Irini Sereti, M.D.

Irini Sereti, M.D.

Chief, HIV Pathogenesis Section

Major Areas of Research

  • Pathogenesis of HIV infection emphasizing mechanisms of immune reconstitution inflammatory syndrome in advanced HIV infection and of serious non-AIDS events in treated HIV-infected patients
  • Pathogenesis of idiopathic CD4 lymphocytopenia (ICL)
  • Immune-based therapeutic strategies of HIV infection and ICL

Program Description

The primary research focus of our group is the study of inflammatory complication in HIV including immune reconstitution inflammatory syndrome (IRIS). IRIS is an aberrant immune response, frequently with an intense inflammatory component, that can occur in the context of immune restoration in patients with HIV infection and severe CD4 lymphopenia after initiation of antiretroviral therapy (ART). Chronically treated patients on the other hand may experience non-infectious complications of HIV, including cardiovascular disease that seem to be driven by chronic residual immune activation and inflammation. The second interest is development of adjuvant immune-based therapies (IBT) to improve immune restoration in CD4 lymphopenic conditions such as HIV and idiopathic CD4 lymphopenia (ICL). ICL is a rare, likely heterogeneous condition characterized by low CD4 T-cell counts in the absence of HIV or other known infection or disease that can cause lymphopenia.

Biography

Dr. Sereti received her M.D. from the University of Athens, Greece, in 1991. She did research for one year in Dr. Greg Spear’s laboratory at Rush Presbyterian Hospital in Chicago and then completed an internship, residency, and chief residency in medicine at Northwestern University. In 1997, Dr. Sereti came to the National Institutes of Health as a clinical associate in the Laboratory of Immunoregulation. She became a staff clinician in 2003. She was appointed to a clinical tenure-track position in 2009 and received tenure in 2015.

Research Group

Ainhoa Perez-Diez
Elizabeth Laidlaw
Xiangdong Liu
Chun-Shu Wong
Silvia Lage
Harry Mystakelis
Luxin Pei
Ornella Sortino
Christopher Grivas
Andrea Lisco (clinical fellow)
Maura Manion (clinical fellow)
 

Publications

Schechter ME, Andrade BD, He T, Richter GH, Tosh KW, Policicchio BB, Singh AP, Raehtz KD, Sheikh VM, Ma D, Brocca-Cofano E, Apetrei C, Tracy R, Ribeiro RM, Sher A, Francischetti IM, Pandrea I, Sereti I. Inflammatory monocytes expressing tissue factor drive SIV and HIV-coagulopathy. Science Translational Medicine. 2017. Epub ahead of print.

Sereti I, Krebs SJ, Phanuphak N, Fletcher JL, Slike B, Pinyakorn S, O'Connell RJ, Rupert A, Chomont N, Valcour V, Kim JH, Robb ML, Michael NL, Douek DC, Ananworanich J, Utay NS; RV254/SEARCH 010, RV304/SEARCH 013 and SEARCH 011 protocol teams. Persistent, albeit reduced, chronic inflammation in persons starting antiretroviral therapy in acute HIV infection. Clin Infect Dis. 2017 Jan 15;64(2):124-131. 

Hsu DC, Ma YF, Hur S, Li D, Rupert A, Scherzer R, Kalapus SC, Deeks S, Sereti I, Hsue PY. Plasma IL-6 levels are independently associated with atherosclerosis and mortality in HIV-infected individuals on suppressive antiretroviral therapy.  AIDS. 2016 Aug 24;30(13):2065-74.

Sheikh V, Porter BO, DerSimonian R, Kovacs SB, Thompson WL, Perez-Diez A, Freeman AF, Roby G, Mican J, Pau A, Rupert A, Adelsberger J, Higgins J, Bourgeois JS Jr, Jensen SM, Morcock DR, Burbelo PD, Osnos L, Maric I, Natarajan V, Croughs T, Yao MD, Estes JD, Sereti I. Administration of interleukin-7 increases CD4 T cells in idiopathic CD4 lymphocytopenia. Blood. 2015 Dec 16.

Hsu DC, Faldetta KF, Pei L, Sheikh V, Utay NS, Roby G, Rupert A, Fauci AS, Sereti I. A paradoxical treatment for a paradoxical condition: Infliximab use in three cases of mycobacterial IRIS. Clin Infect Dis. 2016 Jan 15;62(2):258-61.

Andrade BB, Singh A, Narendran G, Schechter ME, Nayak K, Subramanian S, Anbalagan S, Jensen SM, Porter BO, Antonelli LR, Wilkinson KA, Wilkinson RJ, Meintjes G, van der Plas H, Follmann D, Barber DL, Swaminathan S, Sher A, Sereti I.Mycobacterial antigen driven activation of CD14++CD16- monocytes is a predictor of tuberculosis-associated immune reconstitution inflammatory syndrome. PLoS Pathog. 2014 Oct 2;10(10):e1004433.

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