Cross-talking between baculoviruses and host insects towards a successful infection

Abstract

Baculoviridae is a family of large DNA viruses that infect insects. They have been extensively used as safe and efficient biological agents for the control of insect pests. As a result of coevolution with their hosts, baculoviruses developed unique life cycles characterized by the production of two distinctive virion phenotypes, occlusion-derived virus and budded virus, which are responsible for mediating primary infection in insect midgut epithelia and spreading systemic infection within infected insects, respectively. In this article, advances associated with virus-host interactions during the baculovirus life cycle are reviewed. We mainly focus on how baculoviruses exploit versatile strategies to overcome diverse host barriers and establish successful infections. For example, in the midgut, baculoviruses encode enzymes to degrade peritrophic membranes and use a series of per os infectivity factors to initiate primary infection. A viral fibroblast growth factor is expressed to attract tracheoblasts that spread the virus for systemic infection. Baculoviruses use different strategies to suppress host defence systems, including apoptosis, melanization and RNA interference. Additionally, baculoviruses can manipulate host physiology and induce 'tree-top disease' for optimal virus replication and dispersal. These advances in our understanding of baculoviruses will greatly inform the development of more effective baculoviral pesticides. This article is part of the theme issue 'Biotic signalling sheds light on smart pest management'.

Keywords: baculovirus; behaviour; immune system; insect; primary infection; systemic infection.

Figure 1.

Model of how baculoviruses overcome different host barriers to establish successful infections. After being ingested by susceptible larvae, OBs are dissolved under the alkaline conditions of the insect midgut to release ODVs. Two enzymes (enhancin and ODV-E66) can degrade the PM to allow the access of ODV to the midgut epithelia. Primary infection is then initiated by a group of ODV-specific envelope proteins (PIFs) (①). To egress from the BL barrier at the basal side of the midgut epithelial cells, baculoviruses use vFGF for the chemotaxis of tracheoblasts to facilitate BV passage, and they use BV-specific envelope proteins (GP64 or F proteins) to spread systemic infection (②). Baculoviruses exploit different strategies to suppress host defence systems, including melanization, apoptosis and RNAi for efficient virus replication (③). Baculoviruses can also regulate host physiology and behaviour, such as inducing a ‘tree-top disease’ via PTP and EGT (④) and ‘liquefaction of infected larval bodies' by chitinase and cathepsin (⑤) for optimal virus dispersal. BL: basal laminae; BV: budded virus; ODV: occlusion-derived virus; OB: occlusion body; PM: petritrophic membrane. Viral proteins are in red.