Search Results - (Author, Cooperation:H. Arnheiter)

2011-01-21

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental/radiation effects ; Humans ; Interferon-gamma/*metabolism ; Macrophages/metabolism/radiation effects ; Male ; Melanocytes/*metabolism/radiation effects ; Melanoma/*physiopathology ; Mice ; *Ultraviolet Rays

1749-6632

Blackwell Publishing Journal Backfiles 1879-2005

Natural Sciences in General

Electronic Resource

1600-065X

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1476-4687

Nature Archives 1869 - 2009

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

[Auszug] Macrophages collected from the peritoneal cavity of A2G mice are resistant to influenza virus when first placed in culture6, but become susceptible with time8. We therefore cultivated peritoneal macrophages for 3-4 weeks, at which time they were highly susceptible to the three test viruses used, ...

Electronic Resource

1044-7431

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

1432-119X

Springer Online Journal Archives 1860-2000

Biology

Medicine

Summary The purpose of this paper is to describe the immunocytochemical localization of N and NS nucleocapsid proteins of vesicular stomatitis virus in the cells throughout the infectious cycle. N protein was detected in the cytoplasm at 2h after infection and formed small cytoplasmic clusters which progressively increased in size and number. At 5–6 h, it formed large cytoplasmic inclusions. NS protein was detected in the cytoplasm a little later than N protein and showed almost the same immunostaining pattern. However, diffuse background staining of NS protein was identified throughout the cytoplasm by double immunostaining methods. At electron microscopic level, N protein was mostly granular and occasionally organized in strands at 2–3 h. At 5–6 h, numerous immunostained reaction products were organized in strands. The reaction products of NS protein were almost the same as those of N protein with the exception that diffuse background staining was observed. Cos cells, transfected with SV40 vector containing N gene obtained by recombinant DNA technique, showed clusters of N protein, but virtually no strand at electron microscopic levels. The rapid-freezing and deep-etching replica method demonstrated that loosely coiled VSV genome coated with N protein was localized on cytoplasmic sides of cell membranes in the infected cells. These results showed that complete virus genome replication was needed for strand formation of N and NS proteins and suggested that they were bound to VSV genomes in the infected cells.

Electronic Resource

1432-8798

Springer Online Journal Archives 1860-2000

Medicine

Summary Primary monolayer cultures of adult mouse hepatocytes isolated by collagenase perfusion of the liverin situ were exposed to 2 hepatotropic viruses, an avian influenza A virus adapted to grow in mouse liverin vivo and a herpes simplex type I virus. Influenza virus infection led to lysis of individual hepatocytes and total monolayer destruction within 18 to 120 hours after infection according to the virus dose used. Virus replication was evidenced by assaying hepatocyte supernates for hemagglutinin and infectivity, by immunofluorescent staining and by electron microscopy. Herpes virus infection resulted in polykaryocyte formation followed by nuclear pycnosis and cell lysis. Virus replication was assayed by titration of supernate infectivity.

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