Relationships of varicella zoster virus (VZV)‐specific cell‐mediated immunity and persistence of VZV DNA in saliva and the development of postherpetic neuralgia in patients with herpes zoster

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.

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Varicella-zoster virus-specific cell-mediated immunity and herpes zoster development in multiple myeloma patients receiving bortezomib- or thalidomide-based chemotherapy

Journal of Clinical Virology ◽

10.1016/j.jcv.2015.10.018 ◽

2015 ◽

Vol 73 ◽

pp. 64-69 ◽

Cited By ~ 16

Author(s):

Ji-Won Kim ◽

Chang-Ki Min ◽

Yeung-Chul Mun ◽

Yong Park ◽

Byung Soo Kim ◽

...

Keyword(s):

Multiple Myeloma ◽

Herpes Zoster ◽

Varicella Zoster Virus ◽

Cell Mediated Immunity ◽

Specific Cell ◽

Varicella Zoster

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Kestabilan Model Matematika Infeksi Primer Penyakit Varicella Dan Infeksi Rekuren Penyakit Herpes Zoster Oleh Virus Varicella Zoster

JURNAL ILMIAH MATEMATIKA DAN TERAPAN ◽

10.22487/2540766x.2020.v17.i1.15180 ◽

2020 ◽

Vol 17 (1) ◽

pp. 82-91

Author(s):

Hardiyanti ◽

R Ratianingsih ◽

Hajar

Keyword(s):

Herpes Zoster ◽

Stability Analysis ◽

Varicella Zoster Virus ◽

Critical Point ◽

Postherpetic Neuralgia ◽

Primary Infection ◽

Skin Diseases ◽

Varicella Zoster ◽

Stable Conditions ◽

Disease Free

Varicella and herpes zoster are two infectious skin diseases of human that caused by varicella zoster virus, where varicella disease is a primary infection that often infected younger people while herpes zoster disease is a recurrent disease that often infected older people because of reactivation of latent varicella-zoster virus. If the pain caused by herpes zoster after recurrent phase is a appeared then the condition is known as postherpetic neuralgia. This study builds a mathematical model of primary infection (varicella disease) and recurrent infection (herpes zoster disease) developed from the SIR model (Susceptible, Infected, Recovered). The human population is divided into seven subpopulations, namely susceptible, infection, recovered of varicella, herpes zoster and postherpetic neuralgia subpopulation. Stability analysis at the critical point by linearization method gives a critical point 𝑇1 that guaranted to exist and unstable if 𝛼 𝜇(𝛽1+𝜇) 𝐴 , while the critical point 𝑇1 does not have any reqruitment. Stability analysis at the endemic disease-free critical point is represented 𝑇1 that will be unstable if 𝑇2 exist and stable 𝑇1 if 𝑇2 exist. Numerical simulations by simulated to describe such temporary disease-free conditions and an endemic stable conditions.

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Herpes Zoster and Postherpetic Neuralgia: Past, Present and Future

Pain Research and Management ◽

10.1155/2009/380384 ◽

2009 ◽

Vol 14 (4) ◽

pp. 275-282 ◽

Cited By ~ 20

Author(s):

Gary J Bennett ◽

C Peter N Watson

Keyword(s):

Herpes Zoster ◽

Varicella Zoster Virus ◽

Recent Work ◽

Postherpetic Neuralgia ◽

Current Understanding ◽

Varicella Zoster

OBJECTIVES: The history behind the current understanding of the varicella-zoster virus and its relationship to the pain conditions caused by shingles and postherpetic neuralgia are reviewed. The framework for the current conceptualization is Hope-Simpson’s latency hypothesis. Data from recent work in virology, neuroanatomy and epidemiology are reviewed, as is work using varicella-zoster virus-infected animals. The recent data largely confirm Hope-Simpson’s hypothesis and extend it significantly.

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Reactivation of Varicella Zoster Virus after Vaccination for SARS-CoV-2

Vaccines ◽

10.3390/vaccines9060572 ◽

2021 ◽

Vol 9 (6) ◽

pp. 572

Author(s):

Mina Psichogiou ◽

Michael Samarkos ◽

Nikolaos Mikos ◽

Angelos Hatzakis

Keyword(s):

Adverse Event ◽

Herpes Zoster ◽

T Cell ◽

Varicella Zoster Virus ◽

Time Window ◽

Vaccine Safety ◽

Cell Mediated Immunity ◽

Varicella Zoster ◽

Increased Risk ◽

Immunocompetent Patients

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.

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