IPNV VP5, a novel anti-apoptosis gene of the Bcl-2 family, regulates Mcl-1 and viral protein expression

Jiann-Ruey Hong, Hong Yi Gong, Jen Leih Wu

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

VP5, a 5′-terminal, small open reading frame in segment A of the aquatic birnavirus (infectious pancreatic necrosis virus, IPNV) genome, encodes a 17-kDa nonstructural protein. We previously reported apoptosis induced by IPNV in a fish cell line. In the present study, we cloned and identified VP5 and tested its function. Comparisons of the amino acid sequence of VP5 with well-known Bcl-2 family member proteins showed that the VP5 protein contains Bcl-2 homology (BH) domains BH1, BH2, BH3, and BH4 but without the transmembrane region. VP5-stable clones enhanced viability, prevented membrane blebbing, delayed DNA internucleosomal cleavage, and decreased virus titer during IPNV infection but, when deleted, BH domains 1 and 2 could lose the preventable ability. In addition, VP5 was demonstrated to be able to enhance or assist in maintaining the functional half-life of survival factor Mcl-1 and regulate specific viral protein expression during the early replication cycle. Finally, we found that VP5 was capable of enhancing cell viability when cells were exposed to UV irradiation. In summary, these results suggest that the aquatic birnavirus may utilize a notable strategy via VP5 to regulate the host apoptosis-off system for enhancing progeny production.

Original languageEnglish
Pages (from-to)217-229
Number of pages13
JournalVirology
Volume295
Issue number2
DOIs
Publication statusPublished - 2002 Jan 1

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Infectious pancreatic necrosis virus
bcl-2 Genes
Viral Proteins
Apoptosis
DNA Cleavage
Proteins
Aptitude
Virus Diseases
Blister
Viral Load
Open Reading Frames
Half-Life
Amino Acid Sequence
Cell Survival
Fishes
Clone Cells
Genome
Cell Line
Membranes

All Science Journal Classification (ASJC) codes

  • Virology

Cite this

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abstract = "VP5, a 5′-terminal, small open reading frame in segment A of the aquatic birnavirus (infectious pancreatic necrosis virus, IPNV) genome, encodes a 17-kDa nonstructural protein. We previously reported apoptosis induced by IPNV in a fish cell line. In the present study, we cloned and identified VP5 and tested its function. Comparisons of the amino acid sequence of VP5 with well-known Bcl-2 family member proteins showed that the VP5 protein contains Bcl-2 homology (BH) domains BH1, BH2, BH3, and BH4 but without the transmembrane region. VP5-stable clones enhanced viability, prevented membrane blebbing, delayed DNA internucleosomal cleavage, and decreased virus titer during IPNV infection but, when deleted, BH domains 1 and 2 could lose the preventable ability. In addition, VP5 was demonstrated to be able to enhance or assist in maintaining the functional half-life of survival factor Mcl-1 and regulate specific viral protein expression during the early replication cycle. Finally, we found that VP5 was capable of enhancing cell viability when cells were exposed to UV irradiation. In summary, these results suggest that the aquatic birnavirus may utilize a notable strategy via VP5 to regulate the host apoptosis-off system for enhancing progeny production.",
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IPNV VP5, a novel anti-apoptosis gene of the Bcl-2 family, regulates Mcl-1 and viral protein expression. / Hong, Jiann-Ruey; Gong, Hong Yi; Wu, Jen Leih.

In: Virology, Vol. 295, No. 2, 01.01.2002, p. 217-229.

Research output: Contribution to journalArticle

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