Journal of Microbiology

Jisu Lee

1 Article

Latent Kaposi’s sarcoma-associated herpesvirus infection in bladder cancer cells promotes drug resistance by reducing reactive oxygen species: Suhyuk Lee , Jaehyuk Jang , Hyungtaek Jeon , Jisu Lee , Seung-Min Yoo , Jinsung Park , Myung-Shin Lee; J. Microbiol. 2016;54(11):782-788. Published online October 29, 2016; DOI: https://doi.org/10.1007/s12275-016-6388-x

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Kaposi’s sarcoma-associated herpesvirus (KSHV) is the major etiologic agent of Kaposi’s sarcoma, primary effusion lymphoma, and multicentric Castleman’s disease. Recent studies have indicated that KSHV can be detected at high frequency in patient-derived bladder cancer tissue and might be associated with the pathogenesis of bladder cancer. Bladder cancer is the second most common cancer of the genitourinary tract, and it has a high rate of recurrence. Because drug resistance is closely related to chemotherapy failure and cancer recurrence, we investigated whether KSHV infection is associated with drug resistance of bladder cancer cells. Some KSHV-infected bladder cancer cell lines showed resistance to an anti-cancer drug, cisplatin, possibly as a result of downregulation of reactive oxygen species. Additionally, drug resistance acquired from KSHV infection could partly be overcome by HDAC1 inhibitors. Taken together, the data suggest the possible role of KSHV in chemo-resistant bladder cancer, and indicate the therapeutic potential of HDAC1 inhibitors in drug-resistant bladder cancers associated with KSHV infection.

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Jisu Lee

1 Article

Infection Dynamics of Dengue Virus in Caco-2 Cells Depending on Its Differentiation Status: Jayoung Nam, Jisu Lee, Geon A Kim, Seung-Min Yoo, Changhoon Park, Myung-Shin Lee; J. Microbiol. 2024;62(9):799-809. Published online August 30, 2024; DOI: https://doi.org/10.1007/s12275-024-00161-w

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Abstract: Dengue virus (DENV), from the Flaviviridae family, is the causative agent of dengue fever and poses a significant global health challenge. The virus primarily affects the vascular system and liver; however, a growing body of evidence suggests its involvement in the gastrointestinal (GI) tract, contributing to clinical symptoms such as abdominal pain, vomiting, and diarrhea. However, the mechanisms underlying DENV infection in the digestive system remain largely unexplored. Prior research has detected viral RNA in the GI tissue of infected animals; however, whether the dengue virus can directly infect human enterocytes remains unclear. In this study, we examine the infectivity of human intestinal cell lines to the dengue virus and their subsequent response. We report that the Caco-2 cell line, a model of human enterocytes, is susceptible to infection and capable of producing viruses. Notably, differentiated Caco-2 cells exhibited a lower infection rate yet a higher level of virus production than their undifferentiated counterparts. These findings suggest that human intestinal cells are a viable target for the dengue virus, potentially elucidating the GI symptoms observed in dengue fever and offering a new perspective on the pathogenetic mechanisms of the virus.

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