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At least 685 records · Page 38Linked to original sources
PubMed1996

Interference of reovirus strains occurs between the stages of uncoating and dsRNA accumulation.

Interference of wild-type reovirus growth by some temperature-sensitive (ts) mutant viruses under non-permissive conditions or by other wild-type isolates has been demonstrated; however, the stage of the virus replication cycle at which interference occurs has not been defined. Examination of the time-course of the yields of T1 Lang (T1L) dsRNA in the progeny of mixed infections of T1L with T3 Dearing (T3D) or with a panel of T3D ts mutants at a non-permissive temperature revealed that interference takes place by 8-10 h post-infection and occurs prior to or at the same time as accumulation of reovirus dsRNA. Taken together with our previous results, these data indicate that interference occurs during a window between virus uncoating and synthesis of dsRNA in the reovirus replication cycle, probably at the stage of assembly of primary reovirus particles.

Capsid↗
PubMed1972

Transient inhibition of polyoma virus synthesis by Sendai virus (parainfluenza I). I. Demonstration and nature of the inhibition by inactivated virus.

Superinfection of polyoma virus-infected mouse embryo cells by beta-propiolactone-inactivated Sendai virus resulted in a 90% inhibition of the synthesis of infectious polyoma progeny. The interference is dependent upon the time of superinfection and the concentration of the inactivated virus. The inhibition of polyoma virus synthesis is transient in nature since normal synthesis of polyoma progeny virus is seen upon prolonged incubation. Interferon does not appear to be implicated in the interference. Various aspects of the biological and synthetic capabilities of beta-propiolactone-inactivated Sendai virus are also described.

Animals↗
PubMed1992

Interference is controlled by segment 2 and possibly by segment 8 of the nondefective interfering influenza virus variant A/FM/1/47-MA.

On mouse adaption of A/FM/1/47, a variant, A/FM/1/47-MA (FM-MA), that had acquired the properties of increased virulence and interference was produced. Coinfection of cells with FM-MA and prototype strains of influenza virus yielded > 100-fold more FM-MA virus than prototype virus, whereas coinfection with the same prototype strains and the parental A/FM/1/47 virus produced equivalent yields, indicating that FM-MA had acquired mutations that confer the property of interference during mouse adaption. FM-MA is a nondefective interfering virus that grows to a high titer in vivo and in vitro. It has previously been shown that segments 4, 7, and 8 and possibly segment 5 account for the increased virulence. In this study we show by genetic analysis of FM-MA x A/HK/1/68 reassortants that segment 2, coding for the polymerase-associated protein PB1, and possibly segment 8, encoding the NS1 and NS2 proteins, control the ability of FM-MA to interfere. Interference could not be overcome by increasing the titer of the coinfecting strain, but delaying FM-MA infection by 4 to 6 h did avoid interference. During interference of A/HK/1/68, protein synthesis was inhibited by less than 65% throughout coinfection. Given the kinetics of interference and the small perturbation in protein synthesis, interference appeared to occur at the level of late genome replication or virus assembly. Virulence and interference in FM-MA were not linked. An interfering avirulent FM-MA x A/HK/1/68 reassortant, E07, was capable of protecting mice against lethal pneumonia due to a virulent noninterfering reassortant, H04.

Genetic Variation↗
PubMed1977

Persistent infections in L cells with temperature-sensitive mutants of reovirus.

