Brain, Vol. 115, No. 2, 383-398, 1992
© 1992 Oxford University Press
research-article |
PRESENCE, DISTRIBUTION AND SPREAD OF PRODUCTIVE VARICELLA ZOSTER VIRUS INFECTION IN NERVOUS TISSUES
1Neurological Institute, University of Vienna Salzburg, Austria 2Landesnervenklinik Salzburg, Austria 3National Institute of Health Tokyo, Japan 4University of Tokyo Tokyo, Japan
Correspondence to:
Correspondence to. Dr M. Schmidbauer, Neurologische Universitatsklmik Wien, Wahringer Gilrtel 18-20, A-1090Vienna, Austria
Nervous tissue lesions were retrospectively studied for detection of productive varicella zoster virus (VZV) infection in 33 autopsied cases, including 19 herpes zoster (HZ) (10 trigeminal, nine spinal) and 14 cases of nodular brainstem encephalitis without HZ. Immunocytochemistry for VZV antigens and in situ hybridization with a brotinylated VZV DNA probe were used on formol-fixed paraffin sections. Peripheral and central nervous system, skin and striated muscle were investigated in serial sections; available tissue blocks, however, varied between cases.
Vanicella zoster virus production (both antigen and DNA) in nervous tissue was found in HZ cases but only of short survival after a rash of up to 7 wks (eight out of 12 patients). Varicella zoster virus was visualized in nerve cells, Schwann cells and blood vessels. In the central nervous system (CNS), VZV was detected in trigeminal nuclei (one out of 10 brains) or disseminated nodular brainstem lesions (one out of 10 brains), in subependymal microvessels (one out of 10 brains) or disseminated nodular braintem lesions vascuhtic arteries (two out of 19 brains or spinal cords). In the peripheral nervous system (PNS), VZV (DNA and antigen) was found in neurons and satellite cells of sensory ganglia (four out of seven cases with sampling of ganglia), and in damaged nerve fibres including a muscle nerve in one case; myositis with VZV in affected muscle fibres was found in the latter case. In nodular brainstem encephalitis, one case contained VZV within nodular lesions
We conclude that (i) VZV neural spread is suggested by detectable virus in ganglia, nerve fibres and CNS target nucle; (ii) haematogenous spread of VZV is suggested by detection of virus in CNS microvessels and in disseminated brainstem encephalitis, (iii) VZV myositis may occur in zosteric myotomes; and (iv) VZV is a possible agent in nodular brainstem encephalitis.
Received May 25, 1991. Revised November 5, 1991. Accepted November 21, 1991.
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