Viruses and other pathogens can interrupt host cellular apoptosis to gain benefits, such as sufficient resources and a stable environment that enables them to complete their replication and assembly. It is unusual for viruses to code proteins with homology to caspases, which are commonly recognized as apoptosis regulators.

Feed quality influences insect cannibalistic behavior and gut microbial communities. In the present study,Spodoptera exigualarvae were fed six different artificial diets, and one of these diets (Diet 3) delayed larval cannibalistic behavior and reduced the cannibalism ratio after ingestion. Diet 3-fed larvae had the highest gut bacterial load (1.396 ± 0.556 × 10¹⁴bacteria/mg gut), whereas Diet 2-fed larvae had the lowest gut bacterial load (3.076 ± 1.368 × 10¹²bacteria/mg gut). The gut bacterial composition and diversity of different diet-fedS. exigualarvae varied according to the 16S rRNA gene sequence analysis. Enterobacteriaceae was specific to the Diet 3-fed larval gut. Fifteen culturable bacterial isolates were obtained from the midgut of Diet 3-fed larvae. Of these, ten belonged toEscherichia sp. After administration with Diet 1- or 2-fedS. exigualarvae, two bacterial isolates (SePC-12and-37) delayed cannibalistic behavior in both tested larval groups. Diet 2-fed larvae had the lowest Juvenile hormone (JH) concentration and were more aggressive against intraspecific predation. However,SePC-12loading increased the JH hormone levels in Diet 2-fed larvae and inhibited their cannibalism. Bacteria in the larval midgut are involved in the stabilization of JH levels, thereby regulating host larval cannibalistic behavior.

The pathogenicity of a virus to a specific host species is an inerratic and describable ability of a virus to cause infection but is generally shaped by a variety of abiotic and biotic factors. In this investigation, the variations in pathogenicity of Heliothis virescens ascovirus 3h (HvAV-3h) to five noctuid pests were assessed based on mass spectrometry analysis on the virion compositions. Twenty-nine common HvAV-3h proteins were shared across all hosts, and different flexible proteins were identified in the virions of each specific host. Different host proteins were identified as HvAV-3h virion-associated proteins, including different detoxification enzyme proteins. Furthermore, a relatively fixed relationship between viral replication and changes in host detoxification enzyme activity caused by deficiencies in various viral structural proteins was found in the host larvae using a correlation matrix analysis: the host larval carboxylesterase and cytochrome P450 monooxygenases generally had highly similar responses to the viruses blocked by different structural proteins’ antisera and their effects on viral DNA replication. Different interaction patterns for the virion structural proteins were found in different host larvae-produced virions, and the interactions between Spodoptera litura glutathione S-transferases and viral structural proteins were confirmed. The different host responses after viral infection could be the reason for the changes in viral pathogenicity, while the virus responses gradually adapted to the different hosts and there were flexible changes in the virion structures. IMPORTANCE: Different pathogenic processes of a virus in different hosts are related to the host individual differences, which makes the virus undergoes different survival pressures. Here, we found that the virions of an insect virus, Heliothis virescens ascovirus 3h (HvAV-3h), had different protein composition when they were purified from different host larval species. These “adaptive changes” of the virions were analyzed in detail in this study, which mainly included the differences of the protein composition of virions and the differences in affinity between virions and different host proteins. The results of this study revealed the flexible changes of viruses to help themselves adapt to different hosts. Also, these interesting findings can provide new insights to improve our understanding of virus adaptability and virulence differentiation caused by the adaptation process.