Inhibition of pseudorabies virus replication by a dominant-negative mutant of early protein 0 expressed in a tetracycline-regulated system

T. Tasaki, S. Taharaguchi, T. Kobayashi, S. Yoshino, Etsuro Ono

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Pseudorabies virus (PRV) early protein 0 (EP0) consisting of 410 amino acids is a transactivator of viral genes. A mutant consisting of amino acids 1-113 exhibits dominant-negative properties. In order to assess the antiviral potential of the EP0 mutant, Vero cells were transformed with the EP0 mutant gene expressed in a tetracycline-regulated system. The transformed cell lines showed marked resistance to PRV infection when expression of the EP0 mutant gene was induced. In the transformed cell line infected with PRV, synthesis of the immediate-early protein (IE180) and of EP0 was inhibited, whereas the levels of IE and EP0 messenger RNA (mRNA) were not decreased, as compared with those of the control cell line. The present results suggest that the EP0 mutant may not alter the efficiency of the viral gene transcription but rather translation efficiency of the viral mRNA.

Original languageEnglish
Pages (from-to)195-203
Number of pages9
JournalVeterinary Microbiology
Volume78
Issue number3
DOIs
Publication statusPublished - Feb 12 2001
Externally publishedYes

Fingerprint

Suid Herpesvirus 1
Suid herpesvirus 1
Mutant Proteins
Virus Replication
virus replication
Tetracycline
tetracycline
mutants
Transformed Cell Line
Viral Genes
proteins
Amino Acids
Messenger RNA
Proteins
Vero Cells
Trans-Activators
cell lines
Viral RNA
Virus Diseases
messenger RNA

All Science Journal Classification (ASJC) codes

  • Microbiology
  • veterinary(all)

Cite this

Inhibition of pseudorabies virus replication by a dominant-negative mutant of early protein 0 expressed in a tetracycline-regulated system. / Tasaki, T.; Taharaguchi, S.; Kobayashi, T.; Yoshino, S.; Ono, Etsuro.

In: Veterinary Microbiology, Vol. 78, No. 3, 12.02.2001, p. 195-203.

Research output: Contribution to journalArticle

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