Varicella zoster virus (VZV) causes
varicella (
chickenpox), becomes latent in cranial nerve, dorsal root, and autonomic ganglia; and reactivates decades later to produce
zoster (
shingles). The main complication of
zoster is
postherpetic neuralgia (PHN),
pain that persists for months and often years after
zoster. VZV also causes chronic radicular
pain without
rash (
zoster sine herpete).
Viremia is associated with each stage of VZV
infection.
Viral DNA has been found in peripheral blood mononuclear cells (MNCs) of patients with
varicella,
zoster, PHN, and
zoster sine herpete. In
varicella,
viremia contributes to the widespread distribution of skin lesions and
infection of multiple organs. Although the role of
viremia in other VZV-associated diseases is not as clear, the detection of VZV
DNA (and sometimes VZV
RNA and
proteins) helps diagnose neurological diseases produced by VZV, has indicated that PHN may reflect a chronic VZV ganglionitis, and has established that VZV reactivates subclinically, especially in immunocompromised humans. In vitro studies have established that VZV can productively infect MNCs for a short time and have identified the subpopulations of MNCs that are infected. Finally, simian
varicella virus (SVV)
infection of nonhuman primates shares clinical, pathological, and virologic features with VZV in humans. Like VZV, SV
viremia in nonhuman primates during acute
infection plays an important role in the pathogenesis of SVV. Infectious virus can be isolated from MNCs, and SVV
DNA can be detected in MNCs during
varicella. Further, SVV
DNA can be detected for months in MNCs of monkeys after experimental
infection with SVV. Herein, we review the current literature related to VZV
infection of MNCs during naturally occurring
varicella, PHN, and
zoster sine herpete in humans, including studies of experimental
infection of human MNCs with VZV. We also review SVV MNC interaction during naturally occurring simian
varicella and after experimental
infection of primates with SVV.