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Dive into the research topics where Giampiero D'Offizi is active.

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Featured researches published by Giampiero D'Offizi.


The Journal of Allergy and Clinical Immunology | 1995

Immunologic aspects of hyperimmunoglobulinemia E–like syndrome in patients with AIDS

Roberto Paganelli; Enrico Scala; Ivano Mezzaroma; Elena Pinter; Giampiero D'Offizi; Emanuele Fanales-Belasio; Rosa Maria Rosso; Ignacio J. Ansotegui; Franco Pandolfi; Fernando Aiuti

In this study we describe a series of nine patients affected by acquired immunodeficiency syndrome (AIDS) or AIDS-related complex who had hypereosinophilia and hyperimmunoglobulinemia E (hyper-IgE) with chronic dermatitis and recurrent staphylococcal infections. These patients had features similar to those present in hyper-IgE syndrome, a primary immunodeficiency disease. In addition, immunologic characterization of these patients with human immunodeficiency virus (HIV) infection, compared with 51 HIV-positive patients without hyper-IgE, both atopic and nonatopic, and three patients affected by the primary hyper-IgE syndrome, also revealed an increase in IgA and a severe decrease in B and CD4+ lymphocytes. Spontaneous in vitro synthesis of IgE by peripheral blood mononuclear cells was confirmed in both hyper-IgE conditions, together with increased levels of circulating eosinophil cationic protein. Serum-soluble CD23, usually increased in atopic conditions and hyper-IgE, was similar to that of normal control subjects in the HIV-positive patients with hyper-IgE. On the basis of our findings, we conclude that a hyper-IgE-like syndrome represents a distinct aspect of the clinical manifestations associated with HIV infection and that the immunologic mechanisms in this condition seem to differ from those known in primary hyper-IgE syndrome, because CD4+ TH2 type cells, which are currently believed to have a role in IgE production, are severely depleted in HIV-positive patients.


The Journal of Infectious Diseases | 2004

Mutations in HIV-1 Reverse Transcriptase Potentially Associated with Hypersusceptibility to Nonnucleoside Reverse-Transcriptase Inhibitors: Effect on Response to Efavirenz-Based Therapy in an Urban Observational Cohort

Valerio Tozzi; Mauro Zaccarelli; Pasquale Narciso; Maria Paola Trotta; Francesca Ceccherini-Silberstein; Patrizio De Longis; Giampiero D'Offizi; Federica Forbici; Roberta D'Arrigo; Evangelo Boumis; Rita Bellagamba; Sandro Bonfigli; Chiarina Carvelli; Andrea Antinori; Carlo Federico Perno

BACKGROUND Hypersusceptibility to nonnucleoside reverse-transcriptase inhibitors (NNRTIs) was described in association with reverse-transcriptase (RT) mutations conferring resistance to nucleoside reverse-transcriptase inhibitors (NRTIs). We evaluated the effect of RT mutations associated with hypersusceptibility to NNRTIs on the response to efavirenz-based therapy. METHODS We analyzed an observational database of patients for whom highly active antiretroviral therapy failed and who received genotypic resistance testing-guided therapy, either efavirenz or protease inhibitor (PI) based. Study end points were achievement of virus load <80 copies/mL, achievement of virus load <80 copies/mL without rebound to >500 copies/mL, and changes in CD4 cell counts. RESULTS The baseline RT mutations M41L, M184V, L210W, and T215Y and the M41L/T215Y and M41L/T215Y/M184V combinations were associated with virological suppression for efavirenz-treated patients, whereas, for PI-treated patients, only the M184V mutation was associated with virological suppression, and the L210W mutation showed a negative correlation; no correlation was found between any mutation and virological response without rebound. CONCLUSIONS The M41L, M184V, L210W, and T215Y mutations were associated with a better, although transient, virological outcome in patients treated with efavirenz-based regimens.


AIDS | 2001

Changes in host cell molecules acquired by circulating HIV-1 in patients treated with highly active antiretroviral therapy and interleukin-2.

Isabella Abbate; Ferdinando Dianzani; Ombretta Turriziani; Guido Antonelli; Giampiero D'Offizi; Vincenzo Galati; Marina Pierdominici; Franco Pandolfi; Maria Rosaria Capobianchi

ObjectiveTo analyse cell membrane proteins (CMP) acquired by HIV-1 present in the plasma of asymptomatic patients, and their modifications after a cycle of highly active antiretroviral therapy (HAART) and interleukin (IL)-2. Design and methodsPlasma samples from eight drug-naive asymptomatic subjects underwent immobilized antibody capture (IAC) to detect CMP on the surface of circulating HIV-1. The CMP considered were lymphocyte subset