Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VIRAL INTERFERENCE”

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 649 records · Page 36Linked to original sources
PubMed1985

Expression of Sendai virus defective-interfering genomes with internal deletions.

Sendai virus strain 7 has been shown to contain four defective interfering (DI) RNA species in which both genome termini and various adjacent fragments of the 3'-terminal NP gene and 5'-terminal L gene are represented, but most or all internal genes and gene boundaries are deleted. Previous sequence analyses of these mutant RNAs suggested that all four possessed the transcription initiation signal of the NP gene and the transcription termination signal of the L gene. The supposition that these signals should specify transcripts has now been supported by oligo(dT) selection of four DI 7 specific RNA species that had apparent molecular weights slightly lower than each DI genome. DI RNA 7a, which contains the entire NP gene, except for two U residues at the end of the poly(A) initiation signal, appeared to be transcribed solely as a readthrough product. Since DI RNA 7a contains the entire NP protein-coding sequence and DI RNAs 7c and 7d contain fragments of it, whereas DI RNA 7b is devoid of it, only transcripts of RNAs 7c and 7d were expected to specify fusion proteins containing NP gene-specific sequences. A strain 7-induced protein that reacted with monoclonal antibodies against the NP protein had the 33,000 Mr size appropriate for the translation product predicted by the sequence of RNA 7d. Other proteins of lower molecular weight were seen only in cells infected by strain 7, but they did not react with NP-specific antibody and their translation in vitro was not blocked by hybridization to an NP gene-specific oligonucleotide. Therefore, at least some of these proteins may be cellular products induced by DI virus infection. These DI transcripts and translation products may influence interference with replication of the parental helper virus.

Antibodies, Monoclonal↗
PubMed1991

Differences in fusogenicity and mouse neurovirulence of Japanese encephalitis viruses.

The fusogenic capacity in AP-61 cell monolayers of 10 strains of Japanese encephalitis (JE) virus from different geographic locations was compared. One strain, isolated from Beijing (JE-Bei), did not fuse AP-61 cells after replication (fusion from within; FFWI), whereas all other strains fused these cells by 72 h post-infection. JE-Bei also readily established a non-cytolytic persistent infection in AP-61 cells. Differences in the envelope proteins of fusogenic and non-fusogenic virus were detected by haemagglutination-inhibition tests and by antigenic analysis using monoclonal antibodies. Yields of infectious virus in either AP-61 or Vero cell cultures were similar if JE-Bei was compared with the fusogenic strain (JE-Sar) but yields of haemagglutinin were 50-100 fold higher with the non-fusogenic virus, implying excessive generation of non-infectious particles. When added directly to AP-61 cell monolayers at pH6, only JE-Bei produced significant fusion from without (FFWO) presumably reflecting the larger quantity of antigen. Cell monolayers persistently infected with JE-Bei or monolayers treated with UV-inactivated JE-Bei, were resistant to superinfection with JE, West Nile and dengue 2 viruses but were susceptible to infection with the alphavirus Sindbis. When administered intracerebrally (I/C) to newborn and weanling mice, the viruses were equally neurovirulent. However, fusogenic JE-Sar was significantly more neurovirulent than JE-Bei for weanling mice after intraperitoneal (I/P) or subcutaneous (S/C) inoculation. Mice given non-fusogenic JE-Bei, resisted the peritoneal challenge with fusogenic JE-Sar, and West Nile but not Semliki Forest virus when given 6 h after the first virus. The potential significance of cell fusion by JE virus and interference through over production of non-infectious virus, is discussed in the context of JE virus virulence.

Aedes↗
PubMed1976

An improved assay for feline leukaemia virus pseudotypes of murine sarcoma virus.

An assay is described for feline leukaemia virus pseudotypes of murine sarcoma virus which increased the virus titre by about 100-fold over conventional assays. The titre is independent of dilution and no secondary focus formation occurs. The assay may be used to study virus neutralization and to detect and type feline leukaemia virus in feline embryo cells by interference.

Adsorption↗
PubMed1980

the influence of the host cell on the inhibition of virus protein synthesis in cells double infected with vesicular stomatitis virus and mengovirus.

