Characterization of viremia at different stages of varicella-zoster virus infection

Abstract

Varicella-zoster virus (VZV) viremia at different stages of infection was characterized. Different approaches were used, polymerase chain reaction (PCR), isothermal transcription based nucleic acid amplification (NASBA), and immunofluorescence to describe and quantitate viral infection of peripheral blood mononuclear cells (PBMC). In patients with acute varicella 200 to 5,000 copies of the viral genome in every 150,000 PBMC were found with quantitative competitive PCR (QCPCR). With NASBA, viral transcriptional activity was detected in these cells. RNA transcribed from the immediate early gene IE 63 as well as from the late gene 68 were found, indicating a productive infection. Glycoprotein gE specific immunofluorescence visualized by confocal laser scanning microscopy revealed that only 1 in 10,000 to 100,000 PBMC was infected. T and B lymphocytes as well as monocytes expressed viral protein on their surface. Similar results were obtained with PBMC from immunocompetent zoster patients. In some cases a transient viremia was found shortly after the onset of rash, although the viral load seemed to be lower than in patients with varicella. Examination of blood samples from 16 persons with postherpetic neuralgia (PHN) signs of viral replication in PBMC were not detected. In conclusion, the data suggest that VZV viremia is a frequent event in patients with varicella and zoster, but not in those with postherpetic neuralgia. Moreover, the results indicated that subclinical reactivations occur both in immunocompromised and immunocompetent individuals.

Varicella-Zoster Virus DNA in Cells Isolated from Human Trigeminal Ganglia

“…As with HSV, it is possible that the latency burden of VZV varies with the severity of the primary illness (29). Consistent with this possibility is the reported variation in virus load during the viremic stage of acute VZV infection (6,25). The number of VZV genome copies per latently infected neuron was 2 to 9 genome copies (mean 4.7).…”

Phylogenetic Analysis of Varicella-Zoster Virus: Evidence of Intercontinental Spread of Genotypes and Recombination

“…The natural history of varicella is of primary infection in childhood following which the virus remains quiescent before reactivating once in adulthood, although recent evidence has confirmed observations that subclinical reactivation of VZV is not uncommon (30). The number of replication cycles before latency is established could be as low as 20 (19), and viral shedding is limited to the duration of lesions (approximately 5 to 7 days).…”

Atypical recurrent varicella in 4 patients with hemopathies

“…Transient subclinical VZV viremia has been demonstrated in peripheral blood mononuclear cells of patients with herpes zoster, and in patients who are VZV seropositive (IgMϪ, IgGϩ) with no sign of VZV-related disease. [26][27][28] In the latter patients, the viremic episodes remain probably subclinical as the patients are VZVseropositive and because of the paucity of viral load compared with that observed during varicella. 27,28 On the other hand, previous vascular injury may create a predilective site for VZV replication, leading to varicella on photodamaged sites, 29 or on other diverse skin injuries.…”

“…[26][27][28] In the latter patients, the viremic episodes remain probably subclinical as the patients are VZVseropositive and because of the paucity of viral load compared with that observed during varicella. 27,28 On the other hand, previous vascular injury may create a predilective site for VZV replication, leading to varicella on photodamaged sites, 29 or on other diverse skin injuries. 30,31 Hence, in our patients, the chemotherapy could have damaged the endothelial cells, creating predilective sites for viral attachment and replication.…”