13.1.6 Histopathology
Marzban et al. (2013), surveyed midgut histopathology of the cotton bollworm
infected with H. armigera cytoplasmic polyhedrosis virus. The symptoms of healthy
and infected larvae were compared. The bodies of infected larvae were swollen and
small milky-white polyhedral inclusion bodies were observed in the columnar cells
after 1 or 2 days. Microvilli of infected columnar cells were affected and degenerated
immediately prior to rupture of the cells. Some infected columnar cells ruptured to
release polyhedral inclusion bodies (PIB) into the gut lumen 3 days after infection.
Also, PIB were found in goblet cells, 5 or 6 days after infection. The results showed
that cytopathic effects caused in the cotton bollworm larvae midgut by HaCPV were
similar to those reported for CPV lepidopteran and dipteran infection.
13.1.7 Virus-Insect Interactions
Among the Baculoviruses, the most studied species is Autographa californica
multiple nucleopolyhedrovirus (AcMNPV). Research on baculovirus-insect interactions has recently begun in Iran. While attempting to find differentially expressed
genes of Spodoptera frugiperda (Sf9) cells in response to AcMNPV, Mehrabadi
et al. (2015) discovered a Dim1-like gene that was upregulated from 4 h postinfection (hpi) up until 24 hpi. The expression level diminished dramatically at
36 hpi up to 120 hpi with no expression detected after 144 hpi. RNAi of SfDim1
resulted in decreased viral DNA levels in comparison to mock-infected cells, which
supports the idea that this gene might be involved in virus replication and infection
(Mehrabadi et al. 2013a). RNA interference (RNAi) is a highly conserved sequencespecific gene silencing mechanism in diverse eukaryotes, involved in the regulation
of many biological processes, including virus-host interactions and antiviral immunity in insects (Mehrabadi et al. 2015). The RNAi-based antiviral response can be
mounted through noncoding small RNAs including virus-derived short interfering
RNAs (vsiRNAs) and microRNA (miRNA). Using deep sequencing of small RNAs,
it was shown that AcMNPV infection induces an RNAi response in Sf9 cells and
produces a huge number of vsiRNAs. The vsiRNAs were unevenly mapped onto the
AcMNPV genome showing that some regions of AcMNPV genome are targeted
more than others (i.e hot spots), while there were some regions in the genome with
low or no vsiRNA mapping (i.e cold spots). Despite the presence of this potent
antiviral machinery in Sf9 cells, AcMNPV can infect these cells and replicate within
them (Mehrabadi et al. 2015). Therefore, there must be a counter defense strategy in
AcMNPV to suppress or avoid this potent cellular antiviral immunity. Furthermore,
it was found that AcMNPV encodes potent viral suppressors of RNAi (VSRs) to
counter cellular antiviral RNAi. The viral p35 gene, which is well known as an
inhibitor of apoptosis, was found to be responsible for suppression of RNAi response
in Sf9 cells using a p35-null AcMNPV and ectopic expression of p35. It was also
516
M. Mehrabadi et al.
Marzban et al. (2013), surveyed midgut histopathology of the cotton bollworm
infected with H. armigera cytoplasmic polyhedrosis virus. The symptoms of healthy
and infected larvae were compared. The bodies of infected larvae were swollen and
small milky-white polyhedral inclusion bodies were observed in the columnar cells
after 1 or 2 days. Microvilli of infected columnar cells were affected and degenerated
immediately prior to rupture of the cells. Some infected columnar cells ruptured to
release polyhedral inclusion bodies (PIB) into the gut lumen 3 days after infection.
Also, PIB were found in goblet cells, 5 or 6 days after infection. The results showed
that cytopathic effects caused in the cotton bollworm larvae midgut by HaCPV were
similar to those reported for CPV lepidopteran and dipteran infection.
13.1.7 Virus-Insect Interactions
Among the Baculoviruses, the most studied species is Autographa californica
multiple nucleopolyhedrovirus (AcMNPV). Research on baculovirus-insect interactions has recently begun in Iran. While attempting to find differentially expressed
genes of Spodoptera frugiperda (Sf9) cells in response to AcMNPV, Mehrabadi
et al. (2015) discovered a Dim1-like gene that was upregulated from 4 h postinfection (hpi) up until 24 hpi. The expression level diminished dramatically at
36 hpi up to 120 hpi with no expression detected after 144 hpi. RNAi of SfDim1
resulted in decreased viral DNA levels in comparison to mock-infected cells, which
supports the idea that this gene might be involved in virus replication and infection
(Mehrabadi et al. 2013a). RNA interference (RNAi) is a highly conserved sequencespecific gene silencing mechanism in diverse eukaryotes, involved in the regulation
of many biological processes, including virus-host interactions and antiviral immunity in insects (Mehrabadi et al. 2015). The RNAi-based antiviral response can be
mounted through noncoding small RNAs including virus-derived short interfering
RNAs (vsiRNAs) and microRNA (miRNA). Using deep sequencing of small RNAs,
it was shown that AcMNPV infection induces an RNAi response in Sf9 cells and
produces a huge number of vsiRNAs. The vsiRNAs were unevenly mapped onto the
AcMNPV genome showing that some regions of AcMNPV genome are targeted
more than others (i.e hot spots), while there were some regions in the genome with
low or no vsiRNA mapping (i.e cold spots). Despite the presence of this potent
antiviral machinery in Sf9 cells, AcMNPV can infect these cells and replicate within
them (Mehrabadi et al. 2015). Therefore, there must be a counter defense strategy in
AcMNPV to suppress or avoid this potent cellular antiviral immunity. Furthermore,
it was found that AcMNPV encodes potent viral suppressors of RNAi (VSRs) to
counter cellular antiviral RNAi. The viral p35 gene, which is well known as an
inhibitor of apoptosis, was found to be responsible for suppression of RNAi response
in Sf9 cells using a p35-null AcMNPV and ectopic expression of p35. It was also
516
M. Mehrabadi et al.