VZV Foundation - A Decade Of Leadership In The Fight Against VZV Infections

	Oral Presentation Abstracts: 37 [37] INDUCED NORADRENALINE SENSITIVITY OF SENSORY NEURONS FROM RAT DORSAL ROOT GANGLIA AFTER INFECTION WITH HUMAN VARICELLA ZOSTER VIRUS *H. Fickenscher (1), M. Schmidt (1) & M. Kress (2) (1) Institut für Klinische und Molekulare Virologie, (2) Institut für Physiologie und Experimentelle Pathophysiologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany The reactivation of varicella-zoster virus (VZV) from sensory neurons induces severe pain and hyperalgesia leading to postherpetic neuralgia. In order to elucidate the mechanisms of VZV-associated hyperalgesia, we have established an in vitro model for the VZV infection of sensory neurons from rat dorsal root ganglia. Up to 50% of the neurons showed strong expression of the immediate-early antigens IE62 and IE63, and the late gE. In individual cells, the intracellular calcium concentration was monitored microfluorimetrically. The sensitivity to GABA or capsaicin was similar in controls and in VZV-infected neurons. The baseline calcium concentration was moderately increased after infection. In contrast to uninfected cells, the neurons became de novo sensitive to adrenergic stimulation after VZV infection. Noradrenaline-responsive neurons were much more frequent and calcium responses to noradrenaline were significantly higher after infection with wildtype strains than with the attenuated vaccine strain OKA. The adrenergic agonists phenylephrine and isoproterenol had similar efficacy. We suggest that the infection with wildtype VZV strains confers noradrenaline sensitivity to sensory neurons via a1- and/or B1-adrenergic receptors. This provides a model for the severe pain associated with the reactivation of VZV. Corresponding Author: H. Fickenscher, Priv.-Doz. Dr. med., Institut für Klinische und Molekulare Virologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Schlossgarten 4, D-91054 Erlangen, Germany

[37]

INDUCED NORADRENALINE SENSITIVITY OF SENSORY NEURONS FROM RAT DORSAL ROOT GANGLIA AFTER INFECTION WITH HUMAN VARICELLA ZOSTER VIRUS

*H. Fickenscher (1), M. Schmidt (1) & M. Kress (2)
(1) Institut für Klinische und Molekulare Virologie, (2) Institut für Physiologie und Experimentelle Pathophysiologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany

The reactivation of varicella-zoster virus (VZV) from sensory neurons induces severe pain and hyperalgesia leading to postherpetic neuralgia. In order to elucidate the mechanisms of VZV-associated hyperalgesia, we have established an in vitro model for the VZV infection of sensory neurons from rat dorsal root ganglia. Up to 50% of the neurons showed strong expression of the immediate-early antigens IE62 and IE63, and the late gE. In individual cells, the intracellular calcium concentration was monitored microfluorimetrically. The sensitivity to GABA or capsaicin was similar in controls and in VZV-infected neurons. The baseline calcium concentration was moderately increased after infection. In contrast to uninfected cells, the neurons became de novo sensitive to adrenergic stimulation after VZV infection. Noradrenaline-responsive neurons were much more frequent and calcium responses to noradrenaline were significantly higher after infection with wildtype strains than with the attenuated vaccine strain OKA. The adrenergic agonists phenylephrine and isoproterenol had similar efficacy. We suggest that the infection with wildtype VZV strains confers noradrenaline sensitivity to sensory neurons via a1- and/or B1-adrenergic receptors. This provides a model for the severe pain associated with the reactivation of VZV.

Corresponding Author: H. Fickenscher, Priv.-Doz. Dr. med., Institut für Klinische und Molekulare Virologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Schlossgarten 4, D-91054 Erlangen, Germany