Cytomegalovirus inhibits major histocompatibility class II expression on infected endothelial cells

Daniel D. Sedmak, Anna M. Guglielmo, Deborah A. Knight, Daniel J. Birmingham, Emina H. Huang, W. James Waldman

Research output: Contribution to journalArticlepeer-review

75 Scopus citations


Persistent human cytomegalovirus (HCMV) infections are responsible for significant morbidity and mortality in immunocompromised individuals. One mechanism by which HCMV may develop persistence after primary infection is through inhibition of host cell human leukocyte antigen (HLA) class II expression with resultant escape from normal antiviral immune surveillance. Immunofluorescence flow cytometry of human endothelial cell (EC) cultures infected with HCMV AD169 and an EC propagated strain, VHL/E, showed a marked reduction in interferon-γ (IFN-γ)-induced surface expression of HLA-DR. This inhibition did not occur when EC were treated with ultraviolet- inactivated virus and IFN-γ. HCMV, as determined by dual-labeling immunohistochemistry, inhibited induction of surface and cytoplasmic class II antigens specifically in infected cells. HCMV infection also inhibited IFN- γ and tumor necrosis factor-α up-regulation of HLA class 1 expression. Northern blot analysis of infected, IFN-γ-treated human umbilical vein endothelial cells revealed an absence of class II mRNA. Persistence of HCMV may result in part from its ability to inhibit HLA class II induction in infected cells.

Original languageEnglish (US)
Pages (from-to)683-692
Number of pages10
JournalAmerican Journal of Pathology
Issue number4
StatePublished - Apr 1994
Externally publishedYes

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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