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.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,711 records · Page 95Linked to original sources

PubMed1975

Inhibition of Herpesvirus hominis replication by human interferon.

The effect of human interferon on single-cycle replication of Herpesvirus hominis type 1 (HV-1) and vesicular stomatitis virus (VSV) in human foreskin fibroblast cultures (HFF) was studied. After treatment of HFF cultures with low concentrations (58 U) of human interferon, a variable but statistically significant inhibition of HV-1 was observed. At higher concentrations (greater than 95 U) yield reduction of HV in interferon-treated cultures approached that of VSV. Preliminary data indicate that antiviral activity decays more rapidly for HV-1 than for VSV after removal of interferon from cultures.

Animals↗

PubMed1975

Effect of human leukocyte interferon on vaccinia-and herpes virus-infected cell cultures and monkey corneas.

Pretreatment of human fibroblast cultures with human leukocyte interferon (HIF, 1,000 IU/ml) resulted in a 24-h delay of virus replication after infection with vaccinia virus and herpes simplex virus type 1 and type 2. Additional HIF treatment 24 h after infection effectively lowered the maximum yield of viral infectivity. Equal results were obtained in simian cells with 3,000 IU of HIF per ml. The spread of two cell-bound herpesviruses, varicella zoster virus and Medical Lake macaque herpesvirus, was inhibited by 2,000 IU of HIF per ml in human fibroblasts and Vero cells, respectively. Varicella zoster virus infectivity was notably reduced by HIF, whereas the latter system showed a low sensitivity. To study the effect of HIF in the infected cornea, keratitis was induced experimentally in both eyes of 12 rhesus monkeys and 12 African green monkeys by inoculation with vaccinia virus and herpes simplex virus, respectively. In each monkey one eye served as a control for the full cycle of disease. In the other eye HIF treatment was initiated prophylactically 15 h before or simultaneously with the challenge virus infection or 6 to 20 h postinfectionally or therapeutically after onset of the disease, and the treatment was continued for 2 to 7 days. Prophylactic and simultaneous administration equally resulted in inhibition of both vaccinia and herpes keratitis. Postinfectional and therapeutic administration of interferon moderated the course of keratitis slightly and shortened the period of virus shedding.

Animals↗

PubMed1981

Effects of cell source, mouse strain, and immunosuppressive treatment on production of virulent and attenuated murine cytomegalovirus.

Murine cytomegalovirus pools from various in vitro and in vivo sources were compared for virulence in suckling mice in an effort to identify the conditions which were necessary for the production of virulent and attenuated viruses. Virus passaged in tracheal ring and salivary gland organ cultures, where virus is produced primarily by epithelial cells, was even more attenuated than virus passaged in mouse embryo fibroblasts. The attenuation observed after passage in all three of these in vitro systems did not appear to be due to defective interfering particles. We also found that virus produced in vivo in salivary glands became attenuated with time after infection. Virus harvested from salivary glands 5 to 6 weeks after infection was highly attenuated compared with both salivary gland-passaged virus harvested 2 to 3 weeks after infection and tissue culture-passaged virus. The attenuation of salivary gland-passaged virus with time was reversed when animals were treated with cyclophosphamide before the virus was harvested. A comparison of virus pools harvested from susceptible and resistant mouse strains indicated that the mouse strain had little effect on the virulence of the virus produced. When the various sources of virus tested in this study were ranked in terms of the virulence of the virus produced, salivary glands in intact mice either 2 to 3 weeks after infection or after cyclophosphamide treatment produced the most virulent virus, followed by mouse embryo fibroblast cultures, tracheal ring and salivary gland organ cultures, and, finally, salivary glands in intact mice 5 to 6 weeks after infection.

Animals↗

PubMed1982

Conditions required for induction of interferon by rotaviruses and for their sensitivity to its action.

Our investigations of interferon induction by rotaviruses showed that only when cells were pretreated with interferon, i.e., primed, could infectious rotaviruses induce significant quantities of interferon. As little as 0.5 U of interferon provided sufficient priming for this induction. UV-irradiated rotaviruses induced significant levels of interferon, and priming only marginally enhanced the yields. Neither heat-inactivated virus nor serum-neutralized virus was able to induce interferon, even when cells were primed. When cells were treated with purified virus double-stranded RNA in the presence of DEAE-dextran to facilitate uptake, interferon was induced, although priming did not enhance yields. These results strongly implicate the viral double-stranded RNA as the effector for interferon induction. The insensitivity of rotaviruses to interferon in vitro was also studied. Results suggested that this lack of sensitivity was not due to any inherent resistance of the virus to the antiviral proteins, but rather to lack of activation of cellular enzymes exhibiting antiviral activity.

