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.
journal_name
Virologyjournal_title
Virologyauthors
Hong JR,Gong HY,Wu JLdoi
10.1006/viro.2001.1336subject
Has Abstractpub_date
2002-04-10 00:00:00pages
217-29issue
2eissn
0042-6822issn
1096-0341pii
S0042682201913364journal_volume
295pub_type
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