The ability of mengovirus to inhibit the synthesis of vesicular stomatitis virus (VSV) proteins and of VSV to inhibit the synthesis of mengovirus proteins during double infection in three different cell lines was investigated. Although cellular protein synthesis was inhibited after infection of cells by each virus, the ability of one virus to decrease translation of the mRNA species of the co-infecting virus varied with the cell type. Superinfection of mengovirus-infected L-929 cells by VSV resulted in essentially no inhibition in the synthesis of either mengovirus or VSV proteins. In HeLa cells and CHO cells the synthesis of both VSV and mengovirus proteins was inhibited under conditions of simultaneous or sequential infection. The inhibition of VSV protein synthesis after infection of HeLa cells by mengovirus was not a result of a modification or inactivation of virus mRNAs. When extracted from double infected cells, the VSV mRNAs manifested normal biological activity, as determined by their ability to stimulate the synthesis of VSV proteins in a micrococcal nuclease-treated cell-free system from L cells. The interference of non-interference of one virus by another in different cell lines was also measured by quantifying the number of infectious particles produced in each cell line. The results were similar to those reported above for protein synthesis inhibition. These experiments suggest that the interference of mengovirus with VSV mRNA translation in HeLa cells is not necessarily reflective of the mechanism by which mengovirus inhibits cellular protein synthesis. Also, the host cell appears to influence the extent or nature of the interference of one virus by the other.

Animals↗
PubMed1982

Intrinsic interference between influenza A and B viruses.

Reproduction and synthesis of virus-specific macromolecules were studied in chick embryo fibroblast cultures co-infected with influenza viruses type A (FPV) and B (B/Japan/73). When a multiplicity of infection (MOI) of B/Japan/73 virus (10 EID50/cell and higher) was equal to, or exceeded that of FPV, formation of infectious FPV virions in coinfected cells was suppressed significantly. At equal MOI of FPV and B/Japan/73 synthesis of all proteins of one partner and some proteins of the other was observed. However, when a MOI of one virus was 10 times higher than that of the other, proteins of the virus used at a higher MOI were formed. Studies of the synthesis of virus-specific cRNAs formed in the presence of cycloheximide have shown that at equal MOI. cRNAs were detected that corresponded only to one of the partners involved in the reproduction. The data obtained suggest that intrinsic interference between A and B viruses occurs at a stage of primary transcription.

Animals↗
PubMed1975

Failure of attenuated temperature-sensitive influenza A (H3N2) virus to induce heterologous interference in humans to parainfluenza type 1 virus.

The present investigation was undertaken to determine if a candidate live vaccine virus, influenza A/Hong Kong/68-ts-1 [E] (H3N2), induced heterologous interference against an interferon-sensitive, wild-type, parainfluenza type 1 challenge virus. The parainfluenza virus was administered 7 days after Hong Kong/68-ts-1 [E] virus infection. The clinical response, daily quantitative virus shedding, interferon production, and serum and nasal wash antibody responses were determined in an experimental group (influenza A virus followed by parainfluenza virus) and 10 volunteers in a control group (parainfluenza virus only). The volunteers were selected on the basis of susceptibility to the two viruses, i.e. serum hemagglutination-inhibition antibody titer of is less than or greater to 1:8 for influenza virus and low nasal wash antibody titer (is less than or greater to 1:8) for parainfluenza virus. Despite a 100% infection rate in the Hong Kong/68-ts-1 [E] vaccinees, no heterologous interference was induced against the parainfluenza type 1 virus challenge.

Animals↗
PubMed2005

Specific anti-viral effects of RNA interference on replication and expression of hepatitis B virus in mice.