Serial passage of reovirus temperature-sensitive (ts) mutant C(447) produced by passage 9 (P9) a heavily defective population of virus from which the double-stranded RNA genomic segments L(1), L(3), and M(1) were largely missing. Viral cores obtained from this P9 population were heterogeneous with respect to buoyant density in CsCl gradients, suggesting that particles were present with different combinations of deleted segments. Similar observations were made with the E(320) ts mutant of reovirus. By serial passage P15, 90% of the E(320) viral population was defective and the major missing genomic segments were L(1) and L(3). Persistent infections were readily established in monolayer cultures of L cells with P9 of C(447) virus and P15 of E(320) virus and in Vero cells with P9 of C(447) virus. Under similar conditions persistent infections could not be initiated with defective-free populations of C(447) or E(320) viruses. The greater the capacity of defective virus in the population to interfere with viral growth, the more readily persistent infection was initiated. During their maintenance persistently infected cells were subcultured approximately twice a week. More than 80% of the cells continuously produced virus. By subculture 6 the original ts infectious viral component had been replaced by a small-plaque mutant with a ts(+) phenotype. Defective virus was always present in the carrier cells. In addition to the more commonly observed defectives whose cores banded at approximately rho = 1.40 to 1.415 g/ml in CsCl gradients, a new class of defective core was seen banding in the region of 1.34 to 1.36 g/ml. This latter particle, which has not been thoroughly characterized as yet, is termed "light defective." Persistently infected cells underwent periodic crises during their maintenance, during which the cultures partially lysed and then rapidly grew to confluence. Crises corresponded to a burst of infectious virus from the cells and a relatively low concentration of light defectives. During quiescent periods the concentration of light defectives amounted to as much as 98% of the total viral population. The function of light defectives is not yet clear, but it seems essential to assign major importance to defective virus in maintaining persistent infections in this system.

Defective Viruses↗
PubMed1982

Incomplete avian influenza virus contains a defective non-interfering component.

Incomplete avian influenza (fowl plague) virus derived by undiluted egg passage, displayed an increased capacity to promote the synthesis of intracellular virus-specific proteins when compared with standard virus. The in vitro virion-bound RNA polymerase activity of incomplete virus was also greater than could be explained by the presence of residual infectious virus. When the titres of infectious and interfering virus species were determined directly, they did not account for all the virus present. The existence of defective non-interfering (DNI) virus, even in standard virus preparations, was inferred. DNI virus is capable of initiating infection, synthesis of mRNA and proteins but cannot complete a productive replication cycle, and does not interfere with multiplication of standard virus. Such DNI virus could exaggerate the true extent of DI virus formation by lowering the PFU:HAU ratio and so account for the failure to correlate infectivity with RNA composition or RNA polymerase activity.

Animals↗
PubMed1998

Interference by a non-defective variant of influenza A virus is due to enhanced RNA synthesis and assembly.

Mouse-adapted influenza A virus, FM-MA, interferes with the replication of wild-type strains on co-infection. The interference phenotype was previously mapped to FM-MA segment 2 encoding a mutant PB1 protein, the catalytic component of the RNA polymerase complex. To identify the point at which FM-MA interferes with wild-type A/HK/1/68 (HK), the relative levels of transcription and genome replication of the PB1, NP and M1 genes were determined for FM-MA and HK viruses in co-infected cells using RT-PCR. All stages of HK macromolecular synthesis (primary and secondary transcription, genomic RNA, complementary RNA and protein synthesis) were suppressed relative to FM-MA. Infection with HK virus alone resulted in the accumulation of similar or greater amounts of RNA at late times post-infection relative to FM-MA thus indicating that the presence of FM-MA specifically compromised HK transcription and replication in co-infected cells. However early in infection FM-MA was ten times more active in mRNA transcription than HK or its parental strain FM. FM-MA's ability to interfere was primarily due to an increased capacity for primary transcription. FM-MA genomes were also selectively assembled into progeny virus from cells co-infected with HK and FM-MA, a step which was distinct from the capacity for enhanced RNA synthesis. This suggests that interference of HK growth by FM-MA in mixed infections results from two distinct events: a preferential synthesis of FM-MA-specific macromolecules which is then augmented by a preferential assembly of FM-MA genomes.

Animals↗
PubMed2003

Inhibition of hepatitis B virus expression and replication by RNA interference.

RNA interference (RNAi) is the process of sequence-specific gene silencing, initiated by double-stranded RNA (dsRNA) that is homologous in sequence to the target gene. Because it has been shown that RNAi can be accomplished in cultured mammalian cells by introducing small interfering RNAs (siRNAs), much effort has been invested in exploiting this phenomenon for experimental and therapeutic means. In this study, we present a series of experiments showing a significant reduction in hepatitis B virus (HBV) transcripts and proteins in cell culture, as well as in the viral replicative forms, induced by siRNA-producing vectors. The antiviral effect is sequence-specific and does not depend on active viral replication. In conclusion, our data suggest that RNAi may provide a powerful therapeutic tool, acting both on replication-competent and on replication-incompetent HBV.

