Differentiation between the Oka Varicella Vaccine Virus and American Wild-Type Varicella-Zoster Virus (VZV)

1990 ◽  
pp. 59-69 ◽  
Author(s):  
Lawrence D. Gelb ◽  
Susan G. Adams ◽  
Dennis E. Dohner
Keyword(s):  
Varicella Zoster Virus ◽  
Varicella Vaccine ◽  
Vaccine Virus ◽  
Wild Type ◽  
Varicella Zoster

scholarly journals Varicella Vaccine Meningitis as a Complication of Herpes Zoster in Twice-Immunized Immunocompetent Adolescents

2020 ◽  
Vol 35 (13) ◽  
pp. 889-895 ◽  
Author(s):  
Veena Ramachandran ◽  
Stephen C. Elliott ◽  
Kathie L. Rogers ◽  
Randall J. Cohrs ◽  
Miles Weinberger ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Herpes Zoster ◽  
Varicella Zoster Virus ◽  
Varicella Vaccine ◽  
The United States ◽  
Vaccine Virus ◽  
Virus Reactivation ◽  
Wild Type ◽  
Varicella Zoster ◽  
Intravenous Acyclovir

Varicella-zoster virus vaccination is recommended for virtually all young children in the United States, Canada, and several other countries. Varicella vaccine is a live attenuated virus that retains some of its neurotropic properties. Herpes zoster caused by vaccine virus still occurs in immunized children, although the rate is much lower than in children who had wild-type varicella. It was commonly thought that 2 varicella vaccinations would protect children against the most serious complication of meningitis following herpes zoster; however, 2 meningitis cases have already been published. We now report a third case of varicella vaccine meningitis and define risk factors shared by all 3 immunized adolescents. The diagnosis in cerebrospinal fluid in this third case was verified by amplifying and sequencing portions of the viral genome, to document fixed alleles found only in the vaccine strain. Viral antibody was also detected in the cerebrospinal fluid by confocal microscopy. When compared with the other 2 cases, remarkably all 3 were 14 years old when meningitis occurred. All 3 were treated with intravenous acyclovir, with complete recovery. The adolescent in our case report also had recurrent asthma, which was treated with both prednisone tablets and beclomethasone inhaler before onset of meningitis. When the 3 cases were considered together, they suggested that immunity to varicella-zoster virus may be waning sufficiently in some twice-immunized adolescents to make them vulnerable to varicella vaccine virus reactivation and subsequent meningitis. This complication rarely happens in children after wild-type varicella.

Rapid Molecular Discrimination between Infection with Wild-Type Varicella-Zoster Virus and Varicella Vaccine Virus

Infection ◽  
2002 ◽  
Vol 30 (5) ◽  
pp. 320-322 ◽  
Author(s):  
U. Lässker ◽  
T. C. Harder ◽  
M. Hufnagel ◽  
M. Suttorp
Keyword(s):  
Varicella Zoster Virus ◽  
Varicella Vaccine ◽  
Vaccine Virus ◽  
Wild Type ◽  
Varicella Zoster

scholarly journals Improved Identification and Differentiation of Varicella-Zoster Virus (VZV) Wild-Type Strains and an Attenuated Varicella Vaccine Strain Using a VZV Open Reading Frame 62-Based PCR

2000 ◽  
Vol 38 (9) ◽  
pp. 3156-3160 ◽  
Author(s):  
Vladimir N. Loparev ◽  
Takele Argaw ◽  
Philip R. Krause ◽  
Michiko Takayama ◽  
D. Scott Schmid
Keyword(s):  
Varicella Zoster Virus ◽  
Vaccine Strain ◽  
Varicella Vaccine ◽  
Open Reading Frame ◽  
Cleavage Sites ◽  
Wild Type ◽  
Reading Frame ◽  
Varicella Zoster ◽  
Enzyme Cleavage ◽  
Type Strains

A new method was developed to identify and differentiate varicella-zoster virus (VZV) wild-type strains from the attenuated varicella Oka vaccine strain. The PCR technique was used to amplify a VZV open reading frame (ORF) 62 region. A single specific amplicon of 268 bp was obtained from 71 VZV clinical isolates and several laboratory strains. Subsequent digestion of the VZV ORF 62 amplicons with SmaI enabled accurate strain differentiation (threeSmaI sites were present in amplicons of vaccine strain VZV, compared with two enzyme cleavage sites for all other VZV strains tested). This method accurately differentiated the Oka vaccine strain from wild-type VZV strains circulating in countries representing all six populated continents. Moreover, the assay more reliably distinguished wild-type Japanese strains from the vaccine strain than did previously described methods.

