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Journal of Virology, September 2003, p. 9412-9421, Vol. 77, No. 17
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.17.9412-9421.2003

Edmonston Measles Virus Prevents Increased Cell Surface Expression of Peptide-Loaded Major Histocompatibility Complex Class II Proteins in Human Peripheral Monocytes

Mamadi Yilla,^* Carole Hickman, Marcia McGrew, Elizabeth Meade, and William J. Bellini

Respiratory and Enteric Viruses Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333

Received 4 March 2003/ Accepted 29 May 2003

Gamma interferon (IFN-) induces expression of the gene products of the major histocompatibility complex (MHC), whereas IFN-/ß can interfere with or suppress class II protein expression. In separate studies, measles virus (MV) was reported to induce IFN-/ß and to up-regulate MHC class II proteins. In an attempt to resolve this paradox, we examined the surface expression of MHC class I and class II proteins in MV-infected peripheral monocytes in the presence and absence of IFN-/ß. Infection of purified monocytes with Edmonston B MV resulted in an apparent increase in cell surface expression of HLA-A, -B, and -C class I proteins, but it had no effect on the expression of HLA-DR class II proteins. MV-infected purified monocytes expressed IFN-/ß, but no measurable IFN- expression was detected in supernatant fluids. Class II protein expression could be enhanced by coculture of purified monocytes with uninfected peripheral blood mononuclear cell (PBMC) supernatant. MV infection of PBMCs also did not affect expression of class II proteins, but the expression of HLA-A, -B, and -C class I proteins was increased two- to threefold in most donor cells. A direct role for IFN-/ß suppression of MHC class II protein expression was not evident in monocytes since MV suppressed class II protein expression in the absence of IFN-/ß. Taken together, these data suggest that MV interferes with the expression of peptide-loaded class II complexes, an effect that may potentially alter CD4⁺-T-cell proliferation and the cell-mediated immune responses that they help to regulate.

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* Corresponding author. Mailing address: Centers for Disease Control and Prevention, 1600 Clifton Rd., MS-C22, Atlanta, GA 30333. Phone: (404) 639-3512. Fax: (404) 639-4187. E-mail: mby7{at}cdc.gov.

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Journal of Virology, September 2003, p. 9412-9421, Vol. 77, No. 17
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.17.9412-9421.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

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