Emily R. Albright, PhD

Position title: Kalejta Laboratory

Email: ealbright@wisc.edu

Address:
627a Robert M Bock Lab
1525 Linden Dr
Madison, WI 53706

Research Title. UL138 Regulates Viral Gene Expression and Innate Immunity during HCMV Latency.

Research Description. Dr. Albright’s current research focuses on the role of innate immune sensors in the establishment and maintenance of Human Cytomegalovirus (HCMV) latency. HCMV is a widespread human pathogen that causes birth defects in neonates and severe disease in immunocompromised individuals. In addition to undergoing productive, lytic replication, HCMV achieves lifelong infection in its host through the establishment of latency. Both the adaptive and innate arms of the immune system play important roles in inhibiting productive viral replication and preventing HCMV-related disease. However, even competent immune systems fail to clear latently infected cells, suggesting that HCMV also effectively evades immune detection during latency. While evasion of both innate and adaptive immune responses during productive replication is relatively well understood, how latently infected cells escape immune detection and clearance remains an important area of inquiry. Dr. Albright’s research is aimed at understanding how innate immune sensors contribute to the establishment of HCMV latent infection. Her work indicates that the cGAS/STING/TBK1 foreign DNA sensing pathway recognizes and responds to latent HCMV infection. Interestingly, her work indicates that activation of this pathway correlates with epigenetic changes to viral chromatin and increased accumulation of lytic viral transcripts, suggesting that recognition by the innate immune system may prevent the efficient establishment of latency. Dr. Albright’s work also suggests that HCMV can evade the innate immune response via the viral latency determinant UL138 which is able to inhibit the type I interferon response during the establishment of latency. Thus, Dr. Albright’s ongoing work is focused on further understanding how foreign DNA sensing pathways, and potentially other innate immune sensors, control latent infection as well as how UL138 counteracts this response to ensure establishment and maintenance of latency.

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