Varicella Vaccine Reflux

PEDIATRICS ◽  
1992 ◽  
Vol 89 (2) ◽  
pp. 354-354
Author(s):  
C. J. WHITE
Keyword(s):  
Varicella Zoster Virus ◽  
Primary Infection ◽  
Lymphoblastic Leukemia ◽  
Varicella Vaccine ◽  
Wild Type Virus ◽  
Type Virus ◽  
Wild Type ◽  
Varicella Zoster ◽  
Attenuated Virus ◽  
Sensory Root

In Reply.— Herpes zoster (shingles) is the dermatomal skin eruption resulting from the reactivation of varicella-zoster virus remaining latent in posterior sensory root ganglia following childhood chickenpox (the primary infection with varicella-zoster virus). Since the live attenuated varicella-zoster virus contained in the vaccine replicates in the vaccinee similar to the wild-type virus, establishment of latency is possible for the attenuated strain. Several publications have addressed latency of the attenuated virus following immunization. Two studies have examined the incidence of zoster in children with acute lymphoblastic leukemia (ALL) following immunization with live attenuated varicella-zoster virus.

Varicella-Zoster Virus (Varicella and Shingles)

2021 ◽  
Author(s):  
Anne Gershon
Keyword(s):  
Varicella Zoster Virus ◽  
Varicella Vaccine ◽  
The United States ◽  
Primary Immune Response ◽  
Wild Type Virus ◽  
High Dose ◽  
Healthy Children ◽  
Zoster Vaccine ◽  
Live Attenuated Vaccine ◽  
Varicella Zoster

A live attenuated vaccine against varicella (later also used to prevent zoster) was developed in 1974 by Takahashi and colleagues. Varicella vaccine was licensed for universal immunization of healthy children in the United States in 1995. It is also now used for this purpose in at least 15 additional countries all over the world. Varicella is disappearing in the US. Varicella vaccine has proven extremely safe and side effects are unusual, mild, and less serious than varicella or its complications. 85% of children are protected completely after 1 dose; the 15% who develop varicella despite immunization usually (but not always) have mild infections. These 15%, however, can transmit the wild type virus to others. Therefore, for optimal effect, 2 doses are required, mostly to address children who did not have an optimal primary immune response after the first dose. Waning immunity does not seem to pose a serious problem, but surveillance of vaccinees is continuing. It was demonstrated in 2005 that at a high dose of vaccine – 15 times higher than that used for prevention of varicella in children - zoster in adults can also be safely prevented. The live attenuated zoster vaccine is effective in approximately 50% of healthy individuals over age 60 who have had varicella in the past, and therefore have latent infection with varicella-zoster virus. It is given as one dose, but its effect runs out about 8 years after vaccination. In 2017, a new vaccine against zoster was also introduced. This is a subunit vaccine which does not contain contagious virus. It is even more effective than the older zoster vaccine and is over 95% effective in adults 50–≥70 years of age in preventing zoster and post herpetic neuralgia.

scholarly journals 2767. Variation in Incidence of Pediatric Herpes Zoster by First- and Second-Dose Varicella Vaccine Formulations

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S975-S976
Author(s):  
Sheila Weinmann ◽  
Stephanie Irving ◽  
Padma Koppolu ◽  
Allison Naleway ◽  
Edward Belongia ◽  
...  
Keyword(s):  
Herpes Zoster ◽  
Varicella Vaccine ◽  
Vaccine Dose ◽  
Varicella Vaccination ◽  
Vaccine Formulation ◽  
Wild Type ◽  
Varicella Zoster ◽  
Dose Formulation ◽  
Using Data ◽  
Rate Ratios

