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 130,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An RNA-synthesizing complex was found in the nucleoplasm of fowl plague virus-infected chicken fibroblast and Ehrlich tumour cells. The complex sedimented at 120 S and banded in caesium chloride at 1-39 to 1-41 g/ml. It contained an influenza nucleocapsid protein as a major protein constituent. The complex functioned late in infection, and RNA synthesis in it was resistant to actinomycin D, the properties expected of influenza virus replicative complex.
J Gen Virol 1975 Oct
PMID:Influenza virus RNA-synthesizing complex in the nucleoplasm of infected cells. 123 35

Thogoto (THO) virus is a tick-borne virus which shares morphological and genetic features with members of the Orthomyxoviridae family although the viral glycoprotein appears to be related to gp64 of baculoviruses. Characterization of THO virus was undertaken to clarify its taxonomic position. Purified virus preparations contained at least six virus-encoded polypeptides with apparent M(r) values ranging from 29K to 92K. A 75K polypeptide was identified as an envelope-associated glycoprotein by Triton X-100 and salt dissociation studies, and by proteolytic degradation of the exposed proteins of the virion. By the same criteria, the nucleoprotein and the matrix protein were identified as the 52K and 29K polypeptides, respectively. Immunofluorescence studies using monoclonal antibodies (MAbs) located the glycoprotein on the external cell membrane and the nucleoprotein in the nucleus of infected cells indicating that virus replication involved a nuclear phase. In addition, the virus displayed haemagglutination and haemolytic activities with an optimum at pH 6. These activities are functions of the viral glycoprotein since they were inhibited by anti-glycoprotein MAbs. The data reported here support the notion that THO virus is a member of the Orthomyxoviridae family but that it should be classified in a group distinct from the other influenza viruses.
J Gen Virol 1992 Nov
PMID:Identification of viral structural polypeptides of Thogoto virus (a tick-borne orthomyxo-like virus) and functions associated with the glycoprotein. 127

To evaluate the effect of laboratory passaging of influenza virus A/USSR/90/77 (H1N1) on the pattern of vRNA synthesis regulation in course of the one step infection cycle, we have used the viral variants adapted to growth in the continuous cell line MDCK or to the reproduction in the mice lungs in vivo. Enhancement of regulation was registered in the adapted variants as compared to the original virus strain. The results are discussed in connection with possible significance of the vRNA synthesis regulation for the efficiency of viral reproduction under natural conditions or in laboratory passaging.
Mol Gen Mikrobiol Virusol
PMID:[Change in regulation of influenza virus vRNA synthesis during adaptation to various hosts]. 129 85

A distinctive feature of these workshops, in addition to those noted in the introductory overview, is the selection of a relatively isolated location for a 1-week period. This, together with a rich and varied program and an ethos of informality, encourages participants to discuss not only the work presented but also their unpublished work and their intuitions based on preliminary data and analyses. Such an interchange is of inestimable value to the schizophrenia research community. In scientific terms, a panel of concluding discussants (Drs Kendell, Torrey, and Waddington) were in some measure of agreement that genetics, particularly molecular genetics, appears to be experiencing a period of retrenchment, while epidemiology is experiencing something of a renaissance. Maternal influenza was a prominent theme, although the data were far from consistent. It was argued by Dr Wessely that risk for schizophrenia putatively attributable to maternal influenza might be 5% to 10% of all cases, indicating a modest effect. Eclectically, Dr Kendell believed the effect to be "real" but slight and fragile, it being sought against large aggregates that almost inevitably result in differing findings from differing countries or from different data bases within a given country. Gender differences were also among the more prominent themes, not just in an epidemiologic context but also in a variety of other studies. This points anew to disturbances in schizophrenia of factors that regulate, or are intimately associated with, sexual dimorphism in brain development. Abnormalities in cerebral asymmetry continue to pervade a variety of research findings and point further to neurodevelopmental anomalies.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Gen Psychiatry 1992 Dec
PMID:Schizophrenia, genetic retrenchment, and epidemiologic renaissance. The Sixth Biennial Winter Workshop on Schizophrenia, Badgastein, Austria, January 26-February 1, 1992. 136 Feb 1

