{"id":5388,"date":"2026-08-24T03:37:47","date_gmt":"2026-08-24T03:37:47","guid":{"rendered":"https:\/\/cognitionconferences.com\/hivaids\/?post_type=speaker&#038;p=5388"},"modified":"2026-08-24T03:38:33","modified_gmt":"2026-08-24T03:38:33","slug":"rajgopal-govindarajan","status":"publish","type":"speaker","link":"https:\/\/cognitionconferences.com\/hivaids\/speaker\/rajgopal-govindarajan\/","title":{"rendered":"Rajgopal Govindarajan"},"content":{"rendered":"<p><strong>Abstract :\u00a0<\/strong><br \/>\nNucleoside\/nucleotide reverse transcriptase inhibitors (NRTIs) are foundational to HIV treatment regimens, yet their clinical utility is often limited by treatment toxicities such as liver failure and pancreatitis. In this study, we identify drug-induced dysfunction of the endolysosomal nucleoside transporter SLC29A3\/ENT3 as a mechanism driving autophagic disruption in NRTI-treated mice. NRTIs markedly impair SLC29A3-mediated adenosine transport, leading to dysregulation of the PRKAA-MTOR-ULK signaling axis and consequent autophagy dysfunction. Genetic ablation of SLC29A3 exacerbates NRTI-induced mortality, whereas forced SLC29A3 expression restores autophagic integrity and improves survival. Tissue-specific deletion of SLC29A3 using Alb-Cre and Pdx-Cre models reveals heightened susceptibility to didanosine-induced hepatic and pancreatic toxicity, respectively, highlighting SLC29A3&#8217;s role in organ-specific vulnerability. Notably, co-administration of rapamycin rescues autophagic flux and enhances both tolerance and survival under acute NRTI exposure. Together, these findings suggest SLC29A3 as a crucial modulator of NRTI toxicity, presenting a promising therapeutic target to optimize HIV treatment outcomes by minimizing adverse effects.<\/p>\n<p><strong>Biography :\u00a0<\/strong><\/p>\n<p>Dr. Rajgopal Govindarajan received his PhD from the University of Nebraska Medical Center at Omaha and postdoctoral fellowship from the University of Washington at Seattle. His training is in the areas of animal sciences, cancer biology and drug transporters and he has extensively used cell and mouse models to evaluate experimental therapeutic agents for pancreatic cancer. Dr. Govindarajan\u2019s laboratory has developed several new insights into the pharmacology of nucleoside analogs used in the treatment of pancreatic ductal adenocarcinomas and HIV. Current focuses in his laboratory are to 1) characterize the link between autophagy, stemness, and therapeutic drug resistance in pancreatic cancer and HIV, and 2) understand the role of transporters in pancreatic tumorigenicity and HIV replication. Dr. Govindarajan\u2019s awards in the areas of cancer research include the American Cancer Society Research Scholar Award and Georgia Cancer Coalition Research Award. His current research is supported by grants from the National Institutes of Health and American Cancer Society.<\/p>\n","protected":false},"featured_media":5348,"template":"","meta":{"_acf_changed":false},"schedule":[7],"speaker-category":[6],"class_list":["post-5388","speaker","type-speaker","status-publish","has-post-thumbnail","hentry","schedule-day-2","speaker-category-speakers"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.6 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Rajgopal Govindarajan | The Ohio State University College of Pharmacy | USA<\/title>\n<meta name=\"description\" content=\"Dr. Rajgopal Govindarajan received his PhD from the University of Nebraska Medical Center at Omaha and postdoctoral fellowship from the University of Washington at Seattle. 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