scholarly journals I-29 The natural history of infections caused by varicella-zoster virus (VZV): primary infection, transmission, latency, and reactivation.

2008 ◽  
Vol 12 ◽  
pp. S11
Author(s):  
M.D. Gershon
PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0176845 ◽  
Author(s):  
Luigi Marangi ◽  
Grazina Mirinaviciute ◽  
Elmira Flem ◽  
Gianpaolo Scalia Tomba ◽  
Giorgio Guzzetta ◽  
...  

1986 ◽  
Vol 7 (6) ◽  
pp. 312-316 ◽  
Author(s):  
Keith Krasinski ◽  
Robert S. Holzman ◽  
Rita LaCouture ◽  
Alfred Florman

AbstractVaricella-zoster virus (VZV), one of the most common highly communicable agents of disease, stimulates aggressive infection control measures. In a 1-year period, at one hospital, at least 93 inpatients (82 adult patients, 11 pediatric patients) and 2 hospital staff with active varicella-zoster infections served as potential sources of nosocomial infection. Six incidents of exposure to the virus that occurred without the protection of standard infection control precautions were investigated by the infection control surveillance team. One hundred fifty-six patients and 353 hospital staff were exposed. Fifty-one patients had no history of varicella-zoster infection, but only five were susceptible by serologic testing. One hundred one staff members had no history of varicella-zoster, but only 11 were susceptible by serologic testing. These exposures resulted in three secondary varicella-zoster infections, six courses of varicella-zoster immune globulin prophylaxis and furlough of 13 staff members. Epidemiologic investigation consumed approximately 356 hours of staff time, and management of exposed persons cost approximately $41,500. Prospective knowledge of the immune status of health care workers would vastly decrease the time and effort required to control hospital VZV exposures.


2020 ◽  
Vol 17 (1) ◽  
pp. 82-91
Author(s):  
Hardiyanti ◽  
R Ratianingsih ◽  
Hajar

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.


2018 ◽  
Vol 10 (1) ◽  
Author(s):  
Thigita A. Pandaleke ◽  
Herry E. J. Pandaleke ◽  
Ratna I. Susanti ◽  
Julieta D. P. Dotulong

Abstract: Herpes zoster (HZ) is an acute vesicular eruption caused by latent varicella zoster virus (VVZ) reactivation in sensory ganglia after primary infection. Its incidence increases with age and it is rarely found in children. We reported a case of 10-year-old male with blisters on the right side of his stomach and back 3 days ago. The patient was suffered from fever, common cold, and cough a week before, and had a history of varicella at 5 years old. Dermatologic status showed multiple vesicles on erythematous base at the anterior dan posterior sides of his right lumbar region. The Tzank test showed multinucletaed giant cells. Acyclovir resulted in significant improvement after 7- day therapy. Conclusion: Diagnosis of herpes zoster was based on anamnesis, physical examination, and laboratory findings. Antiviral drugs was aimed to reduce complications and viral shedding.Keywords: Herpes zoster, childAbstrak: Herpes zoster (HZ) merupakan erupsi vesikuler akut yang disebabkan oleh reaktivasi dari virus varisela zoster (VVZ) laten pada ganglia sensoris yang sebelumnya terpajan dengan infeksi primer varisela. Insiden HZ meningkat seiring pertambahan usia dan jarang ditemukan pada anak-anak. Kami melaporkan kasus seorang anak laki-laki, 10 tahun, dengan bintil-bintil berair di perut dan punggung sebelah kanan sejak 3 hari lalu. Riwayat demam, batuk dan pilek 1 minggu sebelum timbul lesi. Riwayat varisela pada usia 5 tahun. Status dermatologis ditemukan vesikel multipel berisi cairan jernih yang tersusun bergerombol di atas kulit yang eritema di regio lumbar dekstra anterior dan posterior. Tes Tzank memperlihatkan sel raksasa berinti banyak. Pasien diterapi dengan asiklovir oral selama 7 hari dan menunjukkan perbaikan yang bermakna. Simpulan: Anamnesis, pemeriksaan fisik, dan pemeriksaan penunjang kasus ini khas untuk herpes zoster. Pemberian obat antiviral bertujuan untuk mengurangi komplikasi dan menurunkan viral shedding.Kata kunci: herpes zoster, anak


