This study examined the perceptions of authenticity in cultural portrayals by both visitors and indigenous tourism operators in Far North Queensland. Surveys were administered over a two week period to indigenous tour operators and visitors at six locations throughout the region. The results showed that tourists place a high value on authenticity and the majority of them who had participated in an indigenous experience were satisfied with its level of authenticity. The study further found that the use of theatrical effects in cultural presentations was viewed negatively by tourists. A few indigenous tour operators were found to place a higher premium on maintaining the pride of their community's cultural values, rather than work collaboratively with external corporations to provide titillating, but barely authentic, tourism experiences. The overwhelming consensus from all those interviewed was that players in the indigenous tourism market are still grappling with how they could appeal to a broad range of tourists without losing authenticity in their presentation of culture. The solution is likely to be found in local capacity building and multi-stakeholder engagement, not least the involvement of governing authorities and the mainstream tourism sector.

The extent to which unconventional forms of antigen presentation drive T cell immunity is unknown. By convention, CD8 T cells recognize viral peptides in association with classical major histocompatibility complex (MHC) class I, or MHC-Ia, but immune surveillance can in some cases be directed against peptides presented by non-classical MHC-Ib, for example the MHC-E proteins (Qa-1 in mice and HLA-E in humans); however, the overall importance of non-classical responses in antiviral immunity remains unclear. Similarly uncertain is the importance of “cryptic” viral epitopes, defined as those undetectable by conventional mapping techniques. Here, we used an immunopeptidomics approach to search for unconventional epitopes that drive T cell responses in mice infected with influenza A virus (IAV). We identify a nine amino acid epitope, termed M-SL9, that drives a co-immunodominant, cytolytic CD8 T cell response that is unconventional in two ways: first, it is presented by Qa-1, and second, it maps to an alternative reading frame of the influenza matrix protein 1 (M1) mRNA and appears to derive mainly from an unannotated 16-residue peptide that is dispensable for viral replication. Presentation and immunogenicity of M-SL9 were dependent on the second AUG codon of the positive sense matrix RNA segment, supporting translation initiation by leaky ribosomal scanning. This work suggests that non-canonical translation products must be examined in order to fully reveal the T cell repertoire and adds to a growing body of evidence that MHC-E-restricted T cells may have significant therapeutic value.

While MHC class Ia-restricted classical CD8+ T cells have been widely shown to participate in the immune response to viral infection, little is known about the MHC class Ib-restricted non-classical CD8+ T cell response. Our laboratory recently demonstrated that during murine cytomegalovirus (MCMV), a well-established model system for human CMV, adoptively transferred non-classical CD8+ T cells are sufficient to protect KbDb RAG1−/− mice from lethality. We sought to further characterize this protective population, which is largely Qa-1-restricted. Using KbDb−/− and KbDb−/−. SJL mice, we are able to track the same original population of T cells through iterative adoptive transfers in multiple hosts. Following MCMV infection of new hosts, these T cells continue to play an active role in viral protection and exhibit both effector and memory phenotypes. Strikingly, following multiple challenges, an enriched clonal CD8+ T cell response is observed. While certain strains of human CMV encode a mimic of the canonical peptide binding partner for Qa-1, MCMV does not have a similar mechanism. Rather, our data show that these T cells are stimulated by an MCMV-derived antigen that is recognized by CD8+ T cells with limited αβ TCR diversity. The population we describe may act as a compensatory immune mechanism when MHC class Ia is targeted by CMV immunoevasins. Taken together, these data demonstrate that an MCMV-derived peptide is presented by Qa-1, necessary for an MCMV-specific activation of non-classical CD8+ T cells, and may be of importance for viral protection when classical CD8+ T cell immunity is compromised. This work is supported by NIH Research Grants AI046709 and AI12221, and was supported by a T32 Training Grant in Molecular and Cell Biology and Biochemistry in years 2019-2020. Shanelle Reilly is also supported by research supplement R01 3AI046709-18S1 to promote diversity.

Murine cytomegalovirus (MCMV) is a well-established model system for human CMV (HCMV), a ubiquitous herpesvirus that affects over 70% of people worldwide. Although the classical CD8 +T cell response to MCMV has been well characterized, little is known about the non-classical CD8 +T cell response. Our laboratory recently demonstrated that Qa-1-restricted CD8 +T cells are sufficient to protect mice from MCMV induced lethality. Our recent data shows that this protective T cell population has limited αβ TCR diversity. To identify the MCMV peptide(s) presented by Qa-1, we utilized bioinformatic tools that predict MHC binding, including NetMHC 4.0 and T Cell Epitope Prediction tools available on the Immune Epitope Database and Analysis Resource. Using these tools, we queried the entire MCMV coding sequence to identify potential nonamers predicted to bind to Qa-1. Furthermore, these candidates were also queried to identify protease cleavage sites to ensure that they are predicted to exist in vivo. Approximately 40 potential peptides were selected and tested in an in vitroscreen using Qa-1 expressing cell lines. Our results suggest that several candidate peptides bind to Qa-1 as strongly as well-defined canonical binding partners. Taken together, these data suggest that an MCMV-responsive T cell population with limited αβ TCR diversity recognizes MCMV-derived peptides presented by Qa-1. This population is likely to be of importance for viral protection when classical CD8 +T cell immunity is compromised. This work is supported by the NIH Research Grant AI046709. Shanelle Reilly is supported by research supplement R01 3AI046709-18S1 to promote diversity.