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Title: Slow cell infection, inefficient primary infection and inability to replicate in fat body determine host-range of Thysanoplusia orichalcea M Nucleopolyhedrovirus (ThorMNPV)

Author
item WANG, LIHUA - MIAMI, UNIV
item SALEM, TAMER - MIAMI, UNIV.
item LYNN, DWIGHT - RETIRED-USDA-IBL
item CHENG, XIAO-WEN - MIAMI, UNIV

Submitted to: Journal of General Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/25/2008
Publication Date: 7/15/2008
Citation: Wang, L., Salem, T.Z., Lynn, D., Cheng, X. 2008. Slow cell infection, inefficient primary infection and inability to replicate in fat body determine host-range of Thysanoplusia orichalcea M Nucleopolyhedrovirus (ThorMNPV). Journal of General Virology. 89:1402-10.

Interpretive Summary: Insect viruses are potential alternatives to chemical pesticides for control of agricultural pests. One of these from the soybean looper (Thysanoplusia orichacea) has a smaller host range than many related viruses but is very potent against susceptible insects. The current study examines factors responsible for the restricted host range, using cell culture systems and fluorescently tagged viruses as tools. We have found dual infection of some cells normally insusceptible to this virus with both it and a wide host range virus allows productive infections. These results suggest that some of the genes in the wide host range virus affect the infectivity of the narrow host range virus. Further studies will use recombinant DNA techniques to identify genes involved in the host range. These studies will be of interest to researchers involved in investigations with other virus host range studies.

Technical Abstract: An enhanced green fluorescence protein (EGFP) gene expression cassette was inserted at the gp37 locus of Thysanoplusia orichacea M nucleopolyhedrovirus (ThorMNPV) to produce vThGFP to study host-range mechanisms. Using EGFP to monitor infection in vitro, many cell lines showed EGFP expression suggesting infection of vThGFP. Detailed infection kinetics showed that vThGFP infection in Sf21 cells was too slow to suppress the cell growth. Wide host-range Autographa californica MNPV (AcMNPV) could speed up vThGFP infection by 40 times and enhance vThGFP infection rate in Sf21 by 138 folds. Per os infection using vThGFP polyhedra did not kill third instar larvae of Spodoptera frugiperda, S. exigua and Helicoverpa zea but was vertically transmitted. However, intrahaemocoelic injection using budded viruses (BV) of vThGFP killed third instar larvae of S. frugiperda, S. exigua and H. zea. Bioassay results showed a LD50 of 240 BVs/larva of vThGFP to third instar S. frugiperda larvae. This suggested that insufficient BVs were generated during the primary infection in the midgut. Fluorescence examination showed that vThGFP infected hemolymph, tracheae and Malpighian tubules but not fat body of larvae of S. frugiperda, S. exigua and H. zea. Third instar S. frugiperda larvae co-infected by injection with vThGFP and vAcRED, an AcMNPV expressing red fluorescent protein gene, showed EGFP expression in the fat body. This result suggests that vAcRed could help vThGFP replicate in the fat body or trans-activate EGFP expression in the fat body. All these results suggested that slow cell infection, insufficient primary infection and inability to replicate in fat body control the host-range of ThorMNPV.