Search Results - (Author, Cooperation:P. Staeheli)

2016-04-23

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

Adaptor Proteins, Signal Transducing/genetics/metabolism ; Adult ; Aged ; Aged, 80 and over ; Animals ; Bacterial Infections/etiology/*immunology ; Caspase 1/metabolism ; Caspases/metabolism ; Female ; Humans ; Immunity, Innate/genetics/*immunology ; Influenza A virus/*immunology ; Influenza, Human/complications/*immunology ; Interferon-beta/immunology ; Male ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Monocytes/immunology ; Myxovirus Resistance Proteins/genetics/*physiology ; Neutrophils/immunology ; Orthomyxoviridae Infections/*immunology ; Respiratory Tract Infections/*immunology/microbiology ; Toll-Like Receptor 7/genetics/metabolism ; Viral Load ; Young Adult

0962-8924

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Medicine

Electronic Resource

0167-7799

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Process Engineering, Biotechnology, Nutrition Technology

Electronic Resource

1420-9071

Springer Online Journal Archives 1860-2000

Biology

Medicine

Electronic Resource

1432-0886

Springer Online Journal Archives 1860-2000

Biology

Medicine

Abstract. Type I interferons (IFNs) are a family of proteins that are predominantly expressed in response to viral infection. Two serologically distinct forms of type I IFN, designated ChIFN1 and ChIFN2, have recently been recognized in the chicken. ChIFN1 is encoded by a cluster of ten or more intronless genes, whereas ChIFN2, whose primary sequence is 57% identical, is encoded by a single intronless gene. By fluorescence in situ hybridization we now demonstrate that the genes for ChIFN1 and ChIFN2 are all located on the short arm of the chicken Z chromosome. This assignment was confirmed by results that showed that DNA from male (ZZ) chickens yielded approximately twofold stronger Southern blot signals with ChIFN1 and ChIFN2 hybridization probes than DNA from females (ZW). Attempts to determine differences in IFN production between male and female chickens failed owing to a high degree of variation in virus-induced IFN expression between individuals of both sexes. Sex linkage of IFN genes was also observed in domestic ducks: fluorescence in situ hybridization of duck metaphase chromosomes with a duck type I IFN probe was confined to the terminal region of the long arm of the Z chromosome. Thus, in contrast to mammals, which have their IFN genes on autosomes, birds have the type I IFN genes on the sex chromosome.

Electronic Resource

1432-8798

Springer Online Journal Archives 1860-2000

Medicine

Summary.  It has previously been reported that de novo infection of primary rabbit brain cells with Borna disease virus (BDV) can be blocked with interferon-α/β (IFN), whereas this cytokine has no inhibitory effect on BDV in persistently infected rat lung cells [v. Rheinbaben et al., J. Gen. Virol. (1985) 66: 2 777–2 780]. It remained unclear, however, whether these results indicated that IFN exclusively targets early steps of the BDV replication cycle or whether they simply reflected cell line differences. We now show that BDV replication was effectively inhibited by IFN in both acutely and persistently infected monkey Vero cells. By contrast, IFN had no clear protective effect on either de novo or persistent BDV infections of rat C6 glioblastoma cells. IFN protected C6 cells from the cytopathic effects of vesicular stomatitis virus, excluding the possibility that these cells are devoid of a functional IFN system. In primary rat fibroblasts and in a human oligodendroglial cell line, IFN induced an efficient antiviral state against BDV. These results indicate that BDV is highly susceptible to the antiviral effect of IFN in some cell lines, while others seem to lack undefined components of the IFN system which mediate protection against BDV.

Electronic Resource

1432-8798

Springer Online Journal Archives 1860-2000

Medicine

Summary Adult but not newborn mice bearing the alleleMx display a specific resistance toin vivo infection with orthomyxoviruses.In vitro, cells isolated from adultMx-animals exhibit a several hundred-fold higher sensitivity to the action of interferon (IFN) against influenza viruses than do cells fromMx-negative mice. We here tested whether or not cells from immatureMx-bearing animals would likewise express the virus-specific higher sensitivity to IFN. Cultured cells from 16-day gestation mouse embryos with and withoutMx were equally permissive for an influenza virus when single cycle virus growth was measured. However, influenza virus plaques were smaller inMx-cells. Treatment of cells with mouse interferon reduced viral protein synthesis, single cycle virus yields and the number of virus plaques more efficiently inMx-cells than in non-Mx-cells. The smaller size of influenza virus plaques inMx-cells not treated with IFN seems to be due to the action of endogenous IFN: inclusion of anti-interferon antibodies in the agar overlay during plaque formation resulted in plaques of approximately the size seen in control cells. When treated with the same dose of IFN, cells withMx developed protection against influenza virus more rapidly than cells withoutMx. However, after removal of IFN, the antiviral protection decayed more rapidly in cells withoutMx. No differences in sensitivity to IFN, viral plaque formation and kinetics of induction and decay of the antiviral state were observed between the two cell types when the rhabdovirus VSV was used as challenge. Thus, the alleleMx is expressed in cultured embryo cells much as in cells from adult animals, and susceptibility of newbornMx-animals to influenza virus infection cannot be due to inability of their cells to respond to IFN appropriately.

Electronic Resource

1432-8798

Springer Online Journal Archives 1860-2000

Medicine

Summary.  Successful inhibition of Borna disease virus (BDV) by amantadine in cultured cells and in an infected human individual has been reported [Bode et al. (1997) Lancet 349: 178–179]. We now found that infection of monkey Vero cells by laboratory strains of BDV was not influenced by amantadine under conditions that reduced the yields of influenza A virus by about 400 fold. Amantadine treatment of Vero cells persistently infected with BDV did not result in reduced viral RNA levels, and application of the drug to persistently infected BALB/c mice had no effect on the concentration of BDV in their brains. Thus, susceptibility to amantadine is not a characteristic of BDV, although it may be observed with certain primary virus isolates.

Electronic Resource