Animals↗

PubMed1982

Pathogenesis of herpes simplex labialis: correlation of vesicle fluid interferon with lesion age and virus titer.

Of 51 patients with herpes simplex labialis, 50 had detectable interferon (IFN) in samples of lesion vesicle fluid. The median titer of vesicle fluid IFN was 8,200 U. and the range of values was 400 to 63,600 U. The amount of vesicle fluid IFN was correlated with lesion age (r = 0.32, P = 0.024) and vesicle fluid virus titer (r = 0.59, P = 0.00004), but not with the clinical severity of the disease. The presence of vesicle fluid IFN (1,500 to 28,600 U) in 15 lesions less than 12 h old emphasizes the need for early treatment in studies of antiviral agents for herpes simplex labialis.

Adult↗

PubMed1982

Induction of alpha and beta interferons during the hyporeactive state of gamma interferon by Mycobacterium bovis BCG cell wall fraction in Mycobacterium bovis BCG-sensitized mice.

Characterization of interferon (IFN) induced by a second challenge with specific antigen was investigated during the development of hyporeactivity established after challenge of Mycobacterium bovis BCG-sensitized mice with BCG cell wall fraction (BCG-CW). When BCG-sensitized mice were challenged with BCG-CW, IFN-gamma was detected in the circulation 4 h later and rapidly disappeared. After IFN-gamma disappeared from their blood, mice became completely hyporeactive to the second challenge with BCG-CW for 1 day, and thereafter they recovered from this hyporeactive state. However, we always observed that IFN induced at first by the second challenge with BCG-CW during the hyporeactive state was type I IFN-alpha/beta, but thereafter was entirely IFN-gamma. Induction of IFN-alpha/beta by the specific antigen during restoration from the hyporeactive state in BCG-sensitized mice is discussed.

Animals↗

PubMed1982

Defective parvoviruses acquired via the transplacental route protect mice against lethal adenovirus infection.

Adeno-associated virus type 1 (AAV-1) interfered with the replication of its murine adenovirus (MAV) helper in primary mouse kidney cells and in 1-day-old ICR mice. Mice carrying AAV-1 acquired via the transplacental route were protected against lethal infection with MAV. The replication of AAV-1 in these mice could be triggered by multiple challenges with MAV, and antibodies to AAV-1 were subsequently detected.

Adenoviridae↗

PubMed1982

Mediators of protection against lethal systemic vesicular stomatitis virus infection in hamsters: defective interfering particles, polyinosinate-polycytidylate, and interferon.

Homologous defective interfering (DI) particles protected adult Syrian hamsters against lethal systemic infection with vesicular stomatitis virus (VSV) serotype Indiana. The DI particles had to be biologically active, but did not have to be administered at the same inoculation site as the infectious virus. Serum and tissue levels of VSV postinoculation were significantly lower in DI-protected animals than in unprotected controls, suggesting that true autointerference was occurring. However, some aspects of protection also must be mediated through nonspecific mechanisms, since susceptible hamsters could be protected against VSV Indiana by coinjection with heterologous DI particles prepared from VSV serotype New Jersey or by simultaneous administration of polyinosinic acid-polycytidylic acid. By measuring serum levels of putative hamster interferon (type 1), we found that animals coinjected with VSV and DI particles or polyinosinic acid-polycytidylic acid produced significant levels of interferon. Since similarly high serum levels of interferon were measured in recipients of VSV alone (animals that eventually died from infection), there appeared to be no correlation between protection against lethal disease and induced levels of serum interferon. Instead, serum interferon levels correlated positively with amounts of VSV PFU found in serum and tissues of infected animals, the lowest levels being found in serum of animals protected with homologous DI particles. The data are consistent with the hypothesis that autointerference by DI particles as well as various host defense mechanisms (possibly including induction of interferon) participates in protecting hamsters against lethal VSV infection.

Animals↗

PubMed1985

Interferon-induced inhibition of Chlamydia trachomatis: dissociation from antiviral and antiproliferative effects.

