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PubMed1970

Effect of persistent fibroma virus infection on susceptibility of cells to other viruses.

Shope fibroma virus establishes a persistent cytoplasmic infection in primary (RK) and serially cultivated (DRK(3)) rabbit kidney cells which is accompanied by a morphological alteration of the cells. The response of such cells to superinfection by other viruses was compared with that of control cells by determining plaque production and virus yield of superinfecting viruses. It was found that the growth of other poxviruses, myxoma and vaccinia, was greatly inhibited in the fibroma virus-infected cells, but that of pseudorabies and herpes simplex viruses, which are unrelated deoxyribonucleic acid viruses, was virtually unaffected. The ribonucleic acid (RNA) viruses, poliovirus 1 and coxsackievirus B1, did not produce plaques on either RK or fibroma virus-infected (F-RK) monolayers. However, the growth of several other RNA viruses, vesicular stomatitis virus, encephalomyocarditis virus, Sindbis virus, and Newcastle disease virus, was enhanced in F-RK cells. None of these latter RNA viruses produced any infectious progeny in DRK(3) cells, but they all plaqued on and produced good yields in DRK(3) cells persistently infected with fibroma virus. This phenomenon is termed facilitation. Facilitation results from the infection of DRK(3) cells by fibroma virus. Neither interference nor facilitation were due to changes in the adsorption or eclipse of the superinfecting virus.

Adenoviridae↗
PubMedDate not supplied

[Chronic rubella virus-induced infection of human continuous cells].

A stable chronically rubella virus-infected culture of HEp-2-BK cells existing for over 30 months has been obtained as a result of a single inoculation and further passages. This system is characterized by the lack of cell destruction and permanent production of infectious virus in titres of 2.5-6.3 lg PFU/ml. Synthesis of RNAs of the same classes as in the acute infection was demonstrated in the chronically infected cell culture (CICC) but virion RNA production was less marked. Only a portion of the cells in the population was found to carry the infectious virus. Virus-free cell clones were as susceptible to rubella virus as the control culture. The process of persistence proved to be resistant to virus-specific antibody as well as to the effect of higher (40 degree C) or lower (34 degree C) temperatures. Actinomycin D, 5-bromodeoxyuridine, and 5-iodo-2-deoxyuridine exerted no significant effect on virus reproduction in CICC which, combined with negative results of the experiments on transfection of the susceptible cultures with DNA preparations recovered from CICC, evidenced against the role of integration mechanisms in the establishment and maintenance of the HEp-2-BK system. A clear-cut interference with a heterologous virus was demonstrated in HEp-2-BK culture. The formation of the chronic form of infection in HEp-2-BK culture appears to be due to weak cytocidal properties of rubella virus and formation of endogenous interferon.

Cell Line↗
PubMed1982

Immune impairment of alveolar macrophage phagocytosis during influenza virus pneumonia.

The pathogenesis of viral pneumonia is associated with an intact antiviral immune response. To determine the degree of involvement of the host response in influenza virus-induced impairment of pulmonary antibacterial defenses, mice were immunosuppressed by treatment with antilymphocyte serum (ALS). Eight days after infection, pulmonary defense mechanisms were quantitated by aerogenic challenge with Staphylococcus aureus; the ingestion of opsonized erythrocyte (EA) was used to monitor the phagocytic capability of alveolar macrophages obtained by pulmonary lavage. The ALS treatment alone caused no significant alteration in pulmonary antibacterial defenses or macrophage phagocytosis, nor did it interfere with viral multiplication. In noninfected lungs, less than 1% of the initial viable staphylococci remained viable at 24 h compared with proliferation to 490 +/- 147% in virus-infected lungs. Treatment with ALS prevented staphylococcal multiplication, the bactericidal value being 28 +/- 12% at the same time period. The phagocytic index (EA ingested/100 macrophages) in cells retrieved from normal lungs was 783 +/- 22 compared with 235 +/- 29 in macrophages from virus-infected lungs. The ALS ameliorated the impairment in phagocytic ingestion, the index being 505 +/- 34. Incubation of alveolar macrophages from virus-infected, ALS-treated animals with specific viral antibody reestablished the phagocytic defect in a dose-dependent manner; the index being 215 +/- 30 at the lowest dilution of antiviral globulin. The data demonstrate that the virus-induced suppression of pulmonary antibacterial defenses caused by dysfunction in alveolar macrophage phagocytosis is, in part, immunologically mediated.

