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The varicella-autoantibody syndrome
C Josephson1, R Nuss, L Jacobson
1Departments of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
Pediatric Research
|August 24, 2001
Summary
Varicella zoster virus (VZV) infection in children frequently causes transient autoantibodies to phospholipids and coagulation proteins. These antibodies are common but do not predict thrombotic complications.
Area of Science:
- Immunology
- Pediatrics
- Hematology
Background:
- Varicella zoster virus (VZV) infection can be associated with thrombotic complications.
- The role of autoantibodies in VZV-associated thrombosis requires further investigation.
Purpose of the Study:
- To determine the incidence of autoantibodies to phospholipids and coagulation proteins in children with acute VZV infection.
- To investigate the association between these autoantibodies and thrombotic complications in children with VZV.
Main Methods:
- Cross-sectional study comparing VZV-infected children (with and without complications) to a control group.
- Assay for free protein S (PS), protein C, antithrombin, prothrombin, associated antibodies, lupus anticoagulant, anticardiolipin antibody, antiphospholipid antibodies, and prothrombin fragment 1+2.
- Data on coinfections were collected.
Main Results:
- VZV-infected children showed increased frequency of lupus anticoagulant, anticardiolipin antibody, antiphospholipid antibodies, and autoantibodies to PS, protein C, prothrombin, and antithrombin compared to controls.
- Children with VZV and purpura fulminans/thromboembolism had decreased free PS, increased PS IgG antibody, and increased prothrombin fragment 1+2.
- Elevated PS IgG antibody correlated negatively with free PS and positively with prothrombin fragment 1+2; autoantibodies were transient.
Conclusions:
- Transient antiphospholipid and coagulation protein autoantibodies are common in children with VZV infection.
- These autoantibodies are not predictive of thrombotic complications.
- Further research may explore the mechanisms linking VZV infection to autoantibody production.