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PubMed1998

Heterologous protection of mice from a lethal human H1N1 influenza A virus infection by H3N8 equine defective interfering virus: comparison of defective RNA sequences isolated from the DI inoculum and mouse lung.

We have examined the RNAs involved in the heterologous protection of adult mice from otherwise lethal intranasal infection with mouse-adapted human A/WSN (H1N1) by defective interfering (DI) equine A/equine/Newmarket/7339/79 (H3N8: EQV) influenza virus, as well as the RNAs involved in the protection of WSN- or EQV-infected mice by their homologous DI viruses. The aim of this study was to describe the types of defective RNAs present in protected mice in order to guide the design of potentially protective DI RNAs. The interfering and mouse-protecting activity of DI virus was destroyed by prolonged UV irradiation (iDI virus) demonstrating that protection correlated with an active DI genome, and not viral antigen. Protected mice were all infected but suffered a lower degree of morbidity than those given iDI virus. The DI EQV inoculum contained defective segment 1-8 RNAs while DI WSN inoculum contained only defective segment 1-6 RNAs. However lungs of mice given EQV + DI EQV contained only defective segments 1-4 or 1-6 RNAs (mouse-to-mouse variation), while control mice given EQV or EQV + iDI EQV contained few very defective RNAs. Thus prevention of death was the result of quantitative and/or qualitative differences in defective RNAs administered to the mice. Only defective segments 1-3 RNAs were isolated from the lungs of mice given WSN + DI WSN, confirming the earlier report of Noble and Dimmock (1995). A detailed analysis showed that most defective RNAs isolated from the lungs of mice protected from a lethal WSN infection by DI EQV were EQV in origin. Thus, as no infectious EQV was present, these defective RNAs from the DI EQV inoculum must have been heterologously replicated in mouse lung by WSN. All defective segment 3-6 RNAs isolated were of EQV origin, indicating that they were replicated by WSN in preference to its own. Defective segments 1 and 2 were a mixture of EQV and WSN RNAs. Of 17 defective EQV segment 1-3 sequences from mouse lung, all but three differed in their primary central deletion from 20 defective RNAs isolated from the inoculum. No bias in the break points was evident. A number of minor deletions of 2 or more nts were also present in defective EQV and WSN RNAs in segments 1 and 2, but none in segment 3. Their 5', but not 3', breakpoints were heterogeneous, suggesting that defective RNAs were generated during positive strand synthesis. Two cloned EQV-defective segment 3 RNAs were chimeras containing a 30 nt insert from segment 1. Most defective RNAs possessed at least 178 nts from the 5' end of vRNA. The amount of 5' sequence present in those RNAs correlated with the segment of origin, suggesting that this was the minimum required for propagation of viral RNA in mouse lung and hence possibly for protection also.

Animals↗
PubMed1998

Coat protein interactions involved in tobacco mosaic tobamovirus cross-protection.

To investigate the molecular role of the tobacco mosaic tobamovirus (TMV) coat protein (CP) in conferring cross-protection, a potato X potexvirus (PVX) vector (S. Chapman, Plant J. 2, 549-557, 1992) was used to systemically express a set of TMV mutant CPs in Nicotiana benthamiana prior to challenge inoculation with TMV. PVX-expressed wild-type TMV CP delayed TMV accumulation for up to 2 weeks compared to unprotected plants or plants preinfected with the unmodified PVX vector. Similar delays in TMV accumulation were obtained using TMV CPs that were deficient in virion formation but competent to assemble into helical aggregates. In contrast, TMV CPs that were incapable of helical aggregation or unable to bind viral RNA did not delay the accumulation of TMV. Furthermore, TMV CPs with enhanced intersubunit interactions that favor helical aggregation produced significantly greater delays in the accumulation of challenge TMV than obtained from the wild-type CP. Thus the capabilities of TMV CP to interact with viral RNA and self-associate in a helical fashion appear to be essential to its ability to confer protection. Taken together, these findings support a model for CP-mediated resistance in which the protecting CP recoats the challenge virus RNA as it disassembles.

Capsid Proteins↗
PubMed2000

Synergistic interactions of a potyvirus and a phloem-limited crinivirus in sweet potato plants.