Animals↗
PubMed1998

The host range and interference properties of two closely related feline leukemia variants suggest that they use distinct receptors.

The proviral clones 61E and 61C represent two closely related variants of feline leukemia virus (FeLV) that exhibit significant differences in their biological and pathogenic properties. The major pathogenic determinant has been mapped to the extracellular envelope glycoprotein (Env-SU), but the mechanism by which envelope differences influence pathogenesis is not well understood. Moreover, it is unclear whether these viruses infect the same target cells and/or enter cells using the same receptor. In the present study, we exploited a recently developed single cycle infection assay to examine the host range and interference properties of 61E and 61C FeLVs and found that these two FeLV variants differ significantly in their host ranges and receptor usages. FeLV-61C was found to be an ecotropic virus; the entry of viruses bearing a 61C envelope protein (Env-SU) into cell lines was limited to feline T-cells and feline fibroblasts. In contrast, the host range of 61E includes, in addition to all feline cells examined, some canine, murine, and human cell lines. Feline fibroblast and feline T-cells that expressed 61E envelope were resistant to infection with a virus bearing a 61E Env-SU, whereas these same cells were susceptible to infection by an otherwise similar virus pseudotyped with the 61C Env-SU. This pattern of interference was observed in cells expressing 61E envelope alone, in the absence of other FeLV gene products, demonstrating that interference was mediated specifically by Env-SU. Fibroblast cells chronically infected with a 61C virus were partially resistant to infection with a virus having a 61C Env-SU, but were not resistant to infection by a virus having a 61E Env-SU. On the basis of the current understanding of virus-receptor interactions, the lack of interference between 61E and 61C under conditions where there is significant homologous interference, combined with the differences in their host cell range, leads us to conclude that 61E and 61C use two distinct primary cellular receptors for entry.

3T3 Cells↗
PubMed1984

Detection of herpes simplex virus intertypic recombinant genomes in infected cell DNA.

Intertypic recombination between herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) was detected using DNA from mixedly infected cells. Because HSV-1 and HSV-2 share a 50% base sequence homology along the genome but have markedly different DNA restriction enzyme cleavage patterns, recombination events can be detected and quantified by analysis of restriction endonuclease digests for the presence of novel DNA fragments. We have used this technique to quantify the degree of interference by HSV-2 on HSV-1 replication as well as the effect of limiting the availability of one genome on the frequency of intertypic recombination. Because this technique does not require production of viable progeny virions, it should also be useful for studying early recombination events.

Animals↗
PubMed1975

The demonstration by interference tests of an infective agent in fetuses from ewes inoculated with Border disease tissue.

Fetuses and placental tissues were taken from pregnant ewes at intervals varying between eight and 21 days after inoculation with tissue suspensions from cases of Border disease. Virus isolation procedures involving the detection of a cytopathic effect in tissue cultures with or without interference tests produced universally negative results but interference tests, using a plaque technique with the NADL strain of bovine virus diarrhoea virus as a challenge virus, detected the presence of an agent in tissues from six out of 10 fetuses. Inoculated ewes allowed to proceed to term showed a serological response characteristic of Border disease infection, as measured by four different tests. Although hairy shaker lambs were not seen, the occurence of abortion and stillbirth due to causes other than bacterial agents, was an indication that the Border disease agent was present. Electron microscopy of fetal fluids failed to detect viral particles.

Abortion, Veterinary↗
PubMed1994

Abnormal processing of a recombinant feline leukemia virus envelope polyprotein and its interference with subgroup C virus infection.

