Vargab Baruah

Abstract Human cytomegalovirus (CMV) is a ubiquitous pathogen that establishes life-long, latent infection in hematopoietic cells. Immune-competent individuals are usually asymptomatic for disease. However, immune dysregulation in latently-infected individuals can result in viral reactivation, often causing further complications. Viral gene transcription during latency is restricted, although the CMV-encoded G-protein coupled receptor homologs, US28 and UL78, are expressed.

Abstract Reactivation of latent human cytomegalovirus (CMV) can lead to severe complications in individuals with dysregulated immune systems. While antiviral therapies for CMV are approved, these compounds are limited by their toxicity and inability to specifically target the latent reservoir or prevent reactivation. Herein we show that CMV reactivation in Kasumi-3 cells, a CD34+ hematopoietic cell line, requires mitogen-activated protein kinase (MAPK) activation.

Abstract The innate immune response is the first line of defense against invading pathogens, including the betaherpesvirus, human cytomegalovirus (CMV). The host innate response acts as the first line of defense, and CMV, like other viruses, has consequently evolved multiple mechanisms to manipulate host interferon (IFN) responses.