When infecting alone, Sweet potato feathery mottle virus (SPFMV, genus Potyvirus) and Sweet potato chlorotic stunt virus (SPCSV, genus Crinivirus) cause no or only mild symptoms (slight stunting and purpling), respectively, in the sweet potato (Ipomoea batatas L. ). In the SPFMV-resistant cv. Tanzania, SPFMV is also present at extremely low titers, though plants are systemically infected. However, infection with both viruses results in the development of sweet potato virus disease (SPVD) characterized by severe symptoms in leaves and stunting of the plants. Data from this study showed that SPCSV remains confined to phloem and at a similar or slightly lower titer in the SPVD-affected plants, whereas the amounts of SPFMV RNA and CP antigen increase 600-fold. SPFMV was not confined to phloem, and the movement from the inoculated leaf to the upper leaves occurred at a similar rate, regardless of whether or not the plants were infected with SPCSV. Hence, resistance to SPFMV in cv. Tanzania was not based on restricted virus movement, neither did SPCSV significantly enhance the phloem loading or unloading of SPFMV. It is also noteworthy that SPVD is an unusual synergistic interaction in that the potyvirus component is not the cause of synergism but is the beneficiary. It is hypothesized that SPCSV is able to enhance the multiplication of SPFMV in tissues other than where it occurs itself, perhaps by interfering with systemic phloem-dependent signaling required in a resistance mechanism directed against SPFMV.

Animals↗
PubMed2001

Rubella virus DI RNAs and replicons: requirement for nonstructural proteins acting in cis for amplification by helper virus.

A rubella virus (RUB) replicon was constructed by replacing the 3' proximal structural protein ORF (SP-ORF) in Robo402, a RUB infectious cDNA clone, with a reporter gene, green fluorescent protein (GFP). This replicon, RUBrep/GFP, mimics naturally occurring RUB defective-interfering (DI) RNAs generated during serial undiluted passage that maintain the 5' proximal nonstructural protein ORF (NS-ORF) but contain deletions in the SP-ORF. Following transfection of Vero cells with in vitro RNA transcripts from RUBrep/GFP, replicon replication occurred and the replicon was amplified and spread to other cells in the presence of standard helper virus. GFP expression was a much more sensitive indicator of replicon replication than was Northern analysis to detect replicon-specific RNAs. Most of a series of RUBrep/GFP constructs with deletions in the NS-ORF not only were incapable of self-replication, but were not amplified by standard helper virus. The only exception was a construct with an in-frame deletion between two NotI sites that removed nucleotides 1685-2192 of the genome; this construct did not express GFP by itself, but did express GFP in the presence of standard helper RUB and was spread to other cells. Thus, with the exception of this region, the NS-ORF is required in cis for amplification of RUB replicons by standard helper virus, explaining the selection of DI RNAs that maintain the NS-ORF. Surprisingly, when the NotI deletion was introduced into Robo402, a viable virus resulted that replicated only threefold less efficiently than did Robo402 virus. Thus, the NotI region of the NS-ORF is not necessary for virus replication. This deletion covers a region of the NS-ORF without predicted function, which therefore may function as a spacer or hinge between functional domains. Nevertheless, it was an unexpected finding that a small virus such as RUB could dispense with approximately 10% of its genome.

Animals↗
PubMed1978

Membrane alterations following interferon treatment.

Interferon treatment appears to induce a number of changes in the plasma membrane of uninfected cells. Interferon treatment altered the surface exposure of gangliosides of both Ly and KB cell membranes. The differences were found in the amount and pattern of incorporation of tritium after galactose oxidase treatment. In AKR,C- (AKR-2B) mouse cells, not only was there an apparent increase in the number of intramembranous particles in response to treatment with interferon but also the kinetics of the increase followed that of the establishment of the antiviral activity. The buoyant density of plasma membrane was also found to be significantly increased in interferon-treated cells. Moloney murine leukemia virus produced in interferon-treated mouse thymus and bone marrow cells had a high particle to infectivity ration. This virus contained a prominent glycoprotein with a molecular weight of about 85,000. This large glycoprotein was only a very minor component of Moloney leukemia virus produced in control TB cells and might be an uncleaved precursor to gp 69-71.

Cell Membrane↗
PubMed1977

Dengue viruses.

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Animals↗
PubMed1992

Cytokine-mediated regulation of monocyte/macrophage cytotoxicity in human immunodeficiency virus-1 infection.

