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Journal of Virology, August 2003, p. 8187-8195, Vol. 77, No. 15
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.15.8187-8195.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Placental Extravillous Cytotrophoblasts Persistently Express Class I Major Histocompatibility Complex Molecules after Human Cytomegalovirus Infection

Masakazu Terauchi,1 Hideki Koi,1 Chikako Hayano,1 Noriko Toyama-Sorimachi,2 Hajime Karasuyama,2 Yuji Yamanashi,3 Takeshi Aso,1 and Masaki Shirakata3*

Department of Comprehensive Reproductive Medicine,1 Department of Immune Regulation, Graduate School,2 Department of Cell Regulation, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo, Tokyo 113-8510, Japan3

Received 19 February 2003/ Accepted 5 May 2003

Human cytomegalovirus (HCMV) downregulates the class I major histocompatibility complexes (MHCs), HLA-A and -B, in infected fibroblasts to escape from antigen-specific cytotoxic T lymphocytes. The HCMV genes responsible for the downregulation of MHCs are US2, US3, US6, and US11, which encode type I membrane proteins working at the endoplasmic reticulum (ER). However, it is largely unknown whether HCMV downregulates the class I MHC molecules in placental extravillous cytotrophoblasts (EVT), which express HLA-C, -E, and -G to protect a semiallogenic fetus from maternal natural killer (NK) cells at the fetomaternal interface. Here, we report that differentiated EVT prepared from human first-trimester chorionic villi persistently express class I MHC molecules upon HCMV infection. When these US proteins were expressed in uninfected EVT, they were localized at the ER in the entire cytoplasm. However, subsequent HCMV infection resulted in dissociation of these US proteins from the ER, which relocated toward the cell membrane. In fibroblasts, these US proteins were localized at the ER before and after HCMV infection. These results suggest that the US gene products are not integrated into ER of HCMV-infected EVT and fail to downregulate class I MHC molecules.

* Corresponding author. Mailing address: Department of Cell Regulation, Medical Research Institute, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo, Tokyo 113-8510, Japan. Phone: (81) 3-5803-5815. Fax: (81) 3-5803-0241. E-mail: shirakata.creg{at}mri.tmd.ac.jp.

Journal of Virology, August 2003, p. 8187-8195, Vol. 77, No. 15
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.15.8187-8195.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hannemann, H., Rosenke, K., O'Dowd, J. M., Fortunato, E. A. (2009). The Presence of p53 Influences the Expression of Multiple Human Cytomegalovirus Genes at Early Times Postinfection. J. Virol. 83: 4316-4325 [Abstract] [Full Text]  


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