Processing of the env polyprotein of a noninfectious feline leukemia virus (FeLV) recombinant, named r6gp, was examined in human-transfected cells. The r6gp provirus was previously generated in the frame of FeLV, subgroup B, GA clone with substitution of all but 40 C-terminal amino acid sequences of the surface glycoprotein (SU) from an endogenous FeLV provirus element (CFE-6). Although r6gp produced a normal size (85 kDa) env glycoprotein precursor, the product, unlike the precursor of the parental virus, was neither additionally glycosylated nor further processed into mature env proteins. Biochemical observations were consistent with the idea that the chimeric env polyprotein was trapped in the endoplasmic reticulum (ER) and were directly supported by immunofluorescence microscopy analyses. Interestingly, the residence of the chimeric protein in the ER specifically interfered with FeLV, subgroup C (Sarma) virus infection but not the parental FeLV-B virus infection. Since FeLV-C provirus sequences could be readily detected in the infected cells, it appeared that r6gp env expression did not block entry of the challenge virus. While FeLV-B and CFE-6 env genes share an extensive overall sequence homology, a variable region (region VI) of CFE-6 near the C-terminus of SU, which was retained in the r6gp construct, exhibits a considerably higher degree of homology to FeLV-C than FeLV-B. Thus, we propose that region VI is involved in conferring specificity for the env polyprotein oligomerization in the ER, and that co-oligomerization of the trapped r6gp env with FeLV-C is the reason for specific interference with FeLV-C infection. The results also demonstrate for the first time a functional abnormality of a recombinant FeLV env gene which is structurally similar to those commonly detected in FeLV-induced feline lymphosarcomas.

Amino Acid Sequence↗
PubMed2003

Antiviral inhibition of the HIV-1 capsid protein.

During the assembly stage of the human immunodeficiency virus (HIV) replication cycle, several thousand copies of the viral Gag polyprotein associate at the cell membrane and bud to form an immature, non-infectious virion. Gag is subsequently cleaved by the protease, which liberates the capsid proteins for assembly into the polyprotein shell of the central core particle (or capsid) of the mature virus. Viral infectivity is critically dependent on capsid formation and stability, making the capsid protein a potentially attractive antiviral target. We have identified compounds that bind to an apical site on the N-terminal domain of the HIV-1 capsid protein and inhibit capsid assembly in vitro. One compound, N-(3-chloro-4-methylphenyl)-N'-[2-[([5-[(dimethylamino)-methyl]-2-furyl]-methyl)-sulfanyl]ethyl]urea) (CAP-1), is well tolerated in cell cultures, enabling in vivo antiviral and mechanistic studies. CAP-1 inhibits HIV-1 infectivity in a dose-dependent manner, but does not interfere with viral entry, reverse transcription, integration, proteolytic processing, or virus production, indicating a novel antiviral mechanism. Significantly, virus particles generated in the presence of CAP-1 exhibit heterogeneous sizes and abnormal core morphologies, consistent with inhibited CA-CA interactions during virus assembly and maturation. These findings lay the groundwork for the development of assembly inhibitors as a new class of therapeutic agents for the treatment of AIDS.

Anti-HIV Agents↗
PubMed2006

Human cytomegalovirus protein pp71 disrupts major histocompatibility complex class I cell surface expression.

The human cytomegalovirus tegument protein pp71 is the product of the UL82 gene. Roles for pp71 in stimulating gene transcription, increasing infectivity of viral DNA, and the degradation of retinoblastoma family proteins have been described. Here we report a novel function for pp71 in limiting accumulation of cell surface major histocompatibility complex (MHC) class I complexes. MHC molecules were analyzed in glioblastoma cells exposed to a replication-defective adenovirus expressing UL82 (Adpp71) or after transient transfection of the UL82 gene. Accumulation of cell surface MHC class I levels diminished in a specific and dose-dependent manner after exposure to Adpp71 but not after exposure to an adenovirus expressing beta-galactosidase (Adbeta gal). UL82 expression did not interfere with accumulation of either MHC class I heavy-chain transcript or protein, nor did UL82 expression correlate with markers of apoptosis. Rather, UL82 expression correlated with an increased proportion of MHC class I molecules exhibiting sensitivity to endoglycosidase H treatment. Finally, we show that, in cells infected with recombinant virus strain missing all of the unique short region MHC class I evasion genes, disruption of UL82 expression by short, interfering RNAs led to increased accumulation of cell surface MHC class I complexes. These findings support a novel role for HCMV pp71 in disruption of the MHC class I antigen presentation pathway.

Antigen Presentation↗
PubMed1993

Herpes simplex virus interferes with monocyte accessory cell function.

