A polydnaviral genome of Microplitis bicoloratus bracovirus and molecular interactions between the host and virus involved in NF-κB signaling
Polydnaviruses (PDVs) play a critical role in altering host gene expression to induce immunosuppression. However, it remains largely unclear how PDV genes affect host genes. Here, the complete genome sequence of Microplitis bicoloratus bracovirus (MbBV), which is known to be an apoptosis inducer, wa...
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Veröffentlicht in: | Archives of virology 2016-11, Vol.161 (11), p.3095-3124 |
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Zusammenfassung: | Polydnaviruses (PDVs) play a critical role in altering host gene expression to induce immunosuppression. However, it remains largely unclear how PDV genes affect host genes. Here, the complete genome sequence of
Microplitis bicoloratus
bracovirus (MbBV), which is known to be an apoptosis inducer, was determined. The MbBV genome consisted of 17 putative double-stranded DNA circles and 179 fragments with a total size of 336,336 bp and contained 116 open reading frames (ORFs). Based on conserved domains, nine gene families were identified, of which the IκB-like viral ankyrin (
vank
) family included 28 members and was one of the largest families. Among the 116 ORFs, 13 MbBV genes were expressed in hemocytes undergoing MbBV-induced apoptosis and further analyzed. Three
vank
genes (
vank86
,
vank92
,
vank101
) were expressed in hemocytes collected from
Spodoptera litura
larvae parasitized by
M. bicoloratus
, in which host NF-κB/IκBs, including
relish
,
dorsal
, and
cactus
, were also persistently expressed. When Spli221 cells were infected with MbBV viral particles, mRNA levels of host and viral NF-κB/IκB genes were persistent and also varied in Spli221 cells undergoing virus-induced pre-apoptosis cell from 1 to 5 hours postinfection. Both were then expressed in a time-dependent expression in virus-induced apoptotic cells. These data show that viral IκB-like transcription does not inhibit host NF-κB/IκB expression, suggesting that transcription of these genes might be regulated by different mechanisms. |
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ISSN: | 0304-8608 1432-8798 |
DOI: | 10.1007/s00705-016-2988-3 |