Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Alpha/Beta interferon promotes transcription and inhibits replication of borna disease virus in persistently infected cells
Autore:
Staeheli, P; Sentandreu, M; Pagenstecher, A; Hausmann, J;
Indirizzi:
Univ Freiburg, Dept Virol, D-79008 Freiburg, Germany Univ Freiburg Freiburg Germany D-79008 Virol, D-79008 Freiburg, Germany Univ Freiburg, Dept Neuropathol, D-79008 Freiburg, Germany Univ Freiburg Freiburg Germany D-79008 pathol, D-79008 Freiburg, Germany
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 17, volume: 75, anno: 2001,
pagine: 8216 - 8223
SICI:
0022-538X(200109)75:17<8216:AIPTAI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
RNA-POLYMERASE ACTIVITY; INFLUENZA-VIRUS; NEURONAL PROPERTIES; GENE-EXPRESSION; MESSENGER-RNAS; PROTEIN MX; MICE; RESISTANCE; RATS; ASTROCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Staeheli, P Univ Freiburg, Dept Virol, Hermann Herder Str 11, D-79008 Freiburg, Germany Univ Freiburg Hermann Herder Str 11 Freiburg Germany D-79008
Citazione:
P. Staeheli et al., "Alpha/Beta interferon promotes transcription and inhibits replication of borna disease virus in persistently infected cells", J VIROLOGY, 75(17), 2001, pp. 8216-8223

Abstract

Borna disease virus (BDV) is a noncytolytic RNA virus that can replicate in the central nervous system (CNS) of mice. This study shows that BDV multiplication was efficiently blocked in transgenic mice that express mouse alpha-1 interferon (IFN-alpha1) in astrocytes. To investigate whether endogenous virus-induced IFN might similarly restrict BDV, we used IFNAR(0/0) mice,which lack a functional alpha/beta IFN (IFN-alpha/beta) receptor. As wouldbe expected if virus-induced IFN were important to control BDV infection, we found that cultured embryo cells of IFNAR(0/0) mice supported viral multiplication, whereas cells from wild-type mice did not. Unexpectedly, however, BDV spread through the CNSs of IFNAR(0/0) and wild-type mice with similar kinetics, suggesting that activation of endogenous IFN-alpha/beta genes in BDV-infected brains was too weak or occurred too late to be effective. Surprisingly, Northern blot analysis showed that the levels of the most abundant viral mRNAs in the brains of persistently infected IFNAR(0/0) mice wereabout 20-fold lower than those in wild-type mice. In contrast, genomic viral RNA was produced in about a 10-fold excess in the brains of IFNAR(0/0) mice. Human IFN-alpha2 similarly enhanced transcription and simultaneously repressed replication of the BDV genome in persistently infected Vero cells. Thus, in persistently infected neurons and cultured cells, IFN-alpha/beta appears to freeze the BDV polymerise in the transcriptional mode, resultingin enhanced viral mRNA synthesis and suppressing viral genome replication.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/01/20 alle ore 07:07:03