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Unit Code 800196:
Varicella-Zoster Virus (VZV) Antibody, IgG and IgM, Serum

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Useful For

Diagnosing acute-phase infection with VZV

Clinical Information

Varicella-zoster virus (VZV), a herpesvirus, causes 2 exanthematous

(rash-associated) diseases: chickenpox and herpes zoster (shingles).

Chickenpox is a highly contagious disease usually contracted during

childhood and is characterized by a dermal vesiculopustular rash

that develops in successive crops. Although primary infection results

in immunity to subsequent exposure to chickenpox, the virus remains

latent in the body, localized to the dorsal root or cranial nerve ganglia.

Reactivation of latent infection manifests as herpes zoster. On reactivation,

the virus migrates along neural pathways to the skin, producing a

unilateral rash usually limited to a single dermatome. Reactivation

occurs in older adults and in patients with impaired cellular immunity.

 

Several populations are at risk of suffering an unusually severe

reaction to VZV infections. The infection in pregnant women may

spread through the placenta to the fetus, causing congenital

disease in the infant. Immunocompromised patients in hospitals

may contract severe nosocomial infections from others who have

active VZV infections. Therefore, serologic screening of direct

health-care providers (physicians, allied health-care personnel)

and individuals in high-risk groups is necessary to avoid

uncontrolled spread of infection.

 

While the clinical presentation of VZV infection is generally characteristic,

serologic evaluation of patients with atypical and systemic infections is

often required. For example, it is extremely important to serologically

evaluate patients for the early detection of VZV infections in hospital

settings. Nosocomial spread of VZV infection can be life-threatening to

immunocompromised patients susceptible to infection.

Reference Values

IgG

      Negative (reported as positive or negative)

      A negative result indicates nonimmunity.

IgM

      Negative (reported as positive or negative)

 

See "Virology" in Special Instructions for additional interpretive

information.

Interpretation

A positive IgG result coupled with a positive IgM result indicates 

recent infection with VZV.

 

A positive IgG result coupled with a negative IgM result indicates

previous exposure to VZV and immunity.

 

A negative IgG result coupled with a negative IgM result indicates the

absence of prior exposure to VZV and nonimmunity. However, a

negative result does not rule out a VZV infection. The specimen

may have been drawn before the appearance of detectable antibodies.

Negative results in suspected early VZV infections should be followed

by testing a new serum specimen in 2-3 weeks.

 

Equivocal results should be followed up with testing a new serum

specimen within 10-14 days.

Cautions

The performance characteristics with individuals vaccinated with

VZV (OKA Strain) have not been established.

 

The test must be performed on serum. The use of whole blood,

plasma, or cord blood has not been established.

 

Positive results from cord blood or neonates should be interpreted

with caution.

 

Results from immunocompromised patients should be interpreted

with caution.

 

Heterotypic antibody titer rises in response to VZV may occur in

certain patients with herpes simplex virus (HSV) infection who have

experienced a prior infection with VZV.

Special Instructions and Forms

 Virology 

Clinical Reference

1.   Kennedy PG:  Latent varicella-zoster virus is located predominantly

      in neurons in human trigeminal ganglia. Proc Natl Acad Sci USA

      1998;95:4658-4662

 

2.   McPherson RE:  Herpes zoster ophthalmicus and the immuno-

      compromised host: a case report and review. J Am Optom Assoc

      1997;68:527-538

 

3.   Papanicolaou GA, Meyers BR, Fuchs WS, et al:  Infectious

      ocular complications in orthotopic liver transplant patients.

      Clin Infect Dis 1997;24:1172-1177

 

4.   Flamholc L:  Neurological complications in herpes zoster. Scand

      J Infect Dis 1996;100:35-40


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