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At least 37 records · Page 2Linked to original sources
PubMed1986

Inhibition of the in vitro-reactivation of latent herpes simplex virus infection in spinal ganglia: comparison of various immune factors. Brief report.

In order to study whether the latency of herpes simplex virus (HSV) is immunologically controlled, the influence of different immune mechanisms on the in vitro-reactivation of the virus in latently infected lumbosacral ganglia of mice was investigated. Combined addition of macrophages and antibodies to cultures of ganglionic tissue proved most effective in delaying virus reactivation. This was achieved to a lesser degree when applying antibodies only, whereas macrophages alone were not effective, nor were immune lymphocytes, nor was interferon from L-cells or from the peritoneal cavity of mice.

Animals↗
PubMed1995

Interferon-beta strong cytopathic effect on human papillomavirus type 16-immortalized HPK-IA cell line, unexpectedly not shared by interferon-alpha.

We report a novel, unusually severe cytopathic effect of interferon-beta (IFN-beta). Data concerning antibody neutralization, induction and recovery time course, CPE50 dose, impact on oxidative metabolic activity and 1D SDS-PAGE total cellular protein analysis are provided for preliminary characterization. This cytopathic effect appears to be linked to human papillomavirus type 16 (HPV-16) genome presence as it is markedly evident in the HPV-16-immortalized HPK-IA cell line, but is not induced in diploid keratinocytes. It is also not induced in highly malignant SiHa cells suggesting that it also requires a fairly conserved phenotype. This effect is unexpectedly not shared by IFN-alpha pointing to a discrimination between IFN-alpha and -beta signal despite the well-known sharing of a common receptor. It remains to be clarified whether this divergence, undetectable in other cellular systems, represents a direct effect of viral presence or a non-specific consequence of cellular homoeostatic disregulation induced by the papillomavirus genome.

Cell Line, Transformed↗
PubMed1994

Potentiating effect of (2-[2-[(2-amino-1,6-dihydro-6-oxo-9H-purin-9-yl)methyl]-phenyl]ethenyl) -phosphonic acid (MDL 74,428), a potent inhibitor of purine nucleoside phosphorylase, on the antiretroviral activities of 2',3'-dideoxyinosine combined with ribavirin in mice.

2',3'dideoxyinosine (ddI) has potent activity against human immunodeficiency virus (HIV) but is rapidly metabolized by erythrocytic purine nucleoside phosphorylase (PNP), and therefore has a very short plasma half-life in rodents, monkeys and in patients with acquired immunodeficiency syndrome. It is now reported that 100 microM (2-[2-[(2-amino-1,6-dihydro-6-oxo-9H-purin-9-yl)methyl]-phenyl]ethenyl) - phosphonic acid (MDL 74,428), a very potent inhibitor of PNP blocks the intracellular phosphorolysis of ddI in cultured human red blood cells, in T leukemic CEM lymphoblasts and prolongs ddI plasma effective concentration in mice at a dose of 250 mg/kg body weight given i.p. In MDL 74,428-treated CEM cells, despite marked reduction of ddI catabolism, neither further accumulation of ddATP, the active antiviral metabolite of ddI, nor potentiation of the activity of ddI against HIV cytopathogenicity is observed. MDL 74,428 does not also affect the inhibitory effect of ddI combined with ribavirin on the transformation in vitro of C3H/3T3 cells by Moloney murine sarcoma virus (MSV). In mice, on the contrary, MDL 74,428 (200 mg/kg body weight, i.p.) is effective at potentiating the effect of ribavirin used either alone, or combined with ddI on MSV-induced tumour formation and associated mortality. However, in the absence of ribavirin, co-administration of MDL 74,428 with ddI affords, no chemotherapeutic advantage.

3T3 Cells↗
PubMed1990

Clonal analysis of infiltrating T lymphocytes in liver tissue in viral hepatitis A.