HSV is a successful human pathogen that causes severe infections in immunocompromised adults and newborn humans. The possibility that HSV might evade host immune responses by interfering with accessory cell function was investigated in vitro using newborns' monocytes adhered to plastic. These cells lost their ability to present staphylococcal enterotoxin B to resting T cells in a stimulatory form after overnight culture with HSV. The interference with T cell proliferation required live virus and was abolished by heat- or UV inactivation. The T cell proliferative response was restored by the addition of IL-2. Furthermore, HSV-precultured monocytes had a reduced production of IL-1 alpha and TNF-beta after phorbol-ionomycin stimulation. Wild-type HSV and a HSV mutant lacking the primary virion host shutoff protein both interfered with IL-1 synthesis and presentation of staphylococcal enterotoxin B for T cell proliferation. These results suggest that HSV can interfere with the provision by human monocytes of costimulator factors that are essential for T cell stimulation. This effect of HSV may be due to secondary shutoff mechanisms that decrease host protein synthesis or secretion after HSV infection.

Antigen-Presenting Cells↗
PubMed1981

Defective interfering particles of fixed rabies viruses: lack of correlation with attenuation or auto-interference in mice.

Six different fixed strains of rabies virus were analysed for their capacity to produce defective particles following acute infection of BHK-21 cells. Five of the six strains produced one or more defective particle populations with strain-specific sedimentation properties, particle length and abbreviated RNA genome size. These defective particles varied in their capacity to interfere with replication of standard rabies virus in cell culture. Each virus strain characteristically either killed adult mice according to a normal dose-response pattern or to an auto-interference type of pattern, or failed to kill mice. Different strains also varied in their capacity to induce a cytopathic effect in cell culture. However, there was no apparent correlation between the presence of defective particles and the pathogenic potential of rabies virus in mice or in cell culture.

Animals↗
PubMed2003

A genome sequence of novel SARS-CoV isolates: the genotype, GD-Ins29, leads to a hypothesis of viral transmission in South China.

We report a complete genomic sequence of rare isolates (minor genotype) of the SARS-CoV from SARS patients in Guangdong, China, where the first few cases emerged. The most striking discovery from the isolate is an extra 29-nucleotide sequence located at the nucleotide positions between 27,863 and 27,864 (referred to the complete sequence of BJ01) within an overlapped region composed of BGI-PUP5 (BGI-postulated uncharacterized protein 5) and BGI-PUP6 upstream of the N (nucleocapsid) protein. The discovery of this minor genotype, GD-Ins29, suggests a significant genetic event and differentiates it from the previously reported genotype, the dominant form among all sequenced SARS-CoV isolates. A 17-nt segment of this extra sequence is identical to a segment of the same size in two human mRNA sequences that may interfere with viral replication and transcription in the cytosol of the infected cells. It provides a new avenue for the exploration of the virus-host interaction in viral evolution, host pathogenesis, and vaccine development.

Base Sequence↗
PubMed1979

Production of temperature-sensitive and pathogenic virus from Aedes albopictus cells (Singh) persistently infected with Chikungunya virus.

When A. albopictus, clone C6/36, cells were infected with chikungunya (CHIK) virus, high virus yield accompanied by a cytopathic effect in the acute stage of infection was followed by a relatively low yield of virus over a long period of time. Virus produced from persistently infected cultures became gradually of smaller plaque size and more temperature-sensitive; however, such virus still retained pathogenicity for suckling mice even after one year of infection. When the persistently infected cells were subcultured, a dissociation was observed between the time course of cell growth and that of virus production, suggesting some intracellular mechanisms that turn off virus production. The greater part of the interference against CHIK virus by the culture medium of the persistently infected cells appeared to be mediated by the infective virus in the medium. The infective virus was easily removed from the persistently infected cells either by subculture or by cloning in the presence of anti-CHIK serum, yielding cured cultures or virus-negative clones.

Aedes↗
PubMed1997

Murine retroviruses use at least six different receptors for entry into Mus dunni cells.

Murine retroviruses have been divided into six interference groups that use different receptors for cell entry: the ecotropic, xenotropic, polytropic, amphotropic, 10A1, and Mus dunni endogenous virus groups. Some interference is observed between xenotropic and polytropic viruses and between amphotropic and 10A1 viruses, indicating some overlap in receptor specificity between these groups, but otherwise these interference groups appear completely independent. In contrast, one study found interference among many of these groups when Mus dunni wild mouse cells were examined with an immunofluorescence assay to detect infection by the challenge virus. Here we have used a more direct assay for cell entry by using pseudotyped retroviral vectors to measure interference in M. dunni cells, and we find no evidence for extensive interference between members of different murine retrovirus groups. Indeed, our results in M. dunni cells are consistent with interference results observed in other cell types and indicate that the anomalous interference results previously observed in M. dunni cells with the immunofluorescence assay were most likely due to factors other than those that affect receptor-mediated virus entry. In summary, our results show that murine retroviruses use at least six different receptors for entry into M. dunni cells.

