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Journal of Virology, December 2003, p. 12852-12864, Vol. 77, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.23.12852-12864.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Varicella-Zoster Virus-Infected Human Sensory Neurons Are Resistant to Apoptosis, yet Human Foreskin Fibroblasts Are Susceptible: Evidence for a Cell-Type-Specific Apoptotic Response

C. Hood,1 A. L. Cunningham,1 B. Slobedman,1 R. A. Boadle,2 and A. Abendroth1*

Centre for Virus Research, Westmead Millennium Institute and University of Sydney,1 Electron Microscope Laboratory, Westmead Millennium Institute and Institute of Clinical Pathology and Medical Research, Westmead Hospital, New South Wales 2145, Australia2

Received 19 May 2003/ Accepted 20 August 2003

The induction of apoptosis or programmed cell death in virus-infected cells is an important antiviral defense mechanism of the host, and some herpesviruses have evolved strategies to modulate apoptosis in order to enhance their survival and spread. In this study, we examined the ability of varicella-zoster virus (VZV) to induce apoptosis in primary human dorsal root ganglion neurons and primary human foreskin fibroblasts (HFFs). Three independent methods (annexin V, TUNEL [terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling] staining, and electron microscopy) were used to assess apoptosis in these cells on days 1, 2, and 4 postinoculation. By all three methods, apoptosis was readily detected in VZV-infected HFFs. In stark contrast, apoptosis was not detected during productive VZV infection of neurons. The low-passage clinical isolate Schenke and the tissue culture-adapted ROka strain both induced apoptosis in HFFs but not in neurons, suggesting that this cell-type-specific apoptotic phenotype was not VZV strain specific. These data show that the regulation of apoptosis differs markedly between HFFs and neurons during productive VZV infection. Inhibition of apoptosis during infection of neurons may play a significant role in the establishment, maintenance, and reactivation of latent infection by promoting survival of these postmitotic cells.

* Corresponding author. Mailing address: Centre for Virus Research, Westmead Millennium Institute, P.O. Box 412, Westmead, 2145 NSW, Australia. Phone: 61-2-98459123. Fax: 61-2-98459100. E-mail: allison_abendroth{at}wmi.usyd.edu.au.

Journal of Virology, December 2003, p. 12852-12864, Vol. 77, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.23.12852-12864.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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