Viral fibroblast growth factor, matrix metalloproteases, and caspases are associated with enhancing systemic infection by baculoviruses

Abstract

Most arthropod-borne and invertebrate viruses are orally ingested and commence infection in cells of the invertebrate intestine. Infection of secondary sites and eventual transmission to other hosts is hindered by basal lamina, a tightly interwoven and virusimpenetrable noncellular layer, lining the intestine and other organ cell layers. The mechanisms for viral escape across basal laminae are unknown. We describe an elegant mechanism mediated by a baculovirus-encoded fibroblast growth factor (vFGF) that signals a previously undescribed stepwise cascade of protease activation wherein matrix metalloproteases activate effector caspases, leading to remodeling of basal lamina lining tracheal cells associated with the intestine and culminating in the establishment of efficient systemic infections. Because FGFs coordinate diverse functions during development, metabolic processes, and tissue repair, it is plausible that the vFGF-mediated pathway described here is widely used during developmental and pathogenic processes that involve basal lamina remodeling.basal lamina | FGF | midgut | virus

Proteomic Analysis of Frankliniella occidentalis and Differentially Expressed Proteins in Response toTomato Spotted Wilt VirusInfection

“…Consistent with our findings, a putative enolase transcript was also identified as upregulated in RSV-infected L. striatellus compared to results for the naive counterparts (86). Matrix metalloproteases have recently been documented to play a role in baculovirus escape from gut tissue through activation of effector caspases (45). The resulting remodeling of the basal lamina lining of tracheal cells associated with the intestine allows baculoviruses to escape from the midgut epithelial cells and establish systemic infections in their lepidopteran hosts (45).…”

“…Matrix metalloproteases have recently been documented to play a role in baculovirus escape from gut tissue through activation of effector caspases (45). The resulting remodeling of the basal lamina lining of tracheal cells associated with the intestine allows baculoviruses to escape from the midgut epithelial cells and establish systemic infections in their lepidopteran hosts (45). Larval acquisition of TSWV is required for transmission of virus; however, when adult thrips feed on virions, they enter the midgut and replicate but do not escape the gut tissues (76).…”

Transcriptome Responses of the Host Trichoplusia ni to Infection by the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus

“…In addition to genes that regulate and/or mediate viral transcription, translation, and DNA replication, the virus also encodes a variety of genes that modify cellular and organismal physiology, architecture, and defenses. These viral manipulations include effects on development and behavior of the host insect through hormonal control and perhaps other mechanisms (11)(12)(13)(14), a profound modification of cellular physiology and architecture (15)(16)(17), and host tissue breakdown, which results in release of the virus into the environment (18)(19)(20)(21). The AcMNPV infection is completed in a relatively short time period (approximately 24 to 48 h), producing infectious budded and occluded viruses.…”

Pathology of aGammabaculovirusin Its Natural Balsam Fir Sawfly (Neodiprion abietis) Host

“…Sequence data have identified F-protein homologs in betabaculoviruses [34,35] and the Culex nigripalpus Deltabaculovirus (CuniNPV) [36], indicating that F-protein may be more ancestral in baculoviruses [37]. Further evidence of the restriction of gammabaculoviruses and deltabaculoviruses to gut tissues is the absence of viral fibroblast growth factor (vfgf) homologs [1] that aid the establishment of alphabaculovirus systemic infections [38][39][40]. Viral FGFs mimic host FGFs that trigger fibroblast growth factor receptor-mediated migration of tracheal cells to the midgut epithelium.…”