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Journal of Virology, July 2000, p. 6287-6299, Vol. 74, No. 14
Department of Medical Microbiology and
Immunology, University of Alberta, Edmonton, Alberta, Canada T6G
2H7,1 and Department of Pathology and
Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N
3Z52
Received 25 February 2000/Accepted 19 April 2000
During infection with herpes simplex virus type 1 (HSV-1), VP16
serves multiple functions, including transcriptional activation of
viral immediate early genes and downregulation of the virion host
shutoff protein vhs. Furthermore, VP16 has been shown to be involved in
some aspect of virus assembly and/or maturation. Experiments with a
VP16 null virus, 8MA, suggested that VP16 plays a direct role in virion
assembly, since removal of VP16 from the HSV-1 genome results in
reduced levels of encapsidated DNA and a failure to produce
extracellular enveloped particles. However, VP16 null mutants display a
severe translational arrest due to unrestrained vhs activity, thus
complicating interpretation of these data. We examine here the role of
VP16 in virion assembly and egress in the context of a vhs null
background, using the virus 8MA/
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Evidence that Herpes Simplex Virus VP16 Is Required for Viral
Egress Downstream of the Initial Envelopment Event
Sma (VP16
vhs
). Comparison of 8MA and 8MA/
Sma with respect to
viral DNA accumulation and encapsidation and accumulation of the major
capsid protein, VP5, revealed that the 8MA lethal phenotype is only
partially due to uncontrolled vhs activity, indicating that VP16 is
required in HSV-1 virion formation. Electron microscopy confirmed these results and further showed that VP16 is required for HSV-1 egress beyond the perinuclear space. In addition, we describe the isolation and characterization of an 8MA derivative capable of propagation on
Vero cells, due to second site mutations in the vhs and UL53 (gK)
genes. Taken together, these results show that VP16 is required for
viral egress downstream of the initial envelopment step and further
underscore the importance of VP16 in controlling vhs activity within an
infected cell.
*
Corresponding author. Mailing address: Department of
Medical Microbiology and Immunology, 1-41, Medical Sciences Bldg.,
University of Alberta, Edmonton, Alberta, Canada T6G 2H7. Phone: (780)
492-2308. Fax: (780) 492-7521. E-mail:
jim.smiley{at}ualberta.ca.
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