Abstract
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.
Highlights
HAdVs represents a large family of genetically diverse pathogens
early transcription unit 3 (E3) proteins are found in all species, others have counterparts in only a few species, and some E3 proteins are unique to a given species
HAdV-F lacks the common some E3 proteins are unique to a given species
Summary
HAdVs represents a large family of genetically diverse pathogens. To date, more than 100 different HAdVs have been identified and classified into seven species, A toG (http://hadvwg.gmu.edu/ (accessed on 22 November 2019)). E3 is one of the most divergent gene regions between species (see Figure 1) This genetic variability is not well understood, but it strongly suggests that E3 proteins play a role in the manifestation of species-specific tissue tropism and diseases [6]. The 19K protein of HAdV-C binds to and retains MHC class I molecules in the endoplasmic reticulum, thereby rendering HAdV-C-infected cells less efficient at presenting viral antigens and less sensitive to lysis by CD8+ T cells [8,9,10,11,12,13,14,15,16,17,18,19,20,21,22] That this 19K gene is maintained in HAdV-B, -D, and -E
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