Disseminated varicella infection caused by varicella vaccine strain in a child with low invariant natural killer T cells and diminished CD1d expression

Banovic, Tatjana, Yanilla, Mayonelo, Simmons, Russell, Robertson, Ian, Schroder, Wayne A., Raffelt, Neil. C., Wilson, Yana A., Hill, Geoffrey R., Hogan, Patrick and Nourse, Clare B. (2011) Disseminated varicella infection caused by varicella vaccine strain in a child with low invariant natural killer T cells and diminished CD1d expression. Journal of Infectious Diseases, 204 12: 1893-1901. doi:10.1093/infdis/jir660


Author Banovic, Tatjana
Yanilla, Mayonelo
Simmons, Russell
Robertson, Ian
Schroder, Wayne A.
Raffelt, Neil. C.
Wilson, Yana A.
Hill, Geoffrey R.
Hogan, Patrick
Nourse, Clare B.
Title Disseminated varicella infection caused by varicella vaccine strain in a child with low invariant natural killer T cells and diminished CD1d expression
Journal name Journal of Infectious Diseases   Check publisher's open access policy
ISSN 0022-1899
1537-6613
Publication date 2011-12
Sub-type Article (original research)
DOI 10.1093/infdis/jir660
Volume 204
Issue 12
Start page 1893
End page 1901
Total pages 9
Place of publication NC, United States
Publisher Oxford University Press
Collection year 2012
Language eng
Formatted abstract
Background. Live attenuated varicella vaccine is considered a safe vaccine with serious adverse effects reported only in immunocompromised children. We describe a severe life-threatening infection with varicella vaccine virus causing rash and pneumonitis in a 6-year-old boy with no apparent immunodeficiency.
Methods and Results. Polymerase chain reaction (PCR) analysis of vesicle swab samples demonstrated varicella zoster virus (VZV). Sequencing of the PCR product demonstrated 100% homology with human herpesvirus 3 strain VZV-Oka ORF62 gene. Routine immunologic investigations failed to demonstrate any abnormality. Total leukocyte, lymphocyte, and neutrophil counts and lymphocyte subsets were normal. Immunoglobulins, C3, C4, and CH50 were intact. Specific IgG to protein and polysaccharide antigens and to Epstein–Barr virus and cytomegalovirus were present. Normal lymphocyte proliferation to phytohemagglutinin and VZV antigens was detected. Neutrophil function and natural killer (NK) cell activity were normal. The analysis of invariant NK T (iNKT) cell numbers and function revealed diminished iNKT cells, reported once previously and unique to our patient, deficient expression of the cognate receptor, CD1d.
Conclusions. This report provides a further link between deficiency of the iNKT/CD1d pathway and increased susceptibility to varicella vaccine virus, suggesting an important role of this innate pathway in host defense against yet another member of the herpesvirus family.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2012 Collection
School of Medicine Publications
 
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