BACKGROUND: RNA interference (RNAi) is a powerful tool to silence gene expression post-transcriptionally. Our previous study has demonstrated that small interfering RNAs (siRNAs) have sufficiently inhibited hepatitis B virus (HBV) replication and expression in vitro. In this study we observed the RNAi-mediated inhibitory effects on HBV replication in mice models and accessed the specificity of these effects. METHODS: A mutant RNAi vector (pSI-C mut) with two base pairs different from the original target gene sequence at the RNAi vector (pSI-C) was constructed according to the method described in this study. A mouse model of acute hepatitis B virus infection was established by injecting naked plasmid pHBV1.3 via the tail vein with acute circulatory overload. pSI-C, pSI-C mut and the irrelevant RNAi control plasmid for green fluorescent protein (GFP) gene, pSIGFP were respectively delivered with pHBV1.3 by tail vein injection method. Six days post injection, enzyme-linked immunosorbent assay (ELISA) assay was used to measure the concentration of HBV surface antigen (HBsAg) in mouse serum, immunohistochemical straining method was used to visualize the expression of HBV core protein (HBcAg) in liver tissues, and the transcriptional level of HBV C mRNA in liver tissues was detected by reverse transcriptase PCR (RT-PCR) analysis. RESULTS: Injection of pSI-C exerted magnificent and specific inhibitory effects on the replication and expression of HBV in the murine model. After 6-day post-injection (p.i.), the OD values were shown to be 5.07 +/- 1.07 in infecting group and 0.62 +/- 0.59 in pSI-C group. The concentration of HBsAg in pSI-C group was significantly lower than that in infecting group (P < 0.01). Liver intracellular synthesis of viral core protein was sharply reduced to 0.9% +/- 0.1%, compared with 5.4% +/- 1.2% of positive hepatocytes in infecting group (P < 0.01), and the transcriptional level of HBV C mRNA was greatly reduced by 84.7%. However, the irrelevant RNAi control plasmid (pSIGFP), and the pSI-C mut did not show the same robust inhibitory effects as pSI-C. CONCLUSION: pSI-C exert efficient and specific inhibitory effects on HBV replication and expression in mice models.

Animals↗
PubMed1976

Defective-interfering particles of Semliki Forest virus: intracellular events during interference.

Purified defective-interfering (DI) particles of Semliki Forest virus are unable to carry out any of the steps in virus multiplication except uncoating. Cells co-infected with DI particles and standard virus contain several virus-specified RNA species (DI particle-specific species) absent from cells infected with standard virus alone. Moreover, synthesis of all the virus-specified components distinctive of standard virus-infected cells is reduced. The DI particle-specific RNA species comprise two poly A-containing single-stranded RNAs (DIss1 and DIss2), identical to those found in purified DI particles, two double-stranded RNA'S (RFs) and a new size class of replicative intermediate (RI). Hybridization experiments showed that the nucleotide sequences of DIss1 and DIss2 (i) are present in the 42S genome of standard virus but absent from the 26S RNA- the RNA from standard virus-infected cells which encodes the structural proteins of the virion (Clegg & Kennedy, 1975 a) and (ii) are complementary to the negative strands of the DI paritcle-specific RFs and RI. Oligonucleotide fingerprinting revealed extensive nucleotide sequence homology between DIssI and DIss2. Analysis of the mRNA complement of standard virus-infected, co-infected and uninfected cells strongly indicated that neither DIss1 nor DIss2 can serve as a functional messenger RNA. From these studies we propose a mechanism for the multiplication of and interference by DI particles of Semliki Forest virus.

Base Sequence↗
PubMed1976

Homologous interference of lymphocytic choriomeningitis virus: detection and measurement of interference focus-forming units.

Lymphocytic choriomeninigitis (LCM) virus defective interfering (DI) particles form foci of protected cells in a monolayer under an agarose-containing overlay medium. Foci originate from one cell dually infected with at least 1 interference focus-forming unit and infectious virus. As a result, an interfering factor is produced and released which interacts with neighboring cells, thereby protecting them against cytopathic lysis by challenge virus. The property of individual LCM virus DI particles to induce countable foci has been made the basis of quantitative assay that is comparable in every respect to the plaque assay of infectious virus and is much more sensitive and probably more accurate than other procedures used to measure LCM virus DI particles. LCM virus was passaged, undiluted, 10 times in cell cultures. When yields were analyzed as to concentrations of PFU and interference focus-forming units, both entities were found to fluctuate with the pattern expected from theoretical considerations.

Cell Line↗