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Fabio  Romerio
 

Fabio Romerio Ph.D.

Academic Title: Assistant Professor
Primary Appointment: Medicine
Secondary Appointments: Microbiology and Immunology
fromerio@ihv.umaryland.edu
Location: 725 W. Lombard Street, N455
Phone: (410) 706-1978
Fax: (410) 706-4694
Lab: (410) 706-0993

Personal History:

1988-92: School of Mathematical, Physical and Biological Sciences, University of Pavia (Italy); PhD in Molecular Biology
1992-94: School of Mathematical, Physical and Biological Sciences, University of Pavia (Italy); Board-certified Biologist

Research Interests:

Dr. Romerio's laboratory focuses on understanding the mechanisms of AIDS immunopathogenesis along two major lines of research.

The first line of research is to elucidate the role of plasmacytoid dendritic cells (pDC) and interferon alpha (IFN-alpha) in promoting immune suppression in HIV-1 patients. IFN-alpha is a cytokine that orchestrates the innate immune response against viral infections. In addition, it helps shape the adaptive immune response by promoting maturation of antigen presenting cells. However, Dr. Romerio's laboratory found that pDC of HIV-1 patients relocate from peripheral blood to lymphoid tissues, where they produce large amounts of IFN-alpha. Dr. Romerio's laboratory is now investigating the effects of chronic, exacerbated IFN-alpha production on CD4+ T cell activation, differentiation and immune function.

The second line of research aims at elucidating the mechanisms of establishment, maintenance and reactivation of HIV-1 latency in CD4+ T cells. This pool of latently infected cells is established during primary infection, persists throughout the disease, and archives drug-resistant viruses that re-emerge in the context of inadequate therapy. Latent HIV-1 is invisible to immune responses, and is refractory to anti-retroviral drugs. Thus, viral latency is a critical problem in clinical practice, that so far could not be tackled due to insufficient knowledge of the biology of latently infected cells and the mechanisms that regulate the establishment and maintenance of HIV-1 latency. Dr. Romerio's laboratory has established an in vitro model to generate cells that harbor a replication-competent HIV-1 provirus in a state of non-productive infection. These resting, latently infected CD4+ T cells present a phenotype similar to long-lived central memory cells found in vivo (CCR7+CD62L+), and can be used to investigate cellular and molecular mechanisms at play in the establishment and maintenance of HIV-1 latency.


Lab Techniques and Equipment:

Dr. Romerio's laboratory has extensive expertise with techniques of cellular immunology, flow cytometry and molecular biology.

Publications:

Tyagi M, Romerio F. Models of HIV-1 Persistence in the CD4+ T Cell Compartment: Past, Present and Future. In Press.

Iglesias-Ussel MD, Romerio F. HIV reservoirs: The new frontier. AIDS Reviews. 2011 13:13-29.

Lehmann C, Lafferty M, Garzino-Demo A, Jung N, Hartmann P, Falkenheuer G, Wolf JS, van Lunzen J, Romerio F. Plasmacytoid dendritic cells accumulate and secrete interferon alpha in lymph nodes of HIV-1 patients. PLoS ONE. 2010 5:e11110.

Li S, Bozzo L, Wu Z, Lu W, Romerio F. The HIV-1 matrix protein p17 activates the transcription factors c-Myc and CREB in human B cells. New Microbiologica. 2010;33:13-24.

Lehmann C, Taubert D, Jung N, Falkenheuer G, van Lunzen J, Hartmann P, Romerio F. Preferential upregulation of interferon-alpha subtype 2 expression in HIV-1 patients. AIDS Res Hum Retroviruses. 2009;25:577-81.

Marini A, Harper JM, Romerio F. An in vitro system to model the establishment and reactivation of HIV-1 latency. J Immunol. 2008;181:7713-20.

Lehmann C, Harper JM, Taubert D, Hartmann P, Falkenheuer G, Jung N, van Lunzen J, Stellbrink HJ, Gallo RC, Romerio F. Increased interferon alpha expression in circulating plasmacytoid dendritic cells of HIV-1-infected patients. J Acquir Immune Defic Syndr. 2008;48:522-30.

Curreli S, Romerio F, Secchiero P, Zella D. IFN-alpha2b increases interleukin-10 expression in primary activated human CD8+ T cells. J Interferon Cytokine Res. 2002;22:1167-73.

Romerio F, Zella D. MEK and ERK inhibitors enhance the anti-proliferative effect of interferon-alpha2b. FASEB J. 2002;16:1680-2.

Curreli S, Romerio F, Mirandola P, Barion P, Bemis K, Zella D. Human primary CD4 + T cells activated in the presence of IFN-alpha 2b express functional indoleamine 2,3-dioxygenase. J Interferon Cytokine Res. 2001;21:431-7.

Romerio F, Riva A, Zella D. Interferon-alpha2b reduces phosphorylation and activity of MEK and ERK through a Ras/Raf-independent mechanism. Br J Cancer. 2000;83:532-8.

Coull JJ, Romerio F, Sun JM, Volker JL, Galvin KM, Davie JR, Shi Y, Hansen U, Margolis DM. The human factors YY1 and LSF repress the human immunodeficiency virus type 1 long terminal repeat via recruitment of histone deacetylase 1. J Virol. 2000;74:6790-9.

Zella D, Romerio F, Curreli S, Secchiero P, Cicala C, Zagury D, Gallo RC. IFN-alpha 2b reduces IL-2 production and IL-2 receptor function in primary CD4+ T cells. J Immunol. 2000;164:2296-302.

Romerio F, Gallo RC. Novel biologic approaches for the treatment of AIDS. J Lab Clin Med. 1999;134:577-84.

Zella D, Barabitskaja O, Casareto L, Romerio F, Secchiero P, Reitz MS Jr, Gallo RC, Weichold FF. Recombinant IFN-alpha (2b) increases the expression of apoptosis receptor CD95 and chemokine receptors CCR1 and CCR3 in monocytoid cells. J Immunol. 1999;163:3169-75.

Flamand L, Romerio F, Reitz MS, Gallo RC. CD4 promoter transactivation by human herpesvirus 6. J Virol. 1998;72:8797-805.

Zella D, Barabitskaja O, Burns JM, Romerio F, Dunn DE, Revello MG, Gerna G, Reitz MS Jr, Gallo RC, Weichold FF. Interferon-gamma increases expression of chemokine receptors CCR1, CCR3, and CCR5, but not CXCR4 in monocytoid U937 cells. Blood. 1998;91:4444-50.

Romerio F, Gabriel MN, Margolis DM. Repression of human immunodeficiency virus type 1 through the novel cooperation of human factors YY1 and LSF. J Virol. 1997;71:9375-82.