The yield of infectious Chlamydia trachomatis was analyzed in human (HeLa) and mouse (McCoy) cell lines treated with the human interferon (IFN) subtypes IFN-alpha A and IFN-alpha D, with their hybrids [IFN-alpha AD (BglII), IFN-alpha AD (PvuII), and IFN-alpha DA (BglII)] constructed in vitro from their expression plasmids, or with IFN-beta 1 or buffy coat IFN. In HeLa cells, a significant inhibition of Chlamydia infectivity was obtained with IFN-alpha D, IFN-alpha DA (BglII), and buffy coat IFN. In McCoy cells, IFN-alpha AD (BglII) and IFN-alpha AD (PvuII) induced a strong degree of inhibition of Chlamydia infectivity. In McCoy cells, there was a correlation among the antichlamydial, antiviral, and antiproliferative activities of the different IFNs tested. In HeLa cells, however, the ability of a particular IFN subtype to inhibit Chlamydia infectivity did not always correlate with its inhibitory effects on encephalomyocarditis virus replication or with its antiproliferative activity.

Cells, Cultured↗

PubMed1973

Rubella immunization of volunteers via the respiratory tract.

The efficacy of various routes of administration of the live attenuated rubella virus vaccine was evaluated by using 46 seronegative volunteers who were divided into 4 vaccine groups: subcutaneous, nosedrops, spray into posterior oropharynx and nose using large particle aerosol, and inhalation of small particle aerosol through the mouth. Seroconversion was observed in all of the vaccinees regardless of route of immunization. Nasal secretion antibody 6 weeks after immunization was highest in the volunteers who received the vaccine by nose drops (all members of this group had demonstrable nasal secretion antibody after immunization). Only half of the volunteers in the subcutaneous group developed demonstrable nasal secretion antibody. This suggests that nasal secretion antibody was best stimulated when vaccine was given directly into the nose. Volunteers were challenged with the vaccine intranasally at 6 to 8 weeks. None of the volunteers exhibited clinical symptoms or fourfold or greater serum antibody rises after challenge, but fourfold or greater nasal secretion antibody rises were observed in three volunteers in the subcutaneous vaccine group and two in the aerosol group, suggesting that those volunteers had not been protected against challenge. Rubella virus was isolated 8 to 12 days after challenge in two persons in the subcutaneous group and three in the aerosol vaccine group, but none in the nose drops or spray groups. Thus, protection after nasal challenge appeared to be best in those groups which also had the best nasal secretion antibody response after immunization. However, protection did not seem to be correlated with either nasal secretion or serum antibody levels.

Administration, Intranasal↗

PubMed1974

Pathogenesis and autointerference in a virus disease of crabs.

The course of an infection apparently caused by a filterable virus of the blood of the shore crab. Carcinus maenas, has been experimentally studied in this host both at Roscoff, France. where it was originally found, and at Woods Hole, Mass., where the local species was also found susceptible. Although a portion of the infected animals die with the symptoms of inadequate blood clotting, recovery of this function occurred promptly in about two-thirds of the animals. Half of the animals that recovered this function did so within 4 to 6 days. Recovery was not accompanied by disappearance of the virus from the whole blood. In tests done as late as 40 days after recovery, virus was still present. Autointerference was demonstrated after acute infection. It was found in the serum of animals with manifest disease on all days tested and in whole blood of animals taken more than 2 days after the clotting defect appeared. It was not demonstrable within the whole blood within the first 2 days of disease. The role of this in the recovery phenomenon is discussed.

Animals↗

PubMed1971

Extent of host deletions associated with bacteriophage P2-mediated eduction.

A series of independent Escherichia coli K eductants has been isolated and tested to determine the extent of their deletions. The deletions cover the P2 prophage in location H, the his operon, a suppressor of the recBC phenotype (sbcB), the gene for gluconate-6-phosphate dehydrogenase (gnd), a locus involved in cell wall synthesis (rfb), and in some cases all or part of genes involved in methylgalactoside uptake (mglP). One end of the deletion, the P2 prophage end, appears to be the same for all eductants. The other end, however, can be located before, within, and after the mglP locus.

Carbon Isotopes↗

PubMed1966

Leukocytes and interferon in the host response to viral infections. II. Enhanced interferon response of leukocytes from immune animals.

