Naturally acquired simian varicella virus infection in African green monkeys

Abstract

Simian varicella virus (SVV) infection of primates shares clinical, pathological, immunological, and virological features with varicella-zoster virus infection of humans. Natural varicella infection was simulated by exposing four SVV-seronegative monkeys to monkeys inoculated intratracheally with SVV, in which viral DNA and RNA persist in multiple tissues for more than 1 year (T. M. White, R. Mahalingam, V. Traina-Dorge, and D. H. Gilden, J. Neurovirol. 8:191-205, 2002). The four naturally exposed monkeys developed mild varicella 10 to 14 days later, and skin scrapings taken at the time of the rash contained SVV DNA. Analysis of multiple ganglia, liver, and lung tissues from the four naturally exposed monkeys sacrificed 6 to 8 weeks after resolution of the rash revealed SVV DNA in ganglia at multiple levels of the neuraxis but not in the lung or liver tissue of any of the four monkeys. This animal model provides an experimental system to gain information about varicella latency with direct relevance to the human disease.

FIG. 1.

Detection of SVV DNA in skin scrapings of rash areas from monkeys infected naturally or intratracheally with SVV. DNA samples extracted from scrapings of rash from a monkey intratracheally infected with SVV and from two monkeys (no. 190 and 191) exposed to the experimentally infected monkey were analyzed by nested PCR with primers and probes specific for SVV ORF 63 to amplify a 219-bp fragment. No DNA was included in one of the reactions (No DNA). DNA samples from uninfected (BSC-1 DNA) and SVV-infected (SVV-BSC-1 DNA) BSC-1 cells in culture were used as negative and positive controls, respectively.

FIG. 2.

Detection of SVV DNA in ganglia from monkeys naturally infected with SVV. DNA samples extracted from pooled cervical (C), thoracic (T), lumbar (L), and sacral (S) ganglia and from the lungs and livers of two monkeys (no. 165 and 166) exposed to an intratracheally infected monkey (no. 164) were analyzed by nested PCR with primers and probes specific for SVV ORF 63 to amplify a 219-bp fragment. No DNA was included in one of the reactions (No DNA). DNA samples from uninfected (BSC-1 DNA) and SVV-infected (SVV-BSC-1 DNA) BSC-1 cells in culture were used as negative and positive controls, respectively.