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Background. Some human herpesviruses become latent in dorsal-root ganglia. Primary infection with the Varicella Zoster virus causes chickenpox, followed by latency, and subsequent reactivation leading to shingles (zoster), but the frequency and distribution of latent virus have not been established.

Methods. Using the polymerase chain reaction, we performed postmortem examinations of trigeminal and thoracic ganglia of 23 subjects 33 to 88 years old who had not recently had chickenpox or shingles to identify the presence of latent Varicella Zoster viral DNA. Oligonucleotide primers representing the origin of replication of the Varicella Zoster virus and Varicella Zoster virus gene 29 were used for amplification.

Results. Among the 22 subjects seropositive for the antibody to the virus, both the viral origin-of-replication and gene-29 sequences were detected in 13 of 15 subjects (87 percent) in whom trigeminal ganglia were examined and in 9 of 17 (53 percent) in whom thoracic ganglia were examined. Viral DNA was not detected in brain or mononuclear cells from the seropositive subjects. None of three thoracic ganglia from the one seronegative subject contained Varicella Zoster viral DNA.

Conclusions. These findings indicate that after primary infection with Varicella Zoster virus (varicella), the virus becomes latent in many ganglia - more often in the trigeminal ganglia than in any thoracic ganglion -and that more than one region of the viral genome is present during latency. (N Engl J Med 1990; 323: 627-31.)

ALL human herpesviruses establish latent infection. The human herpesviruses - in particular, Epstein-Barr virus, herpes simplex virus, and varicella-zoster virus - have served as models for the study of latency. Varicella-zoster virus causes chickenpox (varicella) in children, becomes latent in dorsal-root ganglia, and is reactivated decades later, causing shingles (zoster) in adults. During latency, viral DNA is maintained in infected cells and virions cannot be detected, although virus can often be recovered by explantation of latently infected tissues. The mechanisms of latency and reactivation are not known. That they probably differ among the various herpesviruses is suggested by the establishment [horizontal ellipsis]

Owned, published, and (C) copyrighted, 1990, by the MASSACHUSETTS MEDICAL SOCIETY