Abstract

Abstract Patients with HIV/AIDS are at a 3,400 times higher risk of developing Kaposi's sarcoma when compared to healthy populations. Our hypothesis is that the upregulation of viral associated proteins is causing an increase in DNA damage, allowing for the higher incidence rate of Kaposi's sarcoma in infected populations. The direct mechanisms leading to this increased risk is unknown, but the viral infection with Kaposi's sarcoma-associated herpesvirus (KSHV) is an apparent cause of this risk. The cell is under attack of endogenous threats including oxidative stress, causing DNA damage and leading to mutations, but the viral proteins may interfere with the repair mechanisms. In previous experiments we looked at DNA repair dynamics following X-ray exposure in the two different stages and determined there is an inefficiency in the DNA repair process in the cells during active production of viral particles. This project aimed to compare the transcriptomes of the BCBL-1 cell line during latent and acute phases of KSHV production. Our results are showing that genes involved in genome stability are differently expressed during the lytic stage. Comparison of these two transcriptomes allows for identification of which proteins are being upregulated during active viral production. This may be of importance for the HIV/AIDS cancer patients because it shows the mechanisms behind genome stability in KSHV-infected cells. 1) Research reported in this publication was supported by the National Institute Of General Medical Sciences of the National Institutes of Health under Award Numbers UL1GM118991, TL4GM118992, or RL5GM118990. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. 2) NASA EPSCoR, NNH15ZHA003C Citation Format: Samantha L. Haines, Sabrina R. Bishop, Viktorija Podlutskaya, Andrej Podlutsky. Gene expression profile in BCBL-1 cell line following activation of KSHV [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1394.

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