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At least 613 records · Page 34Linked to original sources
PubMedDate not supplied

[Multiple virus vaccines and the interference phenomena].

It is well known that interference between two viruses simultaneously infecting the same host may bring about the exclusion of one. When administering attenuated viruses for immunization purposes this fact should be theoretically taken into account. The present tendency of associating attenuated virus into multiple vaccines (trivalent polio, mumps-rubella-measles) is supported by their proved effectiveness. The reasons of the non-operativity of the interference mechanism in such conditions are discussed.

Humans↗
PubMed2006

Prospects of RNA interference therapy in respiratory viral diseases: update 2006.

Respiratory viruses, such as influenza, parainfluenza and respiratory syncytial virus (RSV), claim millions of lives annually. At present, there is no completely effective vaccine or drug against these highly mutable RNA viruses. Passive antibody therapies for RSV, despite their limited application and staggering cost, enjoy a virtual monopoly in a multibillion-dollar global market. Recently, however, pioneering discoveries have launched RNA interference as a novel, nucleic acid-based therapy against viral pathogens. Specifically, small interfering RNAs (siRNAs) offered protection against respiratory syncytial virus, parainfluenza and influenza. siRNA against RSV has entered Phase I clinical trials in humans, and preliminary reports are promising. If appropriately formulated for improved specificity, delivery and pharmacokinetics, siRNAs may indeed become effective antivirals in the clinics of the future. This paper provides an overview of the prospects and hurdles facing the antiviral siRNA drugs, with special emphasis on RSV.

Animals↗
PubMed2005

The structure of the flock house virus B2 protein, a viral suppressor of RNA interference, shows a novel mode of double-stranded RNA recognition.

We report the structure of the flock house virus B2 protein, a potent suppressor of RNA interference (RNAi) in animals and plants. The B2 protein is a homodimer in solution and contains three alpha-helices per monomer. Chemical shift perturbation shows that an antiparallel arrangement of helices (alpha2/alpha2') forms an elongated binding interface with double-stranded RNA (dsRNA). This implies a novel mode of dsRNA recognition and provides insights into the mechanism of RNAi suppression by B2.

Amino Acid Sequence↗
PubMed1983

Temperature-sensitive mutants of fowl plague virus (influenza A) generated by undiluted passages at 33 degrees C.

Temperature-sensitive (ts) mutants obtained by undiluted passages of fowl plague virus at 33 degrees C have their defects located mainly in RNA segments 3, 4 and 8 as determined by rescue to wild-type with standard ts mutants. This result is different from that obtained after treatment of virus with mutagens, where the frequency of mutations follows roughly the target size of the RNA segments. Many isolates generated after undiluted passages at 33 degrees C, which seem to have mutations in RNA segments 3 and 4, can be rescued to wild-type. This occurs, however, with certain defined standard ts mutants having a defect in RNA segment 4, but not by other segment 4 mutants. One such mutant, ts 1/93 (ts defect in segment 3), interferes with the multiplication of ts 227 (ts defect in segment 4) at the permissive temperature, presumably at the level of vRNA synthesis, preventing reassortment to wild-type. Similarly, ts 263 (ts defect in segment 3) interferes with the multiplication of ts 1/1 (ts defect in segment 4). For other such interfering mutants, the mechanism preventing reassortment to wild-type is different from that of ts 1/93 or ts 1/1, but is not yet understood. Thus, the number of mutations as determined by rescue with standard ts mutants in isolates obtained by undiluted passages is overestimated due to intrinsic interference.

Animals↗
PubMedDate not supplied

Competition between nonplaquing and plaquing strains of Newcastle disease virus as affected by temperature.

If lentogenic (nonplaquing) strains of Newcastle disease virus were inoculated into a monolayer of chicken embryo fibroblasts before velogenic (plaquing) strains, the plaquing of the latter were inhibited partially or completely. An interval of 22 hours between the two inoculations gave greater inhibition than did 1 hour. In general, lentogenic strains grew better at 37 C (inhibited plaquing more effectively) than at 42 C. Enzootic velogenic strains that produce a neurotropic form of the disease in chickens were inhibited more than were exotic velogenic strains that produce a viscerotropic form. The lentogenic strains differed markedly in ability to interfere with velogenic strains.

Animals↗
PubMed1998

Alpha-glucosidase inhibitors as potential broad based anti-viral agents.

N-Linked oligosaccharides play many roles in the fate and functions of glycoproteins. One function is to assist in the folding of proteins by mediating interactions of the lectin-like chaperone proteins calnexin and calreticulin with nascent glycoproteins. These interactions can be prevented by inhibitors of the alpha-glucosidases and this causes some proteins to be misfolded and retained within the endoplasmic reticulum. In human immunodeficiency virus (HIV) and hepatitis B virus (HBV) the misfolding of key viral envelope glycoproteins interferes with the viral life cycle. It has been demonstrated in an animal model of chronic HBV that glucosidase inhibitors can alter glycosylation and have anti-viral activity. As the mechanism of action of alpha-glucosidase inhibitors is the induction of misfolded or otherwise defective viral glycoproteins, such inhibitors may be useful therapeutics for many viruses, especially those which bud from the endoplasmic reticulum (where protein folding takes place). For example bovine viral diarrhea virus, a pestivirus akin to hepatitis C virus, is also extremely sensitive to glucosidase inhibition.

Animals↗
PubMed2003

Transient expression of homologous hairpin RNA causes interference with plant virus infection and is overcome by a virus encoded suppressor of gene silencing.

Specific post-transcriptional gene silencing (PTGS) of target genes can be induced in a variety of organisms by providing homologous double-stranded RNA (dsRNA) molecules. In plants, PTGS is part of a defense mechanism against virus infection. We have previously shown and patented that direct delivery to nontransgenic plants of dsRNA derived from viral sequences specifically interfere with virus infection. Here, we show that transient expression of constructs encoding hairpin RNA homologous to a rapidly replicating plant tobamovirus also interferes with virus multiplication in a sequence-dependent manner. A three-day lag period between delivery of hairpin RNA and virus into the same tissues completely block virus infectivity. Several hallmarks characteristic of PTGS were associated with viral interference mediated by hairpin RNA: high level of sequence identity between the hairpin RNA and the target RNA, presence of siRNAs in extracts derived from leaves infiltrated with hairpin RNA, and helper component-proteinase (HC-Pro) of potyviruses, a suppressor of PTGS, overcame interference. No evidence for a mobile silencing suppression signal induced by transient expression of HC-Pro was observed. The approach described here has the potential to be used as a versatile tool for studying the onset of PTGS in cases involving virus infection, in opposition to dsRNA-transgenic plants, which allow primarily for the study of PTGS maintenance.

Gene Silencing↗