Glasgow, Lowell A. (University of Rochester School of Medicine and Dentistry, Rochester, N.Y.). Leukocytes and interferon in the host response to viral infections. II. Enhanced interferon response of leukocytes from immune animals. J. Bacteriol. 91:2185-2191. 1966.-The production of interferon was studied under in vitro conditions in peritoneal leukocytes or macrophages from mice immunized with Chikungunya virus (CV). Cultures of leukocytes obtained from animals immune to CV produced 2- to 10-fold greater amounts of interferon when exposed to an inoculum of CV than similar cell preparations from nonimmune, control animals. The viral inhibitor produced in increased quantity by CV-immune leukocytes had the biological and biochemical properties of interferon. The enhanced interferon production was inhibited by actinomycin D. This response of immune leukocytes was specific, and was initiated only by CV; it was not observed in leukocytes from animals immunized against other viruses which were challenged with CV. The presence of neutralizing antibody could not be related to this response. The observed increase in interferon production was not dependent upon an enhanced virus uptake. The data are presented as a possible new dimension of the "immune response" and may suggest a mechanism for the phenomenon of "tissue immunity."

Animals↗

PubMed1966

Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell.

Plagemann, Peter G. W. (Western Reserve University, Cleveland, Ohio), and H. Earle Swim. Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell. J. Bacteriol. 91:2317-2326. 1966.-The replication of mengovirus was studied in two strains of Novikoff (rat) hepatoma cells propagated in vitro. The replicative cycle in both strains required 6.5 to 7 hr. Infection resulted in a marked depression of ribonucleic acid (RNA) and protein synthesis by strain N1S1-63. Inhibition of RNA synthesis was reflected by a decrease in the deoxyribonucleic acid (DNA)-dependent RNA polymerase activity of isolated nuclei. Mengovirus had no effect on either protein or RNA synthesis or on the DNA-dependent RNA polymerase activity of a second strain, N1S1-67. The time course of viral-induced synthesis of RNA by cells was studied in cells treated with actinomycin D. It was first detectable between 2.5 and 3 hr after infection and continued until 6.5 to 7 hr. The formation of mature virus was estimated biochemically by measuring the amount of RNA synthesized as a result of viral infection which was resistant to degradation by ribonuclease in the presence of deoxycholate. Approximately 70% of the deoxycholate-ribonuclease-resistant RNA was located in mature virus, and the remainder was double-stranded. The formation of mature virus began about 45 min after viral-directed (actinomycin-resistant) synthesis of RNA was detectable in the cell, and only about 18 to 20% of the total RNA synthesized was incorporated into virus. Release of virus from cells began about 1 hr after maturation was first detectable. Release of virus from cells was accompanied by a loss of a large proportion of their cytoplasmic RNA and protein.

Animals↗

PubMed1968

Nature of the carrier state of bacteriophage SP-10 in Bacillus subtilis.

Although the association of phage SP-10 with Bacillus subtilis W-23-S(r) persists in heat- and antiserum-resistant form through the spore stage, it is unstable in vegetative cells and frequently terminates in loss of the carried phage or in lysis. On low-tonicity media, the plating efficiency of carrier cells is low. However, high concentrations of succinate or sucrose or a slowed growth rate preserve viability: on 0.48 m succinate-agar, the viable count per optical density unit is the same as that of a noncarrier control culture. Carrier clones retain phage on 0.48 m succinate-agar. At higher succinate levels, many colonies emerge free of phage; at 1 m succinate, all are cured, probably because high succinate inhibits reinfection. Growth of carrier cells in liquid medium with antiphage serum results in rapid curing; events in such cultures with and without succinate were studied quantitatively by tracing the emergence of sensitive cells, the multiplication and induction of carrier cells, and the sensitivity of carrier cells to superinfection with virulent phage. During log phase, 40 to 70% of the carrier cells became sensitive to virulent phage, although the same cells were insensitive during lag and stationary phase. Apparently, fluctuations in repressor levels are responsible. Spontaneous induction of carrier cells followed a qualitatively similar pattern, perhaps in response to changes in level of the same repressor. Production of sensitive segregants by carrier followed a different course, presumably because the repressor does not affect segregation. Many sensitive cells were found two to three divisions after inoculation in antiserum medium. This suggests that each inoculum cell contained one or only a few phage replicons. The data are compatible with the idea that the carrier state in media without antisera is maintained entirely by reinfection and without replication of phage in the latent state. Alternative models which involve replication of latent phage are not ruled out, however.

