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Journal of Virology, July 2003, p. 7872-7879, Vol. 77, No. 14
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.14.7872-7879.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Increased Thymic Output during Acute Measles Virus Infection

Sallie R. Permar,1 William J. Moss,1,2 Judith J. Ryon,1 Daniel C. Douek,3 Mwaka Monze,4 and Diane E. Griffin1*

W. Harry Feinstone Department of Molecular Microbiology and Immunology,1 Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205-2179,2 Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland,3 Virology Laboratory, University Teaching Hospital, Lusaka, Zambia4

Received 22 January 2003/ Accepted 23 April 2003

Measles virus infects thymic epithelia, induces a transient lymphopenia, and impairs cell-mediated immunity, but thymic function during measles has not been well characterized. Thirty Zambian children hospitalized with measles were studied at entry, hospital discharge, and at 1-month follow-up and compared to 17 healthy children. During hospitalization, percentages of naïve (CD62L+, CD45RA+) CD4+ and CD8+ T lymphocytes decreased (P = 0.01 for both), and activated (HLA-DR+, CD25+, or CD69+) CD4+ and CD8+ T lymphocytes increased (P = 0.02 and 0.03, respectively). T-cell receptor rearrangement excision circles (TRECs) in measles patients were increased in CD8+ T cells at entry compared to levels at hospital discharge (P = 0.02) and follow-up (P = 0.04). In CD4+ T cells, the increase in TRECS occurred later but was more sustained. At discharge, TRECs in CD4+ T cells (P = 0.05) and circulating levels of interleukin-7 (P = 0.007) were increased compared to control values and remained elevated for 1 month, similar to observations in two measles virus-infected rhesus monkeys. These findings suggest that a decrease in thymic output is not the cause of the lymphopenia and depressed cellular immunity associated with measles.

* Corresponding author. Mailing address: W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe St., Baltimore, MD 21205. Phone: (410) 955-3459. Fax: (410) 955-0105. E-mail: dgriffin{at}jhsph.edu.

Journal of Virology, July 2003, p. 7872-7879, Vol. 77, No. 14
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.14.7872-7879.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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