Strong Immune Response Can't Keep CMV Down (2 of 2) (IMAGE)
Caption
Major histocompatibility molecules (MHC-I, in red) alert killer T cells to ongoing infections by presenting fragments of viral proteins at the cell surface. These fragments are generated in the cytoplasm of infected cells, transported by the peptide transported TAP into the endoplasmic reticulum where they are loaded onto MHC-I molecules. Several proteins of cytomegalovirus inhibit this process by i) blocking the production of MHC-I protein (VIHCE), ii) mediating the destruction of MHC-I (US2, US11), iii) inhibiting TAP (US6) or iv) by preventing MHC-I to travel to the cell surface (US3). As a result of the concerted action of these proteins, infected cells become "invisible" to the T cells and the infection goes unnoticed (left side). This T cell evasion allows CMV to repeatedly infect despite the presence of CMV-specific T cells. In contrast, CMV-specific T cells eliminate incoming virus that lacks VIHCE and the US2-11 proteins so that viral protein fragments are presented by MHC-I to T cells at the cell surface (right side). This image relates to an article that appeared in the April 2, 2010, issue of Science, published by AAAS. The study, by Dr. Scott Hansen of Oregon Health and Science University in Beaverton, Ore., and colleagues, was titled, "Evasion of CD8+ T Cells Is Critical for Superinfection by Cytomegalovirus."
Credit
Image courtesy of Andrew Townsend
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