Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus
The enteric human adenoviruses of species F (HAdVs-F), which comprise HAdV-F40 and HAdV-F41, are significant pathogens that cause acute gastroenteritis in children worldwide. The early transcription unit 3 (E3) of HAdVs-F is markedly different from that of all other HAdV species. To date, the E3 pro...
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| Format: | Article |
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MDPI AG
2021-07-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/13/7/1289 |
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| author | Edson R. A. Oliveira Lenong Li Marlene Bouvier |
| author_facet | Edson R. A. Oliveira Lenong Li Marlene Bouvier |
| author_sort | Edson R. A. Oliveira |
| collection | DOAJ |
| description | The enteric human adenoviruses of species F (HAdVs-F), which comprise HAdV-F40 and HAdV-F41, are significant pathogens that cause acute gastroenteritis in children worldwide. The early transcription unit 3 (E3) of HAdVs-F is markedly different from that of all other HAdV species. To date, the E3 proteins unique to HAdVs-F have not been characterized and the mechanism by which HAdVs-F evade immune defenses in the gastrointestinal (GI) tract is poorly understood. Here, we show that HAdV-F41 infection of human intestinal HCT116 cells upregulated the expression of MHC class I-related chain A (MIC A) and MIC B relative to uninfected cells. Our results also showed that, for MIC B, this response did not however result in a significant increase of MIC B on the cell surface. Instead, MIC B was largely sequestered intracellularly. Thus, although HAdV-F41 infection of HCT116 cells upregulated MIC B expression, the ligand remained inside infected cells. A similar observation could not be made for MIC A in these cells. Our preliminary findings represent a novel function of HAdVs-F that may enable these viruses to evade immune surveillance by natural killer (NK) cells in the infected gut, thereby paving the way for the future investigation of their unique E3 proteins. |
| first_indexed | 2024-03-10T09:20:28Z |
| format | Article |
| id | doaj.art-1524e0e51d814704a5f59743b921637b |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-03-10T09:20:28Z |
| publishDate | 2021-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-1524e0e51d814704a5f59743b921637b2023-11-22T05:13:40ZengMDPI AGViruses1999-49152021-07-01137128910.3390/v13071289Intracellular Sequestration of the NKG2D Ligand MIC B by Species F AdenovirusEdson R. A. Oliveira0Lenong Li1Marlene Bouvier2Department of Microbiology and Immunology, University of Illinois at Chicago, 909 S Wolcott Avenue, Chicago, IL 60612, USADepartment of Microbiology and Immunology, University of Illinois at Chicago, 909 S Wolcott Avenue, Chicago, IL 60612, USADepartment of Microbiology and Immunology, University of Illinois at Chicago, 909 S Wolcott Avenue, Chicago, IL 60612, USAThe enteric human adenoviruses of species F (HAdVs-F), which comprise HAdV-F40 and HAdV-F41, are significant pathogens that cause acute gastroenteritis in children worldwide. The early transcription unit 3 (E3) of HAdVs-F is markedly different from that of all other HAdV species. To date, the E3 proteins unique to HAdVs-F have not been characterized and the mechanism by which HAdVs-F evade immune defenses in the gastrointestinal (GI) tract is poorly understood. Here, we show that HAdV-F41 infection of human intestinal HCT116 cells upregulated the expression of MHC class I-related chain A (MIC A) and MIC B relative to uninfected cells. Our results also showed that, for MIC B, this response did not however result in a significant increase of MIC B on the cell surface. Instead, MIC B was largely sequestered intracellularly. Thus, although HAdV-F41 infection of HCT116 cells upregulated MIC B expression, the ligand remained inside infected cells. A similar observation could not be made for MIC A in these cells. Our preliminary findings represent a novel function of HAdVs-F that may enable these viruses to evade immune surveillance by natural killer (NK) cells in the infected gut, thereby paving the way for the future investigation of their unique E3 proteins.https://www.mdpi.com/1999-4915/13/7/1289adenovirusesadenovirus species Fviral tropismgut immune systementeric virusesimmune evasion |
| spellingShingle | Edson R. A. Oliveira Lenong Li Marlene Bouvier Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus Viruses adenoviruses adenovirus species F viral tropism gut immune system enteric viruses immune evasion |
| title | Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus |
| title_full | Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus |
| title_fullStr | Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus |
| title_full_unstemmed | Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus |
| title_short | Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus |
| title_sort | intracellular sequestration of the nkg2d ligand mic b by species f adenovirus |
| topic | adenoviruses adenovirus species F viral tropism gut immune system enteric viruses immune evasion |
| url | https://www.mdpi.com/1999-4915/13/7/1289 |
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