Cells, Cultured↗
PubMed1982

Defective interfering particles of respiratory syncytial virus.

A multiplicity-dependent interference was observed in respiratory syncytial virus preparations (Randall strain) grown in HEp-2 cells, and the factor mediating this interference was characterized. Cloned virus did not demonstrate this multiplicity-dependent interference, but its replication was shown to be inhibited by the interfering factor by assays of reduction of infectious yield assay, the interferon factor was found to be particulate, to be inactivated by UV irradiation, and not to interfere with the replication of a heterologous virus, vesicular stomatitis virus. These characteristics are compatible with the physical properties and biological behavior of defective interfering particles. Defective interfering particles were generated by four undiluted passages of cloned virus but were not apparent after eight passages at a multiplicity of infection of 0.1.

Cytopathogenic Effect, Viral↗
PubMed1973

Prophage-mediated interference affecting the development of Bacillus subtilis bacteriophage phi e.

Bacteriophage phie shows a reduced efficiency of plating on strains of Bacillus subtilis which are lysogenic for the temperate bacteriophage SP02. Although this phenomenon resembles prophage-mediated restriction observed in other bacteria, host-controlled modification of phie was not observed. Mutants of phie which plated with high efficiency on the lysogenic host were isolated.

Adsorption↗
PubMed1990

Induction of monocyte proliferation and HIV expression by IL-3 does not interfere with anti-viral activity of zidovudine.

Myelosuppression is a major symptom in the acquired immunodeficiency syndrome (AIDS). Moreover zidovudine, an anti-retroviral drug used to treat AIDS patients has myelosuppressive side effects. Therefore treatment with IL-3, a multi-lineage hemopoietic growth factor may be beneficial for zidovudine-treated individuals. In this study we examined the effect of IL-3 on human immunodeficiency virus (HIV) expression. The proliferative response to rIL-3 and the effects on the replication of the monocytotropic HIV variant, HTLV-III Ba-L, in the absence or presence of the anti-retroviral drug zidovudine was studied in purified human peripheral blood monocytes. Zidovudine concentrations sufficient for complete inhibition of HIV replication did not affect rIL-3 induced monocyte proliferation. Although rIL-3, like rGM-CSF, was able to augment HIV expression in monocytes, it did not interfere with the anti-retroviral activity of zidovudine. These data indicate that rIL-3 is a potential candidate for use in myelosupportive therapy in AIDS patients treated with anti-retroviral drugs.

Cell Division↗
PubMed1978

A plaque assay for Mount Elgon bat virus based on intrinsic interference.

A plaque count infectivity assay was developed in which chick cells infected with the Mount Elgon bat virus were completely resistant to superinfection with large doses of Sendai virus. Several variables markedly affected the assay sensitivity. The defined plaque assay was simple, highly reproducible and sensitive. It allowed determination of virus neutralizing antibody in a simple and reproducible test. Both actinomycin D and 5-iododeoxyuridine were without effect on plaque formation.

Animals↗
PubMed1995

Isolation of a fully infectious variant of parvovirus H-1 supplanting the standard strain in human cells.

A variant H-1 virus, designated H-1 dr virus, was isolated from stock of the standard H-1 virus strain propagated in the newborn human kidney cell line NB-E. Molecular cloning and sequence analysis revealed an in-frame deletion at map positions 39 to 41. This deletion affects the open reading frames encoding the nonstructural proteins NS-1 and NS-2 and the untranslated leader sequence of the R3 transcripts encoding the capsid proteins. In addition, H-1 dr virus harbors a 58-nucleotide duplication inboard from the right-hand terminal palindrome. Internal deletions and terminal reiterations are hallmarks of H-1 virus type I variants that typically are defective interfering particles. Indeed, H-1 dr virus was found to progressively supplant the standard strain in serially coinfected NB-E cell cultures. However, H-1 dr virus differed from previously described type I variants in its full infectivity, as was apparent from its ability to give yields of replication and progeny virus production that were similar to those of the standard virus strain in NB-E cells. Hence, the interference of H-1 dr virus in the propagation of standard H-1 virus in coinfected cells was not accompanied by a drop in the titer of infectious virus. Moreover, H-1 dr virus proved to induce the same pathogenic effects in newborn hamsters as the standard virus strain did.

