RÉSUMÉ
Minute virus of mice (MVM), an autonomous parvovirus, has served as a model for understanding parvovirus infection including host cell response to infection. In this paper, we report the effect of MVM infection on host cell gene expression in mouse fibroblast cells (LA9 cells), analyzed by differential display. Somewhat surprisingly, our data reveal that few cellular protein-coding genes appear to be up- or downregulated and identify the murine B1 and B2 short interspersed element (SINE) transcripts as being increased upon MVM infection. Primer extension assays confirm the effect of MVM infection on SINE expression and demonstrate that both SINEs are upregulated in a roughly linear fashion throughout MVM infection. They also demonstrate that the SINE response was due to RNA polymerase III transcription and not contaminating DNA or RNA polymerase II transcription. Furthermore, expression of MVM NS1, the major nonstructural protein, by transient transfection also leads to an increase in both murine SINEs. We believe this is the first time that the B1 and B2 SINEs have been shown to be altered by viral infection and the first time parvovirus infection has been shown to increase SINE expression. The increase in SINE transcripts caused by MVM infection does not appear to be due to an increase in either of the basal transcription factors TFIIIC110 or 220, in contrast to that which has been shown for other viruses.
Sujet(s)
Fibroblastes/virologie , Virus minute de la souris/pathogénicité , Éléments SINE/physiologie , Transcription génétique , Régulation positive , Animaux , Lignée cellulaire , Analyse de profil d'expression de gènes , Régulation de l'expression des gènes , Souris , Virus minute de la souris/génétique , Éléments SINE/génétiqueRÉSUMÉ
Genome sequences of chicken (low pathogenic avian influenza [LPAI] and highly pathogenic avian influenza [HPAI]) and human isolates from a 2004 outbreak of H7N3 avian influenza in Canada showed a novel insertion in the HA0 cleavage site of the human and HPAI isolate. This insertion likely occurred by recombination between the hemagglutination and matrix genes in the LPAI virus.
Sujet(s)
Épidémies de maladies/médecine vétérinaire , Virus de la grippe A/génétique , Grippe chez les oiseaux/épidémiologie , Séquence d'acides aminés , Animaux , Colombie-Britannique/épidémiologie , Poulets , Humains , Virus de la grippe A/pathogénicité , Grippe chez les oiseaux/virologie , Modèles moléculaires , Données de séquences moléculaires , Mutagenèse par insertion , Conformation des protéines , Alignement de séquences , Protéines virales/composition chimiqueRÉSUMÉ
We sequenced the 29,751-base genome of the severe acute respiratory syndrome (SARS)-associated coronavirus known as the Tor2 isolate. The genome sequence reveals that this coronavirus is only moderately related to other known coronaviruses, including two human coronaviruses, HCoV-OC43 and HCoV-229E. Phylogenetic analysis of the predicted viral proteins indicates that the virus does not closely resemble any of the three previously known groups of coronaviruses. The genome sequence will aid in the diagnosis of SARS virus infection in humans and potential animal hosts (using polymerase chain reaction and immunological tests), in the development of antivirals (including neutralizing antibodies), and in the identification of putative epitopes for vaccine development.