The immune-mediated lethal influenza in C3H/He-mg (H-2k) mice infected with A/WSN influenza virus (H1N1) was investigated. A primary class I major histocompatibility complex-restricted, CD8+ cytotoxic T lymphocyte (CTL) response was found in the lungs with a peak activity at 5 days post-infection. Monoclonal antibody depletion in vivo showed that a lethal CD8+ cell response as well as a lethal CD4+ response was generated during infection. Mice survived infection only if both CD8+ and CD4+ cells were depleted. Mice infected with the same dose of virus, but treated with defective interfering (DI) A/WSN virus develop only a transient sub-lethal respiratory disease even though multiplication of virus in the lungs is undiminished, and we have shown here that this correlates with a reduction in the local CTL response. The mechanism by which DI virus beneficially modulates the immune response is discussed; it is proposed that there is classical, but cell type-specific DI virus interference in lymphocytes but not in the cells of the lung in which virus multiplies productively.
J Gen Virol 1992 Feb
PMID:Protection of mice from lethal influenza by defective interfering virus: T cell responses. 137 42

The matrix (M1) protein isolated from influenza A/WSN/33 virus, when reconstituted with ribonucleoprotein (RNP) cores of vesicular stomatitis virus (VSV), resulted in inhibition of VSV transcription in vitro. The presence of endogenous wild-type (wt) or mutant (tsO23) VSV matrix (M) protein on RNP cores did not prevent down-regulation of VSV transcription by reconstituted influenza virus M1 protein. In fact, endogenous VSV wt M protein augmented transcription inhibition by M1 protein reconstituted with RNP/M protein cores, whereas mutant tsO23 M protein endogenous to RNP cores had no effect on down-regulation of VSV transcription by M1 protein. These data suggest that VSV M protein and influenza virus M1 protein recognize two different sites on RNP cores responsible for down-regulation of VSV transcription. Monoclonal antibodies (MAbs) directed to epitope 2 of M1 protein had been previously shown to reverse transcription inhibition by M1 protein on influenza virus RNP cores, but the same epitope 2-specific MAb had little effect on transcription inhibition by M1 protein reconstituted with VSV RNP cores. VSV M protein bears a striking resemblance biologically and genetically to the M1 protein, including, as shown here, their capacity to bind viral RNA. However, the VSV wt M protein exhibited no capacity to down-regulate transcription by influenza virus RNP cores. The significance of these studies is the identification on VSV RNP templates of at least two separate sites for recognition of protein factors that repress VSV transcription.
J Gen Virol 1992 Mar
PMID:Down-regulation of vesicular stomatitis virus transcription by the matrix protein of influenza virus. 137 41

A T cell epitope of the influenza virus NS1 molecule was identified and shown to be a determinant used in class II major histocompatibility complex-restricted T cell responses to infectious virus. An I-Ed-restricted BALB/c mouse T hybridoma clone recognizing influenza virus A/Puerto Rico/8/34 (PR8; subtype H1N1) but not A/Udorn/72 (subtype H3N2) secreted lymphokines in response to purified recombinant NS1 or fusion proteins containing amino acids 1 to 81 or 1 to 42 of NS1. As expected for recognition of a non-virion protein, the clone failed to respond to u.v.-inactivated virus. The antigenic determinant was localized by synthetic peptides to amino acids 13 to 32 of NS1, explaining the lack of recognition of A/Udorn/72 virus which has an alanine to valine substitution at position 23 within the determinant. A single intranasal dose of infectious PR8 virus was found to elicit T cells that responded to peptide NS1 13-32, suggesting that this determinant is a significant target of T cells in normal infections. To stimulate helper T cell responses similar to those achieved with infectious virus, influenza virus vaccines may therefore have to include NS1 in addition to virion components.
J Gen Virol 1992 Jun
PMID:Influenza virus infection elicits class II major histocompatibility complex-restricted T cells specific for an epitope identified in the NS1 non-structural protein. 137 67

