Frequency and Abundance of Alphaherpesvirus DNA in Human Thoracic Sympathetic Ganglia

Alphaherpesvirus reactivation from thoracic sympathetic ganglia (TSG) and transaxonal spread to target organs cause human visceral disease. Yet alphaherpesvirus latency in TSG has not been well characterized. In this study, quantitative PCR detected varicella-zoster virus (VZV), herpes simplex virus 1 (HSV-1), and HSV-2 DNA in 117 fresh TSG obtained postmortem from 15 subjects. VZVDNAwas found in 76 (65%) ganglia from all subjects, HSV-1 DNAwas found in 5 (4%) ganglia from 3 subjects, and no HSV-2 was found. After primary infection, varicella-zoster virus (VZV) becomeslatent in cranial nerve ganglia, dorsal root ganglia, and auto-nomic ganglia along the entire neuraxis (1–7), herpes simplex virus 1 (HSV-1) DNA becomes latent in cranial nerve, dorsal root, and autonomic ganglia (2, 5–10), and HSV-2 DNA becomes latent primarily in sacral ganglia as well as in cranial nerve and other dorsal root ganglia (5, 9). Alphaherpesvirus reactivation from tho-racic sympathetic ganglia (TSG) and transaxonal spread to target organs cause human visceral disease. However, latency in TSG has not been well characterized because earlier studies used formalin-fixed paraffin-embedded (FFPE) tissue. To assess autonomic gan