Infectivity Difference Between the Two Phenotypes of Autographa californica Nuclear Polyhedrosis Virus: Importance of the 64K Envelope Glycoprotein

Abstract

SUMMARY Two phenotypes of Autographa californica nuclear polyhedrosis virus (AcNPV), occluded virus and budded virus (BV), are responsible for causing disease in Trichoplusia ni. Virus released from occlusion bodies by alkali (LOVAL) is more infectious in the gut than in the haemocoel whereas BV is more infectious in the haemocoel than in the gut. Reduction of infectivity of BV in the haemocoel by the monoclonal antibody AcV1 to a level comparable to LOVAL clearly implicates its target, a 64K phosphoglycoprotein abundant in the BV envelope but not detected in LOVAL, as being involved in BV×s greater infectivity in that location. Homologous antiserum reduces the infectivity of LOVAL in the gut to that of LOVAL in the haemocoel, suggesting an analogous envelope component may account for its greater infectivity in the gut.