Search PubMed⌕ Search

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.

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

At least 505 records · Page 28Linked to original sources

Replication-defective viruses modulate immune responses.

By immunizing inbred mice with purified replication-competent, defective virus particles, or an admixture of the two, differential effects on the cellular immune system have been uncovered. Defective virus, exemplified by the vesicular stomatitis virus (VSV) defective interfering particle (DI 0.33), induced in BALB/c mice low levels of proliferating, IL-2 secreting, and cytolytic Ag-specific T lymphocytes. This was not caused by a dominant suppressor cell response, or by a failure to stimulate lymphokine-secreting cells, but appeared to reflect a reduced efficiency of priming as compared with standard virus. Mice primed with a mixture of wt and DI virus showed reduced proliferation compared with mice primed with wt virus. When histocompatible target cells were sensitized by pure DI particles, they were neither recognized nor lysed by CD8+ CTL. Cells co-infected with wt and DI particles were not as readily lysed by CD8+ CTL as cells infected by VSV alone. The extent of this reduction was dependent on the concentration of DI particles. This suggests that DI particles may have prevented the proper presentation of endogenously synthesized Ag for recognition by CD8+ CTL. Metabolic labeling studies indicated that the presence of DI particles suppressed the synthesis of viral proteins in dually infected cells. However, CD4+ T lymphocyte clones recognized and efficiently lysed histocompatible Ia+ cells infected with DI particles alone or co-infected with replication-competent and defective virus.

Animals↗

[Importance of replacing the support medium for viral interferonogenesis in tissue culture].

Interferonogenesis in the cells of chick embryos induced by strain Lee of influenza B virus was studied. The levels of interferon production with and without changing the medium before the cell inoculation with the interferonogens were compared. It was shown that preliminary changing of the medium resulted in a statistically reliable increase in production of interferon as compared to that without the medium changing. It was found that the increase in the synthesis of interferon under the conditions of the maintaining medium changing was accompanied by an increase in the levels of synthesis of the cellular protein and RNA determined by incorporation of C14-leucine and H3-uridine into the acid insoluble fraction of the cells. It is concluded that metabolic changes in the cells at the moment of interferonogenesis induction due to the maintaining medium changing should be considered in estimation of the experiments on the mechanism of the virus induced interferonogenesis in the tissue culture.

Animals↗

Coinfection with a rhabdovirus: vesicular stomatitis virus of Indiana and New-Jersey serotypes.

Coinfection of cells with vesicular stomatitis virus (VSV) of Indiana and New-Jersey serotypes were performed. Thermosensitive mutants (ts) of VSV Indiana and the wild type strain (+) of New-Jersey were used. Harvests and titrations were made at permissive(PT) and nonpermissive (NPT) temperatures. It was shown that the harvest was mainly composed of one parental-like infectious particles. The dominance of one serotype over the other was shown to be a function of the relative multiplicity of the two viruses; the presence of a thermosensitive lesion imparts a disadvantage to the corresponding serotype. Non parental-like particles were also detected. As expected, these particles were detected only in two conditions. 1) Harvest performed at NPT and titrations allowed at PT.- Most of the infectious particles (i.e. twin particles) resistant to anti-Nj serum developped a plaque (i.e. mixed-plaque)containing virions of both serotypes: Indiana (ts) and New-Jersey (+). After sonication or EDTA treatment of the harvest, prior to titrations, no more mixed-plaques were formed. Examination of the harvest by electron microscopy showed that 7-17 % of the particles formed aggregates; therefore, it is likely that the twin-particles are in fact aggregates. 2) Harvest performed at PT and titrations allowed at NPT.-It has been shown that 1 % of the wild type infectious particles was resistant to anti-Nj serum even though being of Nj genotype. It was inactivated by a mixture of anti-Nj and anti-In sera and therfore behave as pseudotypes. But since twin particles, when plated at Nt, would give rise to an homogenous progeny from New-Jersey (+), they could be confused with pseudotypes. Under those conditions there is no absolute evidence that phenotypic mixing really occurs between VSV of Indiana and New-Jersey serotypes.

