Varicella-zoster virus-specific cell-mediated immunity in subjects with herpes zoster

2012 ◽  
Vol 377 (1-2) ◽  
pp. 53-55 ◽  
Author(s):  
Naruhito Otani ◽  
Kiyofumi Yamanishi ◽  
Yoshiko Sakaguchi ◽  
Yasutomo Imai ◽  
Masayuki Shima ◽  
...  
2012 ◽  
Vol 19 (9) ◽  
pp. 1411-1415 ◽  
Author(s):  
Stephen K. Tyring ◽  
Jon E. Stek ◽  
Jeffrey G. Smith ◽  
Jin Xu ◽  
Marco Pagnoni ◽  
...  

ABSTRACTVaricella-zoster virus (VZV)-specific cell-mediated immunity (CMI) responses were compared over time following an episode of herpes zoster (HZ) with those of age-, race-, and gender-matched healthy controls (HC) without HZ, using a validated gamma interferon (IFN-γ) enzyme-linked immunospot (ELISPOT) assay. The zoster brief-pain inventory (ZBPI) was used to assess zoster-associated pain. HZ patients (n= 140) had significantly higher IFN-γ ELISPOT responses to VZV antigen than did HC (n= 140). ELISPOT geometric mean count (GMC) responses (with 95% confidence intervals [CI]) for subjects who presented within 72 h were as follows: for HZ patients ≥ 60 years of age, at day 0 the GMC was 110 and at week 2 the GMC was 235; for HZ patients 21 to 59 years of age, at day 0 the GMC was 111 and at week 2 the GMC was 198; for HC ≥ 60 years of age, at day 0 the GMC was 19 and at week 2 the GMC was 18; and for HC 21 to 59 years of age, at day 0 the GMC was 59 and at week 2 the GMC was 56. The mean pain score (95% CI) across age groups at 1 week postrash (n= 106) was 6.0 (5.5, 6.5) and at 2 weeks postrash (n= 119) was 3.5 (2.9, 4.0). The percentage of HZ patients with substantial pain (score ≥ 3) at 6 weeks postrash increased with age from 8% for patients 21 to 49 years of age to 16% for patients 50 to 59 years of age to 22% for patients ≥ 60 years of age. The VZV-specific CMI response was substantially boosted by an episode of HZ, as measured by ELISPOT results. Older adults had lower VZV-specific cellular immunity than younger subjects at baseline, but the boosting effect of HZ was substantial for all age groups. HZ patients experienced considerable zoster-associated acute (1 to 2 weeks after rash) pain across age groups, while chronic pain increased with age.


Vaccines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 572
Author(s):  
Mina Psichogiou ◽  
Michael Samarkos ◽  
Nikolaos Mikos ◽  
Angelos Hatzakis

Seven immunocompetent patients aged > 50 years old presented with herpes zoster (HZ) infection in a median of 9 days (range 7–20) after vaccination against SARS-CoV-2. The occurrence of HZ within the time window 1–21 days after vaccination defined for increased risk and the reported T cell-mediated immunity involvement suggest that COVID-19 vaccination is a probable cause of HZ. These cases support the importance of continuing assessment of vaccine safety during the ongoing massive vaccination for the COVID-19 pandemic and encourage reporting and communication of any vaccination-associated adverse event.


2014 ◽  
Vol 151 (1_suppl) ◽  
pp. P215-P215
Author(s):  
Takahiro Ichihara ◽  
Shin-Ichi Haginomori ◽  
Atsuko Mori ◽  
Atsuko Kanazawa ◽  
Akira Nishikado ◽  
...  

2008 ◽  
Vol 198 (9) ◽  
pp. 1327-1333 ◽  
Author(s):  
Kay Sadaoka ◽  
Shigefumi Okamoto ◽  
Yasuyuki Gomi ◽  
Takeshi Tanimoto ◽  
Toyokazu Ishikawa ◽  
...  

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1356 ◽  
Author(s):  
Don Gilden ◽  
Maria Nagel ◽  
Randall Cohrs ◽  
Ravi Mahalingam ◽  
Nicholas Baird

Varicella zoster virus (VZV) is a ubiquitous, exclusively human alphaherpesvirus. Primary infection usually results in varicella (chickenpox), after which VZV becomes latent in ganglionic neurons along the entire neuraxis. As VZV-specific cell-mediated immunity declines in elderly and immunocompromised individuals, VZV reactivates and causes herpes zoster (shingles), frequently complicated by postherpetic neuralgia. VZV reactivation also produces multiple serious neurological and ocular diseases, such as cranial nerve palsies, meningoencephalitis, myelopathy, and VZV vasculopathy, including giant cell arteritis, with or without associated rash. Herein, we review the clinical, laboratory, imaging, and pathological features of neurological complications of VZV reactivation as well as diagnostic tests to verify VZV infection of the nervous system. Updates on the physical state of VZV DNA and viral gene expression in latently infected ganglia, neuronal, and primate models to study varicella pathogenesis and immunity are presented along with innovations in the immunization of elderly individuals to prevent VZV reactivation.


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