Base Sequence↗
PubMed1983

Persistent infection of cultivated cells with lymphocytic choriomeningitis virus: regulation of virus replication. Brief report.

L cells were infected with lymphocytic choriomeningitis virus (LCM virus). They were subcultivated and infectious virus and interfering virus were quantified at intervals. Both entities fluctuated in perfect parallelism. Superinfection with LCM virus revealed a pattern of interference that bore no simple relationship with the quantity of interfering virus present. We explain the oscillating pattern of virus replication, which characterizes this type of LCM virus carrier cultures, as being due to spontaneous shutdown of virus synthesis in conjunction with the action of a resistance factor produced by cells coinfected with infectious virus and interfering virus.

Animals↗
PubMed1983

A replication-efficient mutant of West Nile virus is insensitive to DI particle interference.

A previous report described the isolation of a mutant of West Nile virus (WNV) from culture fluid obtained from persistently infected genetically resistant C3H/RV mouse cells that replicates significantly more efficiently in cultures of C3H/RV cells than does the parental virus. This replication-efficient mutant, designated RE-WNV, has now been found to be insensitive to interference by WNV defective interfering (DI) particles. This characteristic was demonstrated by several means. The RE-WNV mutant was able to superinfect persistently infected cultures that were no longer producing detectable parental virus, while the parental virus was not. Good yields of the mutant virus were produced during six serial undiluted passages of RE-WNV in both resistant C3H/RV and congenic susceptible C3H/HE cells. In contrast, during passage of parental virus in C3H/RV cells, progeny virus could not be detected after the third passage, due to an enhanced interference by WNV DI particles with standard virus replication in these cells. The RE-WNV was also insensitive to interference by a pool of parental virus enriched for DI particles. Analysis of the mutant genome by oligonucleotide fingerprinting indicated that the genome RNA of the mutant differs by two unique spots from the parental RNA. The relevance of this mutant to the eventual understanding of the mechanism by which C3H/RV and C3H/HE cells manifest their flavivirus-specific difference in the efficiency of progeny virus production is discussed.

Animals↗
PubMed1982

Persistent infection with infectious pancreatic necrosis virus mediated by defective-interfering (DI) virus particles in a cell line showing strong interference but little DI replication.

The characteristics of chinook salmon embryo cells persistently infected with infectious pancreatic necrosis virus were consistent with defective-interfering (DI) particle-mediated persistence. All the cells were infected and were slowly releasing virus, but they could be cured of virus in the presence of antiserum. Immunofluorescence showed that the amount of virus antigen in persistently infected cells was low. This fact, coupled with the observation that few DI particles were released by these cells, indicated that DI particles were not replicated to excess in this cell line.

Animals↗
PubMed1994

HIV-1 integrase blocks infection of bacteria by single-stranded DNA and RNA bacteriophages.

Expression of human immunodeficiency virus-1 integrase in Escherichia coli, at levels that had no effect on bacterial cell growth, blocked plaque formation by bacteriophages having single-stranded genomic DNA (M13) or RNA (R17, Q beta, PRR1). Plaque formation by phages having double-stranded genomic DNA (T4, PR4) was unaffected. Integrase also inhibited infection by the phagemid M13KO7, but it had no effect on production of phage once infection by M13KO7 was established. This result indicated that integrase affects an early stage in infection. Integrase also inhibited phage production following transfection by either single-stranded or double-stranded (replicative form) M13 DNA, it blocked M13 DNA replication, as assayed by incorporation of radioactive nucleotides into DNA, and it failed to affect bacterial pilus function. These data suggest that integrase interacts in vivo with phage nucleic acid, a conclusion supported by studies in which integrase was shown to have a DNA-binding activity in its C-terminal portion. This portion of integrase was both necessary and sufficient for interference of plaque formation by M13 in the present study. Expression of the N-terminal portion of integrase at the same level as intact integrase had little effect on phage growth, indicating that expression of foreign protein in general was not responsible for the inhibitory effect. The simple bacteriophage assay described is potentially useful for identifying integrase mutants that lack single-stranded DNA binding activity.

Antiviral Agents↗