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PLoS Pathogens Issue Image | Vol. 7(11) November 2011

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Human herpesvirus-7 (HHV-7) U21 causes redistribution of NK-activating ligands to lysosomes.

Herpesviruses have evolved a stunning array of mechanisms to escape immune detection, both by CTLs and NK cells. The HHV-7 U21 open reading frame encodes a protein that can bind to and reroute both class I MHC molecules and the NK-activating ligand ULBP1 to the lysosomal compartment. This deconvolved widefield epifluorescence micrograph shows co-localization of the NK-activating ligand ULBP1 with lamp2, a lysosomal membrane protein, in U21-expressing astrocytoma cells. Alexafluor-488- and -598-conjugated secondary antibodies were used to label antibodies directed against lamp2 (green) and HHV-7 U21 (magenta). Light green-white indicates co-localization (see Schneider and Hudson, doi:10.1371/journal.ppat.1002362).

Image Credit: Amy W. Hudson and Christine L. Schneider, Department of Microbiology and Molecular Genetics, Medical College of Wisconsin

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Human herpesvirus-7 (HHV-7) U21 causes redistribution of NK-activating ligands to lysosomes.

Herpesviruses have evolved a stunning array of mechanisms to escape immune detection, both by CTLs and NK cells. The HHV-7 U21 open reading frame encodes a protein that can bind to and reroute both class I MHC molecules and the NK-activating ligand ULBP1 to the lysosomal compartment. This deconvolved widefield epifluorescence micrograph shows co-localization of the NK-activating ligand ULBP1 with lamp2, a lysosomal membrane protein, in U21-expressing astrocytoma cells. Alexafluor-488- and -598-conjugated secondary antibodies were used to label antibodies directed against lamp2 (green) and HHV-7 U21 (magenta). Light green-white indicates co-localization (see Schneider and Hudson, doi:10.1371/journal.ppat.1002362).

Image Credit: Amy W. Hudson and Christine L. Schneider, Department of Microbiology and Molecular Genetics, Medical College of Wisconsin

https://doi.org/10.1371/image.ppat.v07.i11.g001