Abstract Background Varicella (VAR) and measles-mumps-rubella (MMR) vaccines are recommended for children at ages 12–15 months and 4–6 years. These are administered as separate MMR and VAR vaccines (MMR+VAR) or as combined measles-mumps-rubella-varicella (MMRV) vaccine. Herpes zoster (HZ), caused by wild-type or vaccine-strain varicella-zoster virus, can occur in children after varicella vaccination. It is unknown whether HZ incidence after varicella vaccination varies by vaccine formulation or simultaneous receipt of MMR. Methods Using data from six integrated health systems, we examined HZ incidence among children who turned 12 months old during 2003–2008 and received varicella and MMR vaccines according to routine recommendations. All HZ cases ≥ 21 days after first varicella vaccination were identified using ICD-9 codes from inpatient, outpatient, emergency room encounters, and claims data, through 2014. HZ incidence was examined by vaccine formulation (MMR+VAR, MMRV, or VAR without same-day MMR) and doses received and compared using incidence rate ratios (IRR). Results Among 199,797 children, we identified 601 HZ cases. Crude HZ incidence after first-dose MMR+VAR (18.6 [95% CI 11.1–29.2] cases/100,000 person-years) was similar to the rate after first-dose MMRV (17.9 [95% CI 10.6–28.3] cases/100,000 person-years), but approximately double the rate among those with first-dose VAR without same-day MMR (7.5 [95% CI 3.1–15.0] cases/100,000 person-years); see Table 1. The IRR for HZ after first-dose MMR+VAR or MMRV, compared with VAR, was 2.5 (95% CI 1.4–4.4; P = 0.002). When examining any first or second dose formulation, crude HZ incidence was lower after the second varicella vaccine dose (13.9 cases/100,000 person-years), than in the period before the second dose (i.e., between first and second doses or after the first dose in children with only one dose; 21.8 cases/100,000 person-years, P < 0.0001). HZ incidence was also lower after two varicella vaccine doses in each of the three first-dose formulation groups. Conclusion HZ incidence among children varied by first-dose varicella vaccine formulation and number of varicella vaccine doses. Regardless of the first-dose varicella vaccine formulation, children who received two vaccine doses had lower HZ incidence after the second dose. Disclosures All authors: No reported disclosures.

Nectin-1 is an entry mediator for VZV infection of human neurons

2021 ◽  
Author(s):  
Labchan Rajbhandari ◽  
Priya Shukla ◽  
Balaji Jagdish ◽  
Abby Mandalla ◽  
Qingxue Li ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Mammalian Cells ◽  
Primary Infection ◽  
Transcriptional Profiling ◽  
Varicella Vaccine ◽  
Ectopic Expression ◽  
Neuronal Model ◽  
Morbidity And Mortality ◽  
Varicella Zoster ◽  
Human Neurons

Varicella zoster virus (VZV) maintains lifelong latency in neurons following initial infection and can subsequently be reactivated to result in herpes zoster or severe neurological manifestations such as encephalitis. Mechanisms of VZV neuropathogenesis have been challenging to study due to the strict human tropism of the virus. While neuronal entry mediators of other herpesviruses, including herpes simplex virus, have been identified, little is known regarding how VZV enters neurons. Here, we utilize a human stem cell based neuronal model to characterize cellular factors that mediate entry. Through transcriptional profiling of infected cells, we identify the cell adhesion molecule nectin-1 as a candidate mediator of VZV entry. Nectin-1 is highly expressed in the cell bodies and axons of neurons. Either knockdown of endogenous nectin-1 or incubation with soluble forms of nectin-1 produced in mammalian cells results in a marked decrease in infectivity of neurons. Notably, while addition of soluble nectin-1 during viral infection inhibits infectivity, addition after infection has no effect on infectivity. Ectopic expression of human nectin-1 in a cell line resistant to productive VZV infection confers susceptibility to infection. In summary, we have identified nectin-1 as a neuronal entry mediator of VZV. IMPORTANCE Varicella zoster virus (VZV) causes chickenpox, gains access to neurons during primary infection where it resides lifelong, and can later be reactivated. Reactivation is associated with shingles and postherpetic neuralgia, as well as with severe neurologic complications including vasculitis and encephalitis. Although the varicella vaccine substantially decreases morbidity and mortality associated with primary infection, the vaccine cannot prevent development of neuronal latency and vaccinated populations are still at risk for reactivation. Furthermore, immunocompromised individuals are at higher risk for VZV reactivation and associated complications. Little is known regarding how VZV enters neurons. Here, we identify nectin-1 as an entry mediator of VZV in human neurons. Identification of nectin-1 as a neuronal VZV entry mediator could lead to improved treatments and preventative measures to reduce VZV related morbidity and mortality.

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