Host–Pathogen Interactions between Metarhizium spp. and Locusts

Abstract

The progress in research on the interactions between Metarhizium spp. and locusts has improved our understanding of the interactions between fungal infection and host immunity. A general network of immune responses has been constructed, and the pathways regulating fungal pathogenicity have also been explored in depth. However, there have been no systematic surveys of interaction between Metarhizium spp. and locusts. The pathogenesis of Metarhizium comprises conidial attachment, germination, appressorial formation, and colonization in the body cavity of the host locusts. Meanwhile, the locust resists fungal infection through humoral and cellular immunity. Here, we summarize the crucial pathways that regulate the pathogenesis of Metarhizium and host immune defense. Conidial hydrophobicity is mainly affected by the contents of hydrophobins and chitin. Appressorial formation is regulated by the pathways of MAPKs, cAMP/PKA, and Ca2+/calmodulin. Lipid droplets degradation and secreted enzymes contributed to fungal penetration. The humoral response of locust is coordinated by the Toll pathway and the ecdysone. The regulatory mechanism of hemocyte differentiation and migration is elusive. In addition, behavioral fever and density-dependent population immunity have an impact on the resistance of hosts against fungal infection. This review depicts a prospect to help us understand host–pathogen interactions and provides a foundation for the engineering of entomopathogenic fungi and the discovery of insecticidal targets to control insect pests.

An entomopathogenic fungus exploits its host humoral antibacterial immunity to minimize bacterial competition in the hemolymph

“…An intriguing finding in the current study is that EPF utilizes host immunity to minimize the competition of opportunistic bacteria in the hemolymph. When EPF germ tubes penetrate the integument and enter the hemocoel, they are exposed to the strong immune reactions of the insect host [ 46 , 47 ]. EPF usually employs two strategies to survive in the hemocoel: evading and suppressing the host immunity [ 6 – 10 ].…”

“…Given that ecdysone triggers the expression of many immune-related genes, such as PRRs and AMPs [ 42 , 63 ], an increased 20E titer upon M. rileyi infection may contribute to the upregulation of AMPs, either directly or indirectly. The humoral antibacterial response of H. armigera upon fungal infection may be coordinated by the Toll pathway and ecdysone, as shown in the locust [ 47 ]. Unlike the decreased 20E levels upon M. rileyi conidial injection [ 41 ], we found that M. rileyi blastospore injection elevated the 20E titers.…”

Recent Advancements in Pathogenic Mechanisms, Applications and Strategies for Entomopathogenic Fungi in Mosquito Biocontrol

“…The fungal infection can lead to the death of the mosquito or disrupt its further development, such as eclosion, pupation, oviposition and reduced life span [13,25,[28][29][30][31]. EPF infection on adult mosquito has been extensively described, showing a similar phenomenon as other insects [27]. Similar as in adults, topical infection of larvae can destroy the host hemocytes after penetrating the cuticle [32].…”

“…They then penetrate the host's cuticle through a combination of mechanical force from turgor pressure and enzymes produced by the appressoria. This penetration allows the fungi to destroy the insect immune system and proliferate inside the insect [25][26][27]. Infection through the cuticle is undoubtedly the main pathway for EPF to target eggs, pupae, and adult mosquitoes with piercing-sucking mouthparts.…”

Phenotypic variation and genomic variation in insect virulence traits reveal patterns of intraspecific diversity in a locust-specific fungal pathogen

“…However, specialization of M. acridum to hosts within Orthoptera is considered to have led to specific patterns of genetic and pathogenic adaptation. For example, unlike generalist Metarhizium species, which typically kill hosts of many insect orders quickly via toxins, M. acridum causes a systemic infection of host tissues along with increased evasion of the host immune system, eliciting a more gradual killing of their orthopteran host (Kershaw et al, 1999; Li & Xia, 2022). In addition, M. acridum has been shown to be more tolerant to physical stressors than other Metarhizium species, such as to ultraviolet light from solar radiation (Brancini et al, 2019; Fernandes et al, 2010).…”