Bacillus subtilis↗

PubMed1990

Human herpesvirus 6 inhibits human immunodeficiency virus type 1 replication in cell culture.

The SF strain of human herpesvirus 6 (HHV-6SF) isolated from the saliva of a human immunodeficiency virus (HIV)-infected individual was shown to inhibit HIV type 1 (HIV-1) replication in both peripheral blood mononuclear cells and purified CD4+ lymphocytes. This suppression of HIV-1 replication led to decreased cytopathic effects of HIV-1 and prolonged survival of CD4+ cells in culture. Even low levels of HHV-6 added to peripheral blood mononuclear cells showed an inhibitory effect on HIV-1 replication. These results differ from those previously reported showing enhanced HIV-1 production following infection with another strain of HHV-6.

Cells, Cultured↗

PubMed1978

Comparison of pseudorabies virus inactivated by bromo-ethylene-imine, 60Co irradiation, and acridine dye in immune assay systems.

Pseudorabies virus infections among animals, especially swine, have become prevalent in the United States in the past few years. The disease in swine is now economically important. Test systems and antigens are being developed for use in control and disease suppression efforts. Pseudorabies virus was inactivated by three methods: chemically, with bromo-ethylene-imine; physically, with 60Co irradiation; and chemically and physically, with 3,9-diaminoacridine dye followed by exposure to white visible light. The antigenicities of the preparations were determined in the presence of specific antibody in immunodiffusion tests and through immunoelectrophoresis. The latter technique permitted quantitation of either antigen or antibody. In the electrophoretic patterns, the antigenic mass in bromo-ethylene-imine preparations was estimated to be 42 mg/ml, the same as in the untreated control material. After 60Co irradiation, 22 mg/ml was present, in comparison with 50 mg/ml in the untreated control antigen. In contrast, 67 mg/ml was present in the acridine dye-light-treated preparation, in comparison with 58 mg/ml in the untreated control material. A possible explanation for the acridine dye-light-treated preparation values is that photodynamic inactivation interferes with viral maturation during the replicative cycle within cells, with a resulting production of a greater amount of antigen, at least some of which is in the form of defective particles.

Acridines↗

PubMed2006

Expression of Nef downregulates CXCR4, the major coreceptor of human immunodeficiency virus, from the surfaces of target cells and thereby enhances resistance to superinfection.

Lentiviral Nef proteins are key factors for pathogenesis and are known to downregulate functionally important molecules, including CD4 and major histocompatibility complex class I (MHC-I), from the surfaces of infected cells. Recently, we demonstrated that Nef reduces cell surface levels of the human immunodeficiency virus type 1 (HIV-1) entry coreceptor CCR5 (N. Michel, I. Allespach, S. Venzke, O. T. Fackler, and O. T. Keppler, Curr. Biol. 15:714-723, 2005). Here, we report that Nef downregulates the second major HIV-1 coreceptor, CXCR4, from the surfaces of HIV-infected primary CD4 T lymphocytes with efficiencies comparable to those of the natural CXCR4 ligand, stromal cell-derived factor-1 alpha. Analysis of a panel of mutants of HIV-1(SF2) Nef revealed that the viral protein utilized the same signature motifs for downmodulation of CXCR4 and MHC-I, including the proline-rich motif P(73)P(76)P(79)P(82) and the acidic cluster motif E(66)E(67)E(68)E(69.) Expression of wild-type Nef, but not of specific Nef mutants, resulted in a perinuclear accumulation of the coreceptor. Remarkably, the carboxy terminus of CXCR4, which harbors the classical motifs critical for basal and ligand-induced receptor endocytosis, was dispensable for the Nef-mediated reduction of surface exposure. Functionally, the ability of Nef to simultaneously downmodulate CXCR4 and CD4 correlated with maximum-level protection of Nef-expressing target cells from fusion with cells exposing X4 HIV-1 envelopes. Furthermore, the Nef-mediated downregulation of CXCR4 alone on target T lymphocytes was sufficient to diminish cells' susceptibility to X4 HIV-1 virions at the entry step. The downregulation of chemokine coreceptors is a conserved activity of Nef to modulate infected cells, an important functional consequence of which is an enhanced resistance to HIV superinfection.

Amino Acid Motifs↗