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Updated: Jun 27, 2025
Evaluation of Caspase Activation to Assess Innate Immune Cell Death
Published on: January 20, 2023
Ben-JNK signaling is required for host mortality during Periplaneta fuliginosa densovirus infection
Dan-Yan Huang1, Jia-Si Qin1, Ren-Ke Dong1
1Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied Technology, Guangzhou Key Laboratory of Insect Development Regulation and Application Research, Institute of Insect Science and Technology, School of Life Sciences, South China Normal University, Guangzhou, China.
Background:
Cockroaches are widely acknowledged as significant vectors of pathogenic microorganisms. The Periplaneta fuliginosa densovirus (PfDNV) infects the smoky-brown cockroach P. fuliginosa and causes host mortality, which identifies the PfDNV as a species-specific and environmentally friendly biopesticide. However, although the biochemical characterization of PfDNV has been extensively studied, the immune response against PfDNV remains largely unclear.
Results:
Here, we investigated the replication of PfDNV and its associated pathological phenotype in the foregut and hindgut. Consequently, we dissected and performed transcriptome sequencing on the foregut, midgut, and hindgut separately. We revealed the up-regulation of immune response signaling pathway c-Jun N-terminal kinase (JNK) and apoptosis in response to viral infection. Furthermore, knockdown of the JNK upstream gene Ben resulted in a decrease in virus titer and delayed host mortality.
Conclusion:
Taken together, our findings provide evidence that the Ben-JNK signaling plays a crucial role in PfDNV infection, leading to excessive apoptosis in intestinal tissues and ultimately resulting in the death of the host. Our results indicated that the host response to PfDNV fosters viral infection, thereby increasing host lethality. This underscores the potential of PfDNV as a viable, environmentally friendly biopesticide. © 2024 Society of Chemical Industry.
Insights
The Periplaneta fuliginosa densovirus (PfDNV) triggers a host immune response involving Ben-JNK signaling, leading to apoptosis and mortality. This clarifies PfDNV
Area of Science:
- Entomology
- Virology
- Immunology
Background:
- Cockroaches transmit pathogens, with Periplaneta fuliginosa densovirus (PfDNV) being a potential biopesticide.
- PfDNV causes mortality in smoky-brown cockroaches (P. fuliginosa).
- The immune response to PfDNV is not well understood.
Purpose of the Study:
- Investigate PfDNV replication and pathology in cockroach gut tissues.
- Elucidate the host immune response pathways involved in PfDNV infection.
- Determine the role of specific signaling pathways in PfDNV-induced mortality.
Main Methods:
- Dissection of cockroach foregut, midgut, and hindgut.
- Transcriptome sequencing of dissected tissues.
- Gene knockdown experiments targeting the Ben gene.
Main Results:
- PfDNV infection up-regulates the c-Jun N-terminal kinase (JNK) signaling pathway and apoptosis.
- Knockdown of the upstream gene Ben reduced PfDNV titer and delayed host death.
- The Ben-JNK pathway activation contributes to excessive apoptosis in intestinal tissues.
Conclusions:
- The Ben-JNK signaling pathway is critical in PfDNV infection, promoting viral replication and host mortality.
- Host immune response to PfDNV paradoxically enhances viral infection and lethality.
- PfDNV demonstrates potential as an environmentally friendly biopesticide due to its species-specific lethality.
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