Proliferation and Apoptosis in Infection with Infectious Bursal Disease Virus: A Flow Cytometric Study

Ojeda, F. Patricio; Skardova, I.; Mi, Guarda; Ulloa, J; Folch, Hugo

doi:10.2307/1592183

Cited by 25 publications

(10 citation statements)

References 10 publications

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“…Previous studies have shown that IBDV induces apoptosis both in vitro and in vivo (26,34,42,45). By transiently expressing the NS protein, VP5, in chicken embryo fibroblasts (CEF) and BSC-1 and Cos-1 cells, Lombardo and coworkers demonstrated that this protein accumulates within the host plasma membrane and induces cell lysis (30).…”

Section: Infectious Bursal Disease Virus (Ibdv) Is the Causative Agenmentioning

confidence: 99%

Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

Liu

Vakharia

2006

J Virol

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Infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, carries a small nonstructural protein (NS). This protein has been implicated to play a role in the induction of apoptosis. In this study, we investigate the kinetics of viral replication during a single round of viral replication and examine the mechanism of IBDV-induced apoptosis. Our results show that it is caspase dependent and activates caspases 3 and 9. Nuclear factor kappa B (NF-B) is also activated and is required for IBDV-induced apoptosis. The NF-B inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-B activation. To study the function of the NS protein in this context, we generated the recombinant rGLS virus and an NS knockout mutant, rGLSNS⌬ virus, using reverse genetics. Comparisons of the replication kinetics and markers for virally induced apoptosis indicated that the NS knockout mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-B activation. These results suggest that the NS protein has an antiapoptotic function at the early stage of virus infection.

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Section: Infectious Bursal Disease Virus (Ibdv) Is the Causative Agenmentioning

confidence: 99%

Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

Liu

Vakharia

2006

J Virol

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“…The VP5 protein has acquired growing relevance in the last years due to its potential role in the onset of apoptosis and necrosis of lymphoid organs [48][49][50][51][52][53][54]. Most of the advances for the comprehension of the VP5 role in the IBDV biology have been achieved studying the amino acid composition of this protein, its localization during the viral infection, and observing its effects on the viral replication cycle using gene expression systems [29,[51][52][53]55].…”

Section: Discussionmentioning

confidence: 99%

Sequence variability and evolution of the terminal overlapping VP5 gene of the infectious bursal disease virus

et al. 2010

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The infectious bursal disease virus (IBDV; Birnaviridae family) constitutes one of the main threats to the poultry industry worldwide. Most of the progress in the molecular epidemiology of this virus has been achieved through the study of the coding region of the capsid protein VP2. Little research has been done regarding the molecular evolution and the epidemiological implications of genetic variability of other IBDV genome regions. In this article, the gene that codes the non-structural protein VP5 was analyzed. Although this protein is not essential for the virus replication, recent evidence indicates that it could be related to the virulent phenotype and the adaptive capacity of the virus. The VP5 gene is also of evolutionary interest because it has an open reading frame that terminally overlaps with the pVP2-VP4-VP3 polyprotein coding region. In the first part of this study, the full VP5 gene of a South American strain was characterized. The results revealed that the VP5 gene of Uruguayan hypervirulent IBDV strains (vvIBDV) lacks the alternative AUG start codon characteristic of the vvIBDV strains that have been described to date. Instead, as occurs in classic and variant strains, this VP5 gene has an AUG start site located four codons downstream and, consequently, it codes for a 145 amino acid long protein rather than the putative 149 amino acid long protein of other vvIBDV. In spite of this, these viruses conserved the VP5 and VP2 amino acid signature of the hypervirulent strains and clustered with reference vvIBDV sequences. This finding may represent evidence that the VP5 gene could be evolving by changing the translation initiation site. In the second part of this study, an evolutionary analysis including the sequences reported in this study together with most of VP5 sequences available in the GenBank, showed the existence of a complex system of selective pressures controlling the evolution of the VP5 gene. Using the dN/dS index, we found a strong purifying selection exerted on the 5' terminal overlapping region of VP2 that would be constraining the evolution of VP5. These results reinforce the hypothesis that the VP5 gene was originated late in the IBDV evolution by a mechanism of genetic overprinting. The results described in this study provided new information about the dynamics of the IBDV genome and revealed some of the mechanisms at play in the evolution of this virus. Since VP5 seems to be related to viral pathogenicity, this evolutionary information might be useful to highlight the impact of the genetic variation of this protein on the epidemiology of IBDV.

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“…In addition, we obtained a monoclonal cell line (7B4) with genomic integration of one copy of the partial sequence of IBDV A-segment and expressing viral protein VP2 only. Previous studies have shown that IBDV induces apoptosis both in vitro and in vivo (Vasconcelos and Lam, 1994;Lam, 1997;Ojeda et al, 1997;Tanimura and Sharma, 1998;Jungmann et al, 2001). An early study showed that transient expression of VP2 could induce apoptosis in BSC40 cells but not in CEF cells (Fernandez-Arias et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Cloned Vero cell lines transfected with full‐length A‐segment or ORF1 cDNA sequence of IBDV

Chen

Zhou

et al. 2007

Cell Biology International

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Recombinant plasmids containing the A-segment or VP2/4/3 gene of infectious bursal disease virus (IBDV) were transfected into Vero cells. Monoclonal Vero cell lines were generated under G418 selection. Genomic (PCR/Southern blot) and transcriptional (RT-PCR/Northern blot) analyses showed that one copy of A-segment or VP2/4/3 or a partial gene of them was randomly and stably inserted into genomic DNA of Vero cells, and was able to transcribe corresponding mRNA. IFA/IPMA and Western blot analyses further confirmed that two of the monoclonal Vero cells with insertion of the A-segment of IBDV into genomic DNA could stably express VP2, VP3 and VP5 proteins, one cell line only expressed VP2 protein, and three monoclonal Vero cell lines with genomic insertion of the VP2/4/3 gene of IBDV could express VP2, VP3 and VP4 proteins. Under G418 selection, integrated foreign genes can be inherited along with cellular genomic DNA during cell replications. Moreover, DNA fragmentation and caspase-3 activity assays illustrated that cell apoptosis did not develop in monoclonal Vero cell lines expressing VP2 and VP5 proteins. The monoclonal IBDV gene-inserted Vero cell lines developed in this study will facilitate better understanding of IBDV and other members of the Birnaviridae in an expression system that would enable investigation of virus-host cell interactions on the cellular and molecular level.

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Proliferation and Apoptosis in Infection with Infectious Bursal Disease Virus: A Flow Cytometric Study

Cited by 25 publications

References 10 publications

Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

Nonstructural Protein of Infectious Bursal Disease Virus Inhibits Apoptosis at the Early Stage of Virus Infection

Sequence variability and evolution of the terminal overlapping VP5 gene of the infectious bursal disease virus

Cloned Vero cell lines transfected with full‐length A‐segment or ORF1 cDNA sequence of IBDV

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