towards lethal challenge by a number of myxoviruses in vivo, yielded peritoneal macrophages which were not affected by M-TUR. Peritoneal macrophages could be classified as resistant or susceptible to M-TUR without sacrificing the cell donor. Backcrosses were arranged between (A2G X A/J)F1 and A/J mice. 64 backcross animals could be tested individually both for resistance of their macrophages in vitro after challenge with M-TUR, and for resistance of the whole animal in vivo after challenge with NWS (a neurotropic variant of human influenza A virus). Macrophages from 36 backcross mice were classified as susceptible, and all of these mice died after challenge. Macrophages from 28 mice were classified as resistant, and 26 mice survived challenge. We conclude that resistance of macrophages and resistance of the whole animal are two facets of the same phenomenon.

Alleles↗
PubMed1983

Involvement of glycolipids in myxovirus-induced membrane fusion (haemolysis).

Myxoviruses (influenza viruses and paramyxoviruses) penetrate their host cells by fusion of viral and cellular membranes. During this process, virus envelopes react with galactose-terminating glycolipids of cellular membranes. This was suggested by experiments showing the ability of these lipids to inhibit fusion (as measured by haemolysis) when reacted with the viruses, and to enhance it when added as enrichment to erythrocytes.

Erythrocytes↗
PubMed1975

Myxovirus-like structures in the glomerular endothelial cell cytoplasm in canine nephritis.

Electron microscopic examinations revealed the presence of myxovirus-like tubular structures, 200A in diameter, in the endothelial cytoplasm of the glomeruli in four dogs with chronic interstitial nephritis and in one healthy control dog. The structures were found inside the endoplasmic reticulum and in some longitudinal sections, the tubuli seemed to have a helical or spiral substructure. The morphology and cellular localization of the structures resembled those seen in systemic lupus erythematosus in man, and in cultures of cells from tissue infected with canine distemper. Precipitating canine distemper virus antibodies were not in evidence in dogs in which such structures were demonstrable by electron microscopy while these antibodies were found in other dogs.

Animals↗
PubMed1977

Demonstration of host antigens in the myxovirus memebrane: lysis of virus by antibody and complement.

Complement-mediated lesions developed in myxovirus membranes in the presence of antibody to host antigens. Intact virions reacted with antibody to the keratosulphate-like host antigen present in the spike layer. Spike-deprived influenza virus reacted in the same way when an antiserum to the Forssman glycolipid was used. The holes in the membrane varied considerably in size, but were otherwise similar to those found in erythrocyte membranes. This immune electron microscopy method proved useful for the localization of host material in viral membranes.

Antibodies, Viral↗
PubMed1967

Myxovirus-like structures in a case of human chronic polymyositis.

Intranuclear and intracytoplasmic aggregates of filaments with tubular structures and transverse striations occurred in muscle tissues biopsied from a patient with chronic polymyositis. The filamentous tubules bear a close resemblance to the incomplete form of myxovirus in which the envelope is missing. Three biopsies from the same patient, taken during a period of 1(1/2) years, all revealed these structures. This finding provides presumptive evidence that a chronic persistent viral infection may be involved in the pathogenesis of chronic polymyositis.

Aged↗