Cell Line↗

Prospects for treatment of human retrovirus-associated diseases.

Overwhelming evidence has been obtained over the past 2 years that human T-cell leukemia virus type III (HTLV-III) is the primary cause of acquired immunodeficiency syndrome. The direct cytopathic effect of the virus on T4 helper cells demonstrated in vitro is probably responsible for the depletion of this critical population of cells in affected individuals which results in a series of devastating immunological abnormalities. It follows that any approaches effective in suppressing the virulent virus would be of benefit to the infected patient. The vast amount of knowledge about retroviruses in general, and the rapidly accumulating information about HTLV-III in particular, makes it likely that a targeted approach for development of antiviral agents will bear fruit. General strategies further making use of chemical and biological agents as well as genetic manipulations are discussed.

Acquired Immunodeficiency Syndrome↗

Early protection to Junín virus of guinea pig with an attenuated Junín virus strain.

Inoculation of guinea pigs with attenuated XJO Junín virus (JV) strain confers protection against challenge with pathogenic XJ-JV strain starting as early as 3 days post infection (p.i.). The protection increased continuously up to 100% by 30 days p.i. Neither stimulation of non-specific cell mediated mechanisms by previous BCG sensitization nor circulating interferon (IFN) seemed essential for such protection. The early detection of the virus in guinea pig organs considered the site of primary JV multiplication suggests that early resistance phenomenon was attributed mainly to direct viral interference.

Animals↗

Interferons and antiviral activity.

Interferons are endogenous antiviral agents which mediate the early defense of the organism against virus infection. The target of interferons is the cell rather than the virus itself. Through binding to specific receptors on the cell surface and subsequent activation of specific genes interferons induce an antiviral state which makes cells less permissive for virus replication. The antiviral state is composed of various antiviral mechanisms which seem to act independently and show some specificity for different viruses. Translational control affecting viral protein synthesis may be the most common mechanism through which virus is inhibited. There is evidence that antiviral and antigrowth activities of interferons share similar mechanisms.

2',5'-Oligoadenylate Synthetase↗

[Analysis of the possible mechanisms for the persistence of the vaccinal strain of the measles virus in a human cell culture].

The mechanisms (factors) of the measles virus vaccine L-16 strain persistence in HEp-2 cell culture were analysed. Among the known mechanisms, most likely is the reduction of the cell-destroying properties of the persisting virus due to mutations in nucleoprotein gene manifested by changes of the isoelectric point of NP protein and temperature sensitivity of its synthesis.

Cells, Cultured↗

Dengue virus vaccine studies in Puerto Rico: a review.

This review summarizes part of the work performed at the Virology Laboratories (Department of Microbiology, University of Puerto Rico School of Medicine) with live attenuated dengue virus vaccines obtained from the Walter Reed Army Institute of Research. Vaccines were tested for their respective immunogenicity and attenuation in rhesus monkeys (Maccaca mulatta) and in mosquitoes (Toxorynchites amboinensis), respectively. This experimental model revealed that out of 6 vaccines tested, only two (DEN-2/S-1 and DEN-4 strain 341750) should be further evaluated for safety and immunogenicity. Further studies are required to develop an effective vaccine to prevent dengue fever and its hemorrhagic manifestations.

Animals↗

[Experimental evaluation of the pathogenicity of Lassa virus variants].

Pathogenicity for guinea pigs and white mice of various Lassa virus variants: native, having had 1 passage in Vero cell culture and 4 passages in newborn white mouse brain; a virus having gone through 10 passages in Vero cells and 8 mouse brain passages (variant No. 10); a small-plaque clone derived from variant No. 10 by the method of plaque-to-plaque cloning (variant No. 11k), was studied. Both the native virus and variant No. 10 were found to be similarly pathogenic for susceptible laboratory animals, while the small-plaque variant of Lassa virus became non-fatal for guinea pigs and white mice. The decline of pathogenic properties in variant No. 11k was shown not to be associated with the presence of temperature-sensitive mutants or defective interfering particles.

Animals↗