2006 ◽  
Vol 80 (19) ◽  
pp. 9772-9778 ◽  
Author(s):  
Louise Jones ◽  
Antony P. Black ◽  
Gathsaurie N. Malavige ◽  
Graham S. Ogg

ABSTRACT Open reading frame 4 (ORF4) of varicella-zoster virus (VZV) encodes an immediate-early protein that is believed to be important for viral infectivity and establishing latency. Evidence suggests that VZV-specific T cells are crucial in the control of viral replication, but there are no data addressing the existence of potential ORF4 protein-specific CD4+ T cells. We tested the hypothesis that VZV ORF4 protein-specific CD4+ T cells could be identified and characterized within the peripheral blood of healthy immune donors following primary infection. Gamma interferon (IFN-γ) immunosorbent assays were used to screen peripheral blood mononuclear cells obtained from healthy seropositive donors for responses to overlapping ORF4 peptides, viral lysate, and live vaccine. High frequencies of ORF4 protein-specific T cells were detected ex vivo in individuals up to 52 years after primary infection. Several immunogenic regions of the ORF4 protein were identified, including a commonly recognized epitope which was restricted through HLA-DRB1*07. Total ORF4 protein-specific responses comprised 19.7% and 20.7% of the total lysate and vaccine responses, respectively, and were dominated by CD4+ T cells. Indeed, CD4+ T cells were found to dominate the overall virus-specific IFN-γ cellular immune response both ex vivo and after expansion in vitro. In summary, we have identified an ORF4 protein as a novel target antigen for persistent VZV-specific CD4+ T cells, with implications for disease pathogenesis and future vaccine development.


2021 ◽  
Author(s):  
Labchan Rajbhandari ◽  
Priya Shukla ◽  
Balaji Jagdish ◽  
Abby Mandalla ◽  
Qingxue Li ◽  
...  

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.


2018 ◽  
Vol 76 (2) ◽  
pp. 234-236
Author(s):  
Claudie Lamoureux ◽  
Charlotte Flatrès ◽  
Sophie Vallet ◽  
Adissa Tran - Minoui ◽  
Christopher Payan ◽  
...  

2019 ◽  
Vol 30 (10) ◽  
pp. 1031-1033
Author(s):  
Emma Wallis ◽  
Bahij Al-Hakim ◽  
Paul Holmes ◽  
Sam Douthwaite ◽  
Ranjababu Kulasegaram

A 34-year-old man recently diagnosed with advanced human immunodeficiency virus infection (CD4 cell count of 139 cells/mm3), not yet started on antiretroviral medications, presented to hospital with a ten-day history of left leg weakness and difficulty walking. He described a childhood history of chickenpox with previous shingles over his buttock over three years ago. Examination revealed reduced power in the left hip and knee flexors and absent knee and adductor reflexes. Lumbar punctures were performed and polymerase chain reaction (PCR) detected varicella-zoster virus (VZV) DNA. Concurrent serum samples for VZV PCR were negative. The patient was diagnosed with VZV radiculopathy and treated with high-dose intravenous acyclovir. Within two days, neurological signs improved. Previous case reports define VZV radiculopathy by a temporal and geographical relationship with a zoster rash. Our diagnosis was based on a clinical picture of radiculopathy with virological evidence in CSF and confirmed by a dramatic clinical response to treatment. We propose that lumbar puncture and detection of VZV DNA by PCR in the cerebrospinal fluid (CSF) is an invaluable investigation that should be considered in the workup of immunosuppressed patients presenting with a radiculopathy.


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