Varicella-zoster virus infection causes two clinically distinct forms of disease, depending on whether an individual is experiencing a primary (chickenpox) or secondary infection (shingles)1. Varicella-zoster virus is highly contagious, spread by exposure to an individual shedding virus from either a varicella or herpes zoster infection. The virus can be spread from person to person by direct contact, inhalation of aerosols from vesicular fluid of skin lesions of acute varicella or zoster and possibly through infected respiratory secretions that also may be aerosolized2.
Common complications of VZV infection are bacterial infections of the skin and soft tissue in children and pneumonia in adults. Severe complications include encephalitis, pneumonia (either direct viral pneumonia or secondary bacterial pneumonia), bronchitis (either viral bronchitis or secondary bacterial bronchitis), visceral dissemination (VZV infection of internal organs) and postherpetic neuralgia in immunocompromised individuals. VZV can also complicate pregnancy; newborns of infected mothers have a small risk of developing congenital varicella syndrome or neonatal varicella2.
Moreover VZV is recognized as one of the leading causes of adult encephalitis and in several studies, VZV was the second most common etiology identified, second only to HSV3. It is estimated that greater than 90 percent of the population will acquire the pathogen by the age of 15 and each of these persons is at risk for developing encephalitis caused by VZV4.
1. Albrecht MA. (2017, May 31). Diagnosis of varicella-zoster virus infection. UpToDate. Retrieved on 06/27/2018 from https://www.uptodate.com/contents/diagnosis-of-varicella-zoster-virus-infection.
2. Centers for Disease Control and Prevention. (2016). Chicken Pox (Varicella). Retrieved from https://www.cdc.gov/chickenpox/hcp/clinical-overview.html.
3. Pahud BA, Glaser CA, Dekker CL, Arvin AM, and Schmid DS. Varicella zoster disease of the central nervous system: Epidemiological, clinical, and laboratory features 10 years after the introduction of the varicella vaccine. J Infect Dis. 2011; 203(3): 316–323.
4. Seward J, Jumaan A. VSV: persistence in the population. In: Arvin A, Campadelli-Fiume G, Mocarski E, et al., editors. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge: Cambridge University Press; 2007. Chapter 40. Available from: https://www.ncbi.nlm.nih.gov/books/NBK47367/.
Why to choose it
A CLIA moderate complexity assay for the direct detection of the VZV DNA polymerase gene from only 50 µl of CSF sample. The assay improves efficiency with a true sample-to-answer workflow without DNA extraction.
Reliable performance that you can count on
The Simplexa® VZV Direct assay demonstrated high performance with excellent clinical agreement against PCR/bi-directional sequencing for both prospective and contrived CSF samples. Contrived samples were tested across the clinical range of the Simplexa® VZV Direct assay. For each of the two strains, VZV Ellen and VZV 9939, 60% of the positive samples were contrived as low positive samples close to the LoD of the test.
Simplexa® VZV Direct Clinical Agreement Study
|Sample TypeCSF Sample Population||Positive % Agreement||Negative % Agreement|
|CSF Sample PopulationProspective||Positive % Agreement100.0% (12/12)
95% CI: 75.7% to 100.0%
|Negative % Agreement99.7% (623/625)a
95% CI: 98.8% to 99.9%
|CSF Sample PopulationContrived||Positive % Agreement100.0% (120/120)
95% CI: 96.9% to 100.0%
|Negative % AgreementN/A|
|a One (1) of two (2) discordant results were positive with an alternate NAAT used by collection site during routine testing.|
The Lowest Sample Volume Requirements
Our Simplexa® VZV Direct assay utilizes only 50 µl of precious CSF sample.
Simplexa® VZV Direct Kit
|Code MOL3650||Reactions 24|
Simplexa® VZV Positive Control Pack
|Code MOL3660||Reactions 10|