TRANSMISSION AND COURSE OF INFECTION OF THE NUCLEOPOLYHEDROSIS VIRUS (BACULOVIRUS) OF THE GYPSY MOTH, LYMANTRIA DISPAR (HEMOCYTES)

Date of Completion

January 1984

Keywords

Biology, Entomology

Degree

Ph.D.

Abstract

The pathway of Lymantria dispar nucleopolyhedrosis virus invasion and infection was studied in the gypsy moth, Lymantria dispar. Polyhedral inclusion bodies dissolved slowly in larval digestive fluids. Significant dissolution occurred only after two hours, and dissolution was complete after four hours. No significant changes were found in the surface morphology of peritrophic membrane which had been exposed to virus in vivo or in vitro. Virus invasion and replication in midgut cells could not be detected, and the mechanism of entry into the hemocoel could not be determined. However, infectious viral material was present in the hemocoel just two hours after ingestion of inclusion bodies. This indicates that direct passage of inoculum virus probably occurred.^ Virus replication in the host was detected first in hemocytes. This occurred 42 hours after ingestion of virus. Mechanisms of virus entry into, and release from hemocytes were described, as were many ultrastructural anomalies connected with virus replication. Throughout the course of infection hemocytes continued to release nucleocapsids into the hemolymph. Cells of the fat body produced many inclusion bodies, but nucleocapsids apparently were not released from these cells.^ During the course of nucleopolyhedrosis, infected larvae experienced significant decreases in total hemocyte count, in the percentage of circulating coagulocytes, and in the ability of the hemolymph to clot. Their hemolymph volume per unit body weight increased significantly. The total hemocyte count, hemolymph volume per unit body weight, and ability of hemolymph to clot in control larvae did not change significantly; the percentage of circulating coagulocytes increased. The body weight and absolute hemocyte counts of both groups increased during the lethal infection period, but increases were significantly smaller in infected larvae. Wound repair was accomplished in a timely, but altered manner in infected larvae.^ Virus susceptibility and lethal times were related to age and weight of the host, but lethal times were not related to dosage. There was no evidence of acquired resistance, or that survivors, or their immediate progeny, were in any measurable way affected by a sublethal dosage of virus. ^

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