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In this study, I investigate the landscape of video game play in terms of gender’s influence on experiences and preferences; relationship to a gaming identity and community; and understandings of success, skill, and leadership within gaming. I use qualitative methods, including interviews with 54 respondents, online observations of forum posts, and content analysis of older forum posts to assess player’s experiences and perceptions. There were three major possibilities for gender’s influence at the beginning of this project. First, due to anincreasing number of female players, there may be equal opportunities, definitions, and understandings among players. Second, gaming spaces could reflect what is seen in other masculine areas, with women being pushed out and seen as not belonging. Finally, players may express support for equality, but continue to leave women at a disadvantage through cultural ideas within the space. Ultimately, it appears that these possibilities all exist in an uneven distribution across gaming culture. In terms of player experiences and preferences, there is a decreasing difference based on gender, with male and female players starting at similar times and enjoying the same aspects of similar games. When considering identity and community, players share a discomfort with a “gamer” label and have a desire not to associate with it. Finally, the starkest differences and examples of the aforementioned possibilities come with player definitions of success, skill, and leadership. When considering success, players describe an openended, nongendered idea of what this means, allowing – for more casual and hobby-based play – the perception of an even playing field for men and women. On the other hand, when asked about or discussing skill, players defaulted to more masculine definitions and ideas, emphasizing men in their lives as examples of exemplary players and placing women at a disadvantage when it comes to more professional or competitive play. Beyond these aspects of gaming, players continued to create a complex idea about who is equipped for what by defining leadership in more feminine ways, but simultaneously considering this a low-prestige position and further presenting obstacles for women in gaming.

Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's Disease. The simian homologue of KSHV, rhesus monkey rhadinovirus (RRV), is highly related to KSHV. The first open reading frames of KSHV and RRV encode for proteins K1 and R1, respectively. Although only 17% similar at the amino acid level, K1 and R1 function similarly, scoring positively in a number of cellular transformation assays and encoding an immunoreceptor -tyrosine-based activation motif (ITAM). Both proteins are capable of activating B lymphocyte signal transduction and interacting with the major B cell kinase, Syk. Expression of K1 in B lymphocytes was found to activate the PI3K/Akt pathway and inhibit PTEN, leading to the inhibition of FKHR transcription factors, key regulators of cell cycle progression and apoptosis. K1 expression inhibited apoptosis induced by FKHR proteins and the FasL/Fas receptor pathway. Expression of K1 promotes cell survival pathways and contributes to KSHV pathogenesis by preventing virally infected cells from undergoing premature apoptosis. Recent evidence suggests that receptor signaling not only occurs at the cell membrane, but from intracellular compartments. K1 was found to internalize in a clathrin-dependent manner, trafficking from the early endosome to the recycling endosome. By blocking signaling of PI3K or Syk, the rate of K1 internalization was diminished. Additionally, blocking clathrin-mediated endocytosis inhibited downstream signaling by K1 to Akt. The above phenomena are dependent on a functional ITAM of K1. This suggests that K1 signaling is strongly associated with internalization. In B-cells, K1 co-internalizes with the BCR, suggesting that K1 scavenges the BCR from the surface. In order to discern what role R1 plays in the virus life-cycle, the R1 ORF was deleted from the RRV genome, by insertion of a GFP expression cassette. By PCR and Southern blot analysis, this virus is identical to the wild-type virus, except for insertion of the transgene. This virus will be used to analyze the contribution of R1 to lytic replication, establishment of latency, and reactivation from latency. Additionally, this virus can be used to observe the role R1 plays in the development of disease in vivo.