A large panel of mouse monoclonal antibodies was produced and tested against field isolates of the equine H7N7 influenza A virus subtype. Only a limited degree of H7 haemagglutinin variation was detected. At least four antigenic sites were identified by selecting variant viruses in eggs. The limited variation in the field did not correlate with the frequency of variant viruses detected in eggs; this frequency was similar to those reported for other influenza viruses. We sought to determine whether the limited amount of variation could be correlated with an epitope-restricted antibody response in vaccinated horses. To this end, limiting dilution cultures were established with peripheral blood leukocytes from vaccinated ponies and the antibodies released into culture supernatants were assayed for binding to variant H7 viruses in ELISA. Three neutralizable antigenic sites mapped by mouse antibodies were also recognized by antibodies in pony limiting dilution culture supernatants, indicating that the equine antibody response against the influenza virus H7 haemagglutinin is diverse, and should be effective in selecting variant viruses.
J Gen Virol 1992 Jun
PMID:Diversity of the antibody responses produced in ponies and mice against the equine influenza A virus H7 haemagglutinin. 137 70

A synthetic peptide that contains a Semliki Forest virus (SFV) B cell epitope, located at amino acid positions 240 to 255 of the E2 protein, and an SFV T helper (Th) cell epitope, located at positions 137 to 151 of the E2 protein, evoked high titres of SFV-reactive antibodies in H-2d mice. Although the peptide-induced antibodies did not neutralize SFV in vitro, 70 to 100% of the peptide-immunized mice were protected against SFV, even when viral challenge was presented 4 months after immunization. The protection could be transferred by anti-peptide serum, indicating that antibodies were responsible for the protection. When the Th cell epitope of this protective peptide was replaced by an influenza virus Th cell epitope or by another SFV Th cell epitope, the resulting peptides induced lower non-neutralizing SFV-reactive antibody titres and protected a correspondingly lower percentage of mice (50% and 30%, respectively). A peptide with the same Th cell epitope as the best protective peptide but with a less effective SFV B cell epitope protected only 33% of the mice. These results indicate that protection against SFV by a synthetic peptide is primarily dependent on its ability to induce adequate amounts of antibodies with relevant specificity and sufficient affinity; the ability to induce a relevant (SFV-specific) T memory response played only a minor role in protection.
J Gen Virol 1992 Sep
PMID:Immunogenicity and vaccine efficacy of synthetic peptides containing Semliki Forest virus B and T cell epitopes. 138 5

The antigenic and genetic characteristics of the haemagglutinins of influenza type B viruses isolated since 1988 during periods of both widespread activity (1990/1991) and sporadic activity (1989/1990) were examined using microneutralization tests and direct RNA sequencing. During 1989/1990, influenza B viruses representative of two distinct lineages antigenically and genetically related to either B/Victoria/2/87 or B/Yamagata/16/88 were isolated, and a minor drift variant of B/Yamagata/16/88, B/Hong Kong/22/89, was identified. In 1990/1991, B/Hong Kong/22/89- or B/Yamagata/16/88-like viruses accounted for the majority of the influenza virus isolates in most countries. Sequence analysis of the HA1 domains of representative viruses confirmed the continued existence of two main lineages among recent strains of influenza B virus and identified unique amino acid changes that could account for the altered antigenic reactivity of some variants. Sequence analysis of the HA2 domains of some of the recent influenza B viruses allowed for a comparison of the evolutionary rates and patterns between the HA1 and HA2 domains.
J Gen Virol 1992 Oct
PMID:Antigenic and genetic characterization of the haemagglutinins of recent cocirculating strains of influenza B virus. 140 7


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