User talk:Eeugenin

Eliseo Eugenin. Ph.D., is a Associate Professor in the Department of Microbiology and Molecular Genetics at Rutgers University and member of the Public Research Institute (PHRI). Eugenin examines the mechanism of pathogenesis of HIV in the brain as well as others viruses including dengue, west nile and Japanese Encephalitic viruses.

Education Universidad Austral de Chile	B.Sc. 1995	Biochemistry

Pontificia Universidad Católica de Chile	MS	 1996	Biological Sciences Pontificia Universidad Católica de Chile	PhD	2001	Physiological Sciences The Albert Einstein College of Medicine	Postdoctoral	2002-2005	Infectious Disease The Albert Einstein College of Medicine	Instructor	2005-2007	Infectious Disease The Albert Einstein College of Medicine	Assistant Prof.	2007-2012	Neurosci/Infectious Disease University of Medical-Dentist (UMDNJ) and Public Health Research Institute (PHRI) Rutgers University Medical School, Rutgers The State University of New Jersey) 	Associate Prof. Associate Prof.	2012-2013 2013-present	Infectious Diseases/Neuroscience Microbiology and Molecular Genetics

Publications 1. Eugenin E.A. and Berman J.W. (2007) Gap junctions mediate HIV-bystander killing in astrocytes. J. Neuroscience. 27 (47): 12844-50. PMID 18032656. Major findings: This publication is the first demonstration that HIV can utilize connexin containing channels, gap junctions, to spread toxicity and inflammation to uninfected cells. 2. Eugenin E.A., Clements J., Zink C.M., and Berman J.W. (2011) HIV infection of human astrocytes disrupts blood brain barrier integrity by a gap junction dependent mechanism. J Neuroscience. 31(26): 9456-65.   PMID 21715610. Major findings: This publication demonstrated that connexin containing channels, gap junctions, play a key role in blood brain barrier disruption and brain inflammation induced by HIV. This paper have more than 60 different associated publications/comments and press releases. 3. Contreras J., Sánchez H., Eugenin E.A., Spiedel D., Theis M., Willecke K., Bukauskas F.F., Bennett M.V and Sáez J.C. (2002) Metabolic inhibition induces opening of unapposed connexin43 gap junction hemichannels and reduces gap junctional communication in cortical astrocytes in culture. Proc. Natl. Acad. Sci. USA. 99 (1) 495-500 PMID 11756680 Major findings: This corresponds to the first demonstration that connexin containing hemichannels are opened under stress conditions. This publication has more than 240 citations. 4. Gaskill P.J., Calderon T.M., Luers A.J., Eugenin E.A., Javitch J.A. and Berman J.W. (2009) Human immunodeficiency virus (HIV) infection of human macrophages is increased by dopamine: a bridge between HIV-associated neurologic disorders and drug abuse. Am J Pathol. 175(3) 1148-59. PMC2731133. Major findings: In this publication we described that dopamine can up regulate HIV replication in human primary macrophages by a mechanism involving endogenous dopamine receptors. 5. Hazleton J.E., Berman J.W. and Eugenin E.A. (2012) Purinergic Receptors are required for HIV-1 Infection of Primary Human Macrophages. J. Immunology. 188(9):4488-95. Major findings: In this manuscript we found that ATP receptors are essential for HIV infection of human primary macrophages by a mechanism that involves HIV entry. 6. Hazleton J., Berman J.W. and Eugenin E.A. (2010) Novel mechanisms of central nervous system damage in HIV infection. HIV/AIDS Research and Pall. Care. 2: 39-49. DOI:59186 Major findings: In this manuscript we integrate that different communication systems, including TNT, gap junctions as well as hemichannels may be important during the pathogenesis of HIV infection. 7. Eugenin E.A., Osiecki K., Lopez L., Goldstein H., Calderon T.M. and Berman J.W. (2006) CCL2/MCP-1 mediates enhanced transmigration of HIV-infected leukocytes across the blood brain barrier: a potential mechanism of HIV-CNS invasion and NeuroAIDS. J. Neuroscience. 26:1098-106 PMID 16436595 Major findings: This is a seminal paper in the field of NeuroAIDS. We demonstrated that CCL2/MCP-1 is one of the key chemokines in mediate transmigration of uninfected and HIV infected leukocytes into the brain. This publication has 143 citations. 8. Eugenín E.A., Eckcart D., Theis M., Willecke K., Bennett M.V. and Sáez J.C. (2001) Microglia at brain stab wounds express connexin43 and in vitro form functional gap junctions after treatment with IFN-γ and TNF-. Proc. Natl. Acad. Sci. USA. 98, 4190-4195. PMID 10775310. 9. Eugenin E.A., Branes M.C., Berman J.W. and Saez J.C. (2003) TNF- plus IFN-γ induce connexin43 expression and formation of gap junctions between human monocytes/macrophages that enhance physiological responses. J Immunology. 170: 1320-1328. PMID 12538692 Major findings: These two papers are the first publications that specific treatments induced expression and formation of functional gap junction channels in immune cells. 10. Eugenin E. A., King J.E., Nath A., Calderon T. M., Zukin S.R., Bennett M.V.L, and Berman J. W. (2007) HIV-tat induces the formation of an LRP-PSD95-NMDAR-nNOS complex necessary for neuronal apoptosis. Proc. Natl. Acad. Sci. USA, 104 (9)3438-3443. PMID 17360663 Major findings: In this publication we showed the mechanism by which HIV-tat protein induced apoptosis in human primary neurons. We identify a membrane complex that is required to trigger apoptosis in neurons exposed to HIV-tat protein.

Website http://phri.org/research/res_pieugenin.asp