Animals↗
PubMed1998

Threshold number of provirus copies required per cell for efficient virus production and interference in moloney murine leukemia virus-infected NIH 3T3 cells.

The gag-pol readthrough mutant of Moloney murine leukemia virus, MLV-B(CAG) (T. Odawara, H. Yoshikura, M. Oshima, T. Tanaka, D. S. Jones, F. Nemoto, Y. Kuchino, and A. Iwamoto, J. Virol. 65:6376-6379, 1991), was poorly complemented by a mutant encoding only Gag. This is because with all the genetic elements necessary for env expression present in MLV-B(CAG), insufficient Env protein was produced by the cells expressing MLV-B(CAG) for efficient virus production. Since the env mRNA expression per provirus in the MLV-B(CAG)- and wild-type-MLV-producing cells were the same and since the cells expressing the former contained eightfold fewer proviral copies, the insufficient Env expression by the former was found to be due to insufficient proviral copies in the cells. Examination of the cell clones having various proviral copies of Deltawt MLV (M. Oshima, T. Odawara, T. Matano, H. Sakahira, Y. Kuchino, A. Iwamoto, and H. Yoshikura, J. Virol. 70:2286-2295, 1996) showed that mRNA level was proportional to the number of proviral copies while interference and virus production followed a sigmoid curve with a sharp rise at the threshold number of proviral copies of around four per cell. Multicycle infection probably continues until the threshold level of proviral copies is attained in natural infection too.

3T3 Cells↗
PubMed1988

Interference between coinoculated viroids.

Experiments were carried out to seek evidence of an interaction between two viroid RNAs introduced to tomato plants in the same inoculum. At the level of symptom expression, the severe isolate of potato spindle tuber viroid (PSTV) dominated the mild isolate. Seventy-five percent of the plants inoculated with a 100-fold excess of the mild isolate developed unattenuated symptoms of severe disease. Other experiments revealed that infectious RNA molecules transcribed from cloned DNA templates containing PSTV sequences reduced the level of hop stunt viroid (HSV) RNA present in nucleic acid extracts of plants which had been inoculated with a mixture of dimeric plus-strand transcripts of these two viroids. Plants inoculated with dual transcripts--containing two copies of PSTV linked to two copies of HSV--developed characteristic symptoms of severe PSTV. Dot hybridization demonstrated that only PSTV replicated to detectable levels in these plants. A likely interpretation of these results is that the HSV portion of the dual transcripts failed to replicate because of interference from PSTV. These results raise questions about how the process of viroid replication is related to symptom expression, and lead to suggested models for the effect of viroid-like RNAs in cells under both normal and pathogenic circumstances.

Plant Diseases↗
PubMed2005

Viral targeting of the interferon-{beta}-inducing Traf family member-associated NF-{kappa}B activator (TANK)-binding kinase-1.

Expression of the antiviral cytokines IFN-alpha/beta is among the most potent innate defenses of higher vertebrates to virus infections, which is controlled by the inducible transcription factor IFN regulatory factor (IRF)3. Borna disease virus (BDV) establishes persistent noncytolytic infections in animals and tissue culture cells, indicating that it can circumvent this antiviral reaction by an unexplained activity. In this study, we identify the BDV P protein as microbial gene product that associates with and inhibits the principal regulatory kinase of IRF3, Traf family member-associated NF-kappaB activator (TANK)-binding kinase 1 (TBK-1). We demonstrate that the P protein counteracts TBK-1-dependent IFN-beta expression in cells and, hence, the establishment of an antiviral state. Furthermore, our data show that the BDV P protein itself is phosphorylated by TBK-1, suggesting that P functions as a viral decoy substrate that prevents activation of cellular target proteins of TBK-1. Thus, our findings provide evidence for a previously undescribed mechanism by which a viral protein interferes with the induction of the antiviral IFN cascade.

Animals↗