Marco Sgarbanti

Dr. Marco Sgarbanti

orcid

Research Focus & Metrics

Academic Career Length

26Years (2001-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
15 February 2001 in Oncogene
Verified
Journal Article
Closed access
PDF file
RLRongtuan Lin
Rongtuan Lin
PGPierre Genin
Pierre Genin
YMYael Mamane
Yael Mamane
MSMarco Sgarbanti
Marco Sgarbanti
ABAngela Battistini
Angela Battistini
JHJohn Hiscott
John Hiscott

20 May 2002 in Journal of Experimental Medicine
Verified
Journal Article
Open access
PDF file
MSMarco Sgarbanti
Marco Sgarbanti
ABAlessandra Borsetti
Alessandra Borsetti
NMNicola Moscufo
Nicola Moscufo
MBMaria C. Bellocchi
Maria C. Bellocchi
BRBarbara Ridolfi
Barbara Ridolfi
ABAngela Battistini
Angela Battistini
Transcription of the human immunodeficiency virus (HIV)-1 is controlled by the cooperation of virally encoded and host regulatory proteins. The Tat protein is essential for viral replication, however, expression of Tat after virus entry requires HIV-1 promoter activation. A sequence in the 5′ HIV-1 LTR, containing a binding site for transcription factors of the interferon regulatory factors (IRF) family has been suggested to be critical for HIV-1 transcription and replication. Here we show that IRF-1 activates HIV-1 LTR transcription in a dose-dependent fashion and in the absence of Tat. This has biological significance since IRF-1 is produced early upon virus entry, both in cell lines and in primary CD4+ T cells, and before expression of Tat. IRF-1 also cooperates with Tat in amplifying virus gene transcription and replication. This cooperation depends upon a physical interaction that is blocked by overexpression of IRF-8, the natural repressor of IRF-1, and, in turn is released by overexpression of IRF-1. These data suggest a key role of IRF-1 in the early phase of viral replication and/or during viral reactivation from latency, when viral transactivators are absent or present at very low levels, and suggest that the interplay between IRF-1 and IRF-8 may play a key role in virus latency.

1 April 2008 in Journal of Virology
Verified
Journal Article
Closed access
MSMarco Sgarbanti
Marco Sgarbanti
ARAnna L. Remoli
Anna L. Remoli
GMGiulia Marsili
Giulia Marsili
BRBarbara Ridolfi
Barbara Ridolfi
ABAlessandra Borsetti
Alessandra Borsetti
ABAngela Battistini
Angela Battistini
Human immunodeficiency virus type 1 (HIV-1) gene expression is controlled by a complex interplay between viral and host factors. We have previously shown that interferon-regulatory factor 1 (IRF-1) is stimulated early after HIV-1 infection and regulates promoter transcriptional activity even in the absence of the viral transactivator Tat. In this work we demonstrate that IRF-1 is also required for full NF-κB transcriptional activity. We provide evidence that IRF-1 and NF-κB form a functional complex at the long terminal repeat (LTR) κB sites, which is abolished by specific mutations in the two adjacent κB sites in the enhancer region. Silencing IRF-1 with small interfering RNA resulted in impaired NF-κB-mediated transcriptional activity and in repressed HIV-1 transcription early in de novo-infected T cells. These data indicate that in early phases of HIV-1 infection or during virus reactivation from latency, when the viral transactivator is absent or present at very low levels, IRF-1 is an additional component of the p50/p65 heterodimer binding the LTR enhancer, absolutely required for efficient HIV-1 replication.

14 April 2014 in Viruses
Verified
Journal Article
Open access
PDF file
ABAngela Battistini
Angela Battistini
MSMarco Sgarbanti
Marco Sgarbanti
The major obstacle towards HIV-1 eradication is the life-long persistence of the virus in reservoirs of latently infected cells. In these cells the proviral DNA is integrated in the host’s genome but it does not actively replicate, becoming invisible to the host immune system and unaffected by existing antiviral drugs. Rebound of viremia and recovery of systemic infection that follows interruption of therapy, necessitates life-long treatments with problems of compliance, toxicity, and untenable costs, especially in developing countries where the infection hits worst. Extensive research efforts have led to the proposal and preliminary testing of several anti-latency compounds, however, overall, eradication strategies have had, so far, limited clinical success while posing several risks for patients. This review will briefly summarize the more recent advances in the elucidation of mechanisms that regulates the establishment/maintenance of latency and therapeutic strategies currently under evaluation in order to eradicate HIV persistence.

1 August 2012 in Cytokine & Growth Factor Reviews
Verified
Journal Article
Closed access
GMGiulia Marsili
Giulia Marsili
ARAnna Lisa Remoli
Anna Lisa Remoli
MSMarco Sgarbanti
Marco Sgarbanti
EPEdvige Perrotti
Edvige Perrotti
AFAlessandra Fragale
Alessandra Fragale
ABAngela Battistini
Angela Battistini

19 February 2003 in Oncogene
Verified
Journal Article
Closed access
MAMeztli Arguello
Meztli Arguello
MSMarco Sgarbanti
Marco Sgarbanti
EHEduardo Hernandez
Eduardo Hernandez
YMYael Mamane
Yael Mamane
SSSonia Sharma
Sonia Sharma
JHJohn Hiscott
John Hiscott