Monocyte/macrophage-mediated tumor cytotoxicity was studied in patients infected with human immunodeficiency virus-1 (HIV-1) at various stages [Center for disease control (CDC) classification] of the disease. using the P-815 tumor cell line as target cells, the results demonstrated reduced monocyte/macrophage cytotoxicity early in HIV-1-related disease (CDCIII, P < 0.01). This cellular dysfunction sustained during the progression of the disease. Evidence could be presented that neither exogenous application of macrophage-stimulating cytokines (e.g. interferons) nor their endogenous induction in vitro restored monocyte/macrophage cytotoxicity. However, enhanced tumor necrosis factor (TNF)-alpha production, which parallels the observed reduced capacity to lyse P-815 tumor cells, might be the major source for monocyte/macrophage-mediated cell lysis. TNF-alpha-induced cytotoxicity can be inhibited by addition of anti-TNF-alpha. Other experimental models using TNF-sensitive tumor target cells may, therefore, mimic monocyte/macrophage-mediated lysis. Suppression of monocyte/macrophage cytotoxicity in later stages of HIV-1 infection (AIDS-related complex, AIDS) could partly be reverted by treatment with the cyclooxygenase blocker, indomethacin. The responsible arachidonic acid product mediating suppression was found to be prostaglandin E2, suggesting that in addition to the direct viral interference cellular dysfunction is at least in part a result of altered cytokine regulation.

Adult↗
PubMed1976

Oncornavirus-like protein expression in human prostatic tissue.

A sensitive competition radioimmunoassay using 125 I-labelled p 30 interspecies antigen, antiserum specific to the interspecies antigen of the feline leukaemia virus, and aqueous tissue extracts from prostate was used to examine benign hyperplastic prostates for the presence of protein components able to complete with the interspecies viral antigens. Six of 20 prostatic nodular hyperplastic tissues were competitive in radioimmunoassay with the 125 I-labelled viral antigen for binding sites on the antiviral antibodies. These findings suggest the presence of oncornavirus-like proteins in prostatic nodular hyperplasia. No correlation could be made between the presence of competing protein and histological features of acute or chronic prostatitis and squamous metaplasia.

Antibodies, Viral↗
PubMed1979

Aberrant immunity behaviour of hybrid lambda imm21 phages containing the DNA of ColE1-type plasmids.

Hybrid lambda and lambda imm21 bacteriophages carrying various ColE1-type plasmids have been constructed in vitro. The lambda imm21/plasmid recombinants display aberrant immunity behaviour, giving clear plaques under conditions where the parental phages give turbid ones and being able to grow on homoimmune lysogens. lambda imm lambda/plasmid recombinants show no such unusual behaviour. Studies with hybrids of a lambda imm21 cITS phage carrying pMB9 DNA showed the operation of the plasmid's replication system to be the basic cause of the aberrant immunity behaviour. The plasmid replication system could act as a complete alternative to the phage system during vegetative phage growth. The probable reason that lambda imm21 phages show such altered phenotypes when carrying a functional plasmid replication origin, whereas lambda imm lambda and lambda imm434 (Mukai et al., 1978) phages do not, is the relative ease of titration of the phage 21 repressor to allow transcription from pR21. Various uses are considered for the altered phenotypic behaviour of lambda imm21/ColE1-type plasmid hybrids.

Bacteriocin Plasmids↗
PubMed1990

A trial of molecular epidemiology using bovine enteroviruses isolated monthly from cattle.

Enteroviruses were isolated monthly for one year from feces in the intestine of 47 cattle. Judging from the isolation panel, it was suggested that endemic infection occurs. Genetic changes of isolated enteroviruses were traced using RNase T1 oligonucleotide fingerprint analysis and nonparametric distance scaling. Using some characteristics transitions of fingerprint patterns we could also trace some strains. These analyses suggested that in some strains drastic genetic changes may occur, which coincide with additional infections transmitted from other cows. Furthermore, it was indicated that the genetic changes of viruses isolated from cow R13 were not very drastic, but genetic changes were drastic for viruses isolated from cow R19. Overall, we could never observe the same fingerprint pattern using RNase T1. This study suggests that genetic changes tend to accumulate as time elapses, and at the same time, infection decreases.

Animals↗