The pathogenic mechanism leading to liver tissue injury in hepatitis caused by hepatitis A virus is unclear. We have randomly established T-cell clones from liver biopsies from four patients with hepatitis A. A total of 578 clones was phenotypically analysed. During the acute phase of the disease CD8+ clones dominated over CD4+ clones, whereas in a biopsy taken late after onset of clinical syndromes more CD4+ than CD8+ clones were obtained. Interestingly, in a patient with a second exacerbation of the disease, more than 20% of all clones had the CD3+ WT31- CD4- CD8- 'NK-like' phenotype. All CD8+ clones had cytotoxic activity and approximately 50% of all CD8+ clones showed specific cytotoxicity against autologous fibroblasts infected with hepatitis A virus. The CD8+ cells also produced IFN-gamma in response to these target cells. Variable IFN-gamma production was observed with all types of T-cell clones. These results suggest that the liver injury in hepatitis A is not caused by a viral cytopathogenic effect but is due to an immunopathological reaction of sensitized cytotoxic T lymphocytes against infected hepatocytes. In addition, these studies show an enrichment of CD4-8-T-cell receptor alpha beta-chain-negative T lymphocytes at the site of an inflammation and suggest a role of these cells in an anti-viral reaction.

Acute Disease↗
PubMed1987

Centrifugation-shell vial technique for rapid detection of herpes simplex virus cytopathic effect in Vero cells.

A centrifugation-shell vial technique for herpes simplex virus detected the virus in 50 (24.6%) of 203 specimens by cytopathic effect at 48 h, compared with detection of the virus in 47 (23.2%) specimens by immunofluorescence at 24 h. The rapid detection of cytopathic effect may be useful to laboratories that are not interested in typing all herpes simplex virus specimens but that wish to reduce the cost of herpesvirus cultures.

Animals↗
PubMed1990

The epithelial neoplasm observed in the cultured coho salmon, Oncorhynchus kisutch.

The epithelial neoplasms were observed on the mouth of the cultured coho salmon, Oncorhynchus kisutch. Histopathologically, the tumors were formed to be proliferative epithelial cells, but no change was observed in other organs. The virus from this tumor was isolated in RTG-2 and CHSE-214 cells and developed the cytopathic effect which characterized to be the formation of syncytia and the migration of chromatin. This virus was neutralized with anti-Oncorhynchus masou virus (OMV) rabbit serum.

Animals↗
PubMed1985

Antiviral activity of phorbol myristate acetate and possible relationships with interferon action.

Signal-induced turnover of membrane phospholipids represents a fundamental transducing mechanism that induces a signal cascade resulting in mobilization of calcium, activation of protein kinase C by diacylglycerol, release of arachidonic acid and stimulation of cyclic GMP production. In this pathway tumor-promoting phorbol esters such as phorbol myristate acetate (PMA) may substitute for diacylglycerol. The interferon-like antiviral effect of PMA described here suggests that the inositol phospholipid-diacylglycerol-protein kinase C signal-transducing mechanism may be involved in interferon action.

Antiviral Agents↗
PubMed1996

HIV-induced apoptosis requires the CD4 receptor cytoplasmic tail and is accelerated by interaction of CD4 with p56lck.

The roles of the CD4 receptor and the src kinase p56lck were examined in the process of HIV-induced apoptosis of CD4+ T lymphocytes. The presence of the CD4 cytoplasmic tail was found to be essential in delivering an apoptotic signal, and interaction of CD4 with p56lck potentiated HIV-induced apoptosis. Apoptosis, but not HIV replication, was abrogated by deleting the NH2-terminal intracytoplasmic tail of CD4, or by mutating the two critical cysteines in this tail that are responsible for CD4-p56lck interaction. Introduction of p56lck in C8166-45 or MT-2 cells, CD4+ T cell lines deficient for this protein, greatly increased HIV-induced apoptosis and syncytium formation. The ability of p56lck to deliver an apoptotic signal did not depend on its kinase function, since a kinase-deficient mutant was as effective as its normal counterpart in inducing apoptosis, suggesting that p56lck may act as an adapter to anchor other proteins to transduce the death signal.

Apoptosis↗
PubMed1993

Induction of micronuclei by HTLV-I Tax: a cellular assay for function.

Cellular chromosomal damage is ubiquitously seen in HTLV-I-transformed lymphocytes. It is also characteristic of cells that have been exposed to mutagens. A sensitive measurement for mutagen-induced DNA damage is the formation of micronuclei in treated cells. Because current evidence suggests that HTLV-I Tax is etiologically linked to transformation, we tested for its activity in inducing micronuclei. We show here that transfection into cells of a Tax-producing plasmid rapidly induced the formation of micronuclei. This effect cooperated with that of a mutagen (mitomycin C) and was correlated with the inherent trans-activation capacity of Tax. These findings suggest that a commonly used mutagen assay could be a quick biological test for putatively oncogenic proteins.

Cell Line↗
PubMed1991

Evaluation of a visual, rapid, membrane enzyme immunoassay for the detection of herpes simplex virus antigen.

We evaluated a 12-min, direct, monoclonal antibody-based enzyme immunoassay (EIA) (SureCell; Kodak, Rochester, N.Y.) which aids in the detection of herpes simplex virus infection; the assay system is also approved for culture confirmation. The test was evaluated from direct clinical samples and compared with conventional culture methodology by using a single swab. A total of 265 specimens from 180 female cervical-urogenital sites, 62 male urogenital sites, 4 rectal sites, 3 skin sites, 6 oral sites, and 10 colposcopy sites were collected on Dacron or cotton swabs and placed in viral transport medium (VTM). Within 6 h of receipt, 0.2 ml of the vortexed VTM was inoculated into each of two replicate cell cultures. Cell monolayers were observed daily for ten days, and cytopathic effect was confirmed by using an indirect immunoperoxidase reagent. The procedure for the SureCell assay conformed to the manufacturer's recommendations. When conventional culture was compared with EIA results, the overall sensitivity, specificity, positive predictive value, negative predictive value, and agreement were 64.4, 98.9, 96.7, 84.4, and 87.2%, respectively. Variables affecting the EIA sensitivity are the stage of the lesion and conventional culture methodologies. A review of culture results for 32 EIA false-negative tests indicated that 15 were detected after 48 h of incubation. Cytopathic effect observed at 48-, 72-, and 96-h cutoffs altered the sensitivity for the EIA. To ensure detection of SureCell herpes simplex virus-negative specimens, it is recommended that an unused aliquot of VTM be tested in cell culture.

Antigens, Viral↗
PubMed1988

A recombinant murine retrovirus expressing v-rel is cytopathic.

A murine retrovirus that expresses the avian v-rel oncogene was constructed. NIH 3T3 cells transfected with this construct expressed v-rel-specific RNA and a 59-kDa protein serologically identical to avian v-rel. The protein expressed from the recombinant retrovirus retained the associated protein kinase activity observed in avian systems. While the detection of v-rel RNA sequences in infected cells verified the infectivity of the retrovirus, the retrovirus did not transform either murine fibroblasts or bone marrow cells. Rather, a cytopathic effect was observed in murine fibroblasts and a pre-B lymphoid cell line that were infected with the murine retrovirus. Growth curves of these infected cells revealed cell death or diminished growth rate in all cases.

Animals↗
PubMed1990

Potentiating effect of ribavirin on the in vitro and in vivo antiretrovirus activities of 2',3'-dideoxyinosine and 2',3'-dideoxy-2,6-diaminopurine riboside.

2',3'-Dideoxyinosine (DDI) and 2',3'-dideoxy-2,6-diaminopurine riboside (ddDAPR) are potent and selective inhibitors of human immunodeficiency virus (HIV) replication in MT-4 cells. They are also inhibitory to the transformation of C3H/3T3 cells by Moloney murine sarcoma virus (MSV). In vivo, they are only marginally effective in delaying MSV-induced tumor formation, and mortality associated therewith in newborn NMRI mice. When combined with ribavirin, DDI and ddDAPR become much more effective in inhibiting MSV and HIV replication in vitro and MSV-induced tumor formation in vivo. These observations point to the potential role of ribavirin in potentiating the anti-HIV activity of DDI in AIDS patients.

Animals↗
PubMed1986

Comparative inhibitory effects of suramin and other selected compounds on the infectivity and replication of human T-cell lymphotropic virus (HTLV-III)/lymphadenopathy-associated virus (LAV).

Suramin and various other selected compounds were evaluated for their in vitro inhibitory effects on the infectivity and replication of human T-cell lymphotropic virus (HTLV/III)/lymphadenopathy-associated virus (LAV). As parameters for infectivity and replication, respectively, we followed the cytopathic effect of HTLV-III/LAV on ATH 8 cells, a T-cell clone with high susceptibility to HTLV-III/LAV, and the expression of HTLV-III/LAV p24 gag protein in H9 cells infected with HTLV-III/LAV. As the most effective inhibitors of HTLV-III/LAV the following substances emerged (in order of decreasing activity): Evans Blue approximately equal to suramin greater than phosphonoformic acid greater than Direct Yellow 50. Several purine nucleoside analogues including vidarabine, tubercidin, neplanocin A, dihydroxypropyladenine, pyrazofurin and ribavirin were not inhibitory to HTLV-III/LAV. In our test systems, involving a high multiplicity of infection, HPA-23, previously reported to be effective against LAV reverse transcriptase, showed no inhibitory effect on HTLV-III/LAV infectivity for ATH 8 cells and proved only weakly inhibitory to HTLV-III/LAV replication in H9 cells. Thus, among the anionic dyes that are structurally related to suramin, compounds were found which were as active as suramin itself, if not more so.

Animals↗
PubMed2000

Unique morphological alterations of the HTLV-I transformed C8166 cells by infection with HIV-1.

C8166 cells express T lymphocyte markers, a monocyte-specific esterase, taxpolypeptide of HTLV-I. In spite of this transactivator, their HIV-1 yield is low. Their culture conditions were modified, and infected cells were immobilized on a poly-L-lysine sheet under semisolid overlays to study their phenotypic alterations and HIV-1 production by microscopy and electron microscopy. Another lymphoid cultures (MT-4, CEM, CEM-ss, AdCEM) similarly treated were infected with either HIV-1/RF or IIIB. Specificity of HIV-1 was compared to the effects of vesicular stomatitis virus (VSV). Unlike other cultures, HIV-1/RF infected C8166 cells in Eagle s MEM exhibited surface projections resembling hairy leukemia cells, which was followed by balloon degeneration and apoptosis. Immobilized HIV-1 infected cultures formed flat syncytia with several interdigitating dendritic projections. Syncytia shrunk with condensed nuclear material and axon-like filaments characteristic for infected macrophages. VSV induced enlargement and necrotic lysis of all cell types. Early postinfection with HIV-1, electron microscopy revealed irreversible membrane fusion above cell nuclei, and transient fusion between filaments. Transient presence of coated vesicles containing intact HIV-1 particles, Birbeck granule-like structures of Langerhans cells, fibrillar-lamellar structures resembling hairy leukemia or Sézary cells were detected. Late postinfection, high proportion of HIV-1 bud from polarized cytoplasm was empty particle, while that bud and entrapped in cytoplasmic vacuoles contained two or multiple cores in a fused envelope. The effect of early gene products of HIV-1 on HTLV-I and C8166 cells might elicit their latent potentials for monocyte or interdigitating dendritic cells, while in the later phase HTLV-I products might alter HIV-1 virion assembly.

Apoptosis↗
PubMed1977

The elimination of herpes simplex plaques by antibody and the emergence of resistant strains.

Established type 1 HSV plaques were eliminated by antibody. Antibody had to remain in contact with infected cells for several days to have a maxi;mum effect. It did not prevent the production of viral induced antigens in a cell when applied after the cell was infected but did prevent the transmission of infection to contiguous cells. Strains which were resistant to elimination by antibody formed syncytia, did not grow to significantly higher titers than nonresistant strains, and were as easily neutralized by antiserum as nonresistant strains.

Antibodies, Viral↗
PubMed1980

Induction of virus multiplication in permissive cells transformed by a temperature-sensitive polyoma virus. I. Isolation and partial characterization of survivors.

A fibroblastic cell line transformed by ts-P155, an early temperature-sensitive mutant of polyoma virus, has been isolated after infection of secondary mouse embryo cells at the restrictive temperature of 39. These cells, designated Cyp, undergo a massive CPE accompanied by the production of infectious, temperature-sensitive virus when transferred to the nonrestrictive temperature of 33. Several independent clones were established from cells which survived the induction of virus multiplication occurring at 33. When routinely cultured at this temperature, these cells, termed R, displayed the growth properties of transformants and produced variable amounts of infectious, temperature-sensitive virus. This shedding of virus could not be "cured' by the addition to the culture medium of antipolyoma serum which had already been found to effectively suppress virus production in Cyp cell cultures transferred to 33. Moreover, R cells seemed to have developed a resistance to superinfection that the parent Cyp cell line did not exhibit. Therefore, virus production in R cell cultures probably reflects the occasional excision and replication of integrated viral genomes rather than a carrier state.

Antigens, Viral↗