shown that VSR activity of p35 is not linked to the antiapoptotic activity of this gene,
as p35 mutant gene with no antiapoptotic activity showed VSR function in Sf9 cells
(Mehrabadi et al. 2015). Following this study, it was shown that the transcript levels
of core siRNA pathway in Sf9 cells including Dicer-2 (Dcr1), Argonaute-2 (Ago2)
increased in response to AcMNPV infection. Silencing of these genes increased viral
genomic DNA replication which indicated their role in the host antiviral defense.
Moreover, silencing of Dcr2 in Sf9 cells resulted in enhanced expression levels of
the selected virus hotspot genes, while the transcript levels of virus cold spots
remained unchanged. Replication of p35-null AcMNPV was significantly increased
in Sf9 cells with reduced transcript levels of Dcr2 and Ago2. Also, overexpression of
p35 as a suppressor of RNAi and anti-apoptosis gene in Sf9 cells increased virus
replication (Karamipour et al. 2018). These results indicate the antiviral role of the
siRNA pathway in Sf9 cells and show that the AcMNPV p35 suppresses the siRNA
pathway.
MicroRNAs (miRNAs) as small non-coding RNAs play important roles in
various biological processes including host-virus interactions by regulating host/
virus gene expression. Mehrabadi et al. (2013b) identified about 90 conserved and
new miRNAs from Sf9 cells using deep sequencing. The majority of the identified
miRNAs were differentially expressed in response to AcMNPV infection. Many of
the miRNAs were downregulated; however, some of them were upregulated in
response to infection (e.g. miR-184, miR-998 and miR-10), highlighting their
potential roles in host–virus interaction. Target analysis of miR-184 – one of the
most expressed miRNAs that is differentially expressed following AcMNPV
infections – showed potential targets on the coding regions of some of host genes.
Using miR-184 agonist and antagonist, it was shown that this miRNA targets
dimethyl adenosine transferase, glycosyl hydrolase, transmembrane protein 14C
and hydroxysteroid dehydrogenase of SF9 cells (Mehrabadi et al. 2013b). This
study revealed the potential roles of miRNAs in host–virus interaction. In a follow
up study, the role of core components of the miRNA pathway (including Dicer-1
(Dcr1), Argonaute-1 (Ago1), Exportin-5 (Exp5), and Ran) in Sf9-AcMNPV interaction was investigated. Gene expression analyses showed that the expression levels
of Dcr1, Ago1, and Exp5 increased following AcMNPV infection; however, Ran
expression declined in response to virus infection. The expression levels of cellular
miRNAs (i.e. miR-184 and let-7), were also diminished after AcMNPV infection
revealed the differential expression of miRNAs. To investigate the role of core
miRNA genes in Sf9-AcMNPV interactions, gene silencing was used and the results
showed that RNAi of Dcr1, Ago1 and Ran enhanced viral DNA replication and
reduced the abundance of miR-184 and let-7. These results provide evidence that the
miRNA pathway is involved in the antiviral immunity of Sf9 cells (Karamipour et al.
2019a). It was shown that Toll and Imd pathways played a role in Sf9 cells after
AcMNPV infection (Karamipour et al. 2019b).
13 Insect Pathogenic Viruses, Microsporidians and Endosymbionts
517
as p35 mutant gene with no antiapoptotic activity showed VSR function in Sf9 cells
(Mehrabadi et al. 2015). Following this study, it was shown that the transcript levels
of core siRNA pathway in Sf9 cells including Dicer-2 (Dcr1), Argonaute-2 (Ago2)
increased in response to AcMNPV infection. Silencing of these genes increased viral
genomic DNA replication which indicated their role in the host antiviral defense.
Moreover, silencing of Dcr2 in Sf9 cells resulted in enhanced expression levels of
the selected virus hotspot genes, while the transcript levels of virus cold spots
remained unchanged. Replication of p35-null AcMNPV was significantly increased
in Sf9 cells with reduced transcript levels of Dcr2 and Ago2. Also, overexpression of
p35 as a suppressor of RNAi and anti-apoptosis gene in Sf9 cells increased virus
replication (Karamipour et al. 2018). These results indicate the antiviral role of the
siRNA pathway in Sf9 cells and show that the AcMNPV p35 suppresses the siRNA
pathway.
MicroRNAs (miRNAs) as small non-coding RNAs play important roles in
various biological processes including host-virus interactions by regulating host/
virus gene expression. Mehrabadi et al. (2013b) identified about 90 conserved and
new miRNAs from Sf9 cells using deep sequencing. The majority of the identified
miRNAs were differentially expressed in response to AcMNPV infection. Many of
the miRNAs were downregulated; however, some of them were upregulated in
response to infection (e.g. miR-184, miR-998 and miR-10), highlighting their
potential roles in host–virus interaction. Target analysis of miR-184 – one of the
most expressed miRNAs that is differentially expressed following AcMNPV
infections – showed potential targets on the coding regions of some of host genes.
Using miR-184 agonist and antagonist, it was shown that this miRNA targets
dimethyl adenosine transferase, glycosyl hydrolase, transmembrane protein 14C
and hydroxysteroid dehydrogenase of SF9 cells (Mehrabadi et al. 2013b). This
study revealed the potential roles of miRNAs in host–virus interaction. In a follow
up study, the role of core components of the miRNA pathway (including Dicer-1
(Dcr1), Argonaute-1 (Ago1), Exportin-5 (Exp5), and Ran) in Sf9-AcMNPV interaction was investigated. Gene expression analyses showed that the expression levels
of Dcr1, Ago1, and Exp5 increased following AcMNPV infection; however, Ran
expression declined in response to virus infection. The expression levels of cellular
miRNAs (i.e. miR-184 and let-7), were also diminished after AcMNPV infection
revealed the differential expression of miRNAs. To investigate the role of core
miRNA genes in Sf9-AcMNPV interactions, gene silencing was used and the results
showed that RNAi of Dcr1, Ago1 and Ran enhanced viral DNA replication and
reduced the abundance of miR-184 and let-7. These results provide evidence that the
miRNA pathway is involved in the antiviral immunity of Sf9 cells (Karamipour et al.
2019a). It was shown that Toll and Imd pathways played a role in Sf9 cells after
AcMNPV infection (Karamipour et al. 2019b).
13 Insect Pathogenic Viruses, Microsporidians and Endosymbionts
517