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Journal of Virology, December 2001, p. 11821-11826, Vol. 75, No. 23
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.23.11821-11826.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Alpha and Gamma Interferons Inhibit Herpes Simplex Virus Type 1 Infection and Spread in Epidermal Cells after Axonal Transmission

Zorka Mikloska and Anthony L. Cunningham*

Centre for Virus Research, Westmead Millennium Institute, Westmead Hospital and University of Sydney, Westmead, New South Wales 2145, Australia

Received 9 April 2001/Accepted 10 August 2001

The ability of alpha interferon (IFN-alpha ) and IFN-gamma to inhibit transmission of herpes simplex virus type 1 (HSV-1) from neuronal axon to epidermal cells (ECs), and subsequent spread in these cells was investigated in an in vitro dual-chamber model consisting of human fetal dorsal root ganglia (DRG) innervating autologous skin explants and compared with direct HSV-1 infection of epidermal explants. After axonal transmission from HSV-1-infected DRG neurons, both the number and size of viral cytopathic plaques in ECs was significantly reduced by addition of recombinant IFN-gamma and IFN-alpha to ECs in the outer chamber in a concentration-dependent fashion. Inhibition was maximal when IFNs were added at the same time as the DRG were infected with HSV-1. The mean numbers of plaques were reduced by 52% by IFN-alpha , 36% by IFN-gamma , and by 62% when IFN-alpha and IFN-gamma were combined, and the mean plaque size was reduced by 64, 43, and 72%, respectively. Similar but less-inhibitory effects of both IFNs were observed after direct infection of EC explants, being maximal when IFNs were added simultaneously or 6 h before HSV-1 infection. These results show that both IFN-alpha and IFN-gamma can interfere with HSV-1 infection after axonal transmission and subsequent spread of HSV-1 in ECs by a direct antiviral effect. Therefore, both IFN-alpha and -gamma could contribute to the control of HSV-1 spread and shedding in a similar fashion in recurrent herpetic lesions.

* Corresponding author. Mailing address: Centre for Virus Research, Westmead Millennium Institute, Westmead Hospital and University of Sydney, P.O. Box 214, Westmead, New South Wales 2145, Australia. Phone: 61 2 9845 9001. Fax: 61 2 9845 9100. E-mail: tony_cunningham{at}wmi.usyd.edu.au.

Journal of Virology, December 2001, p. 11821-11826, Vol. 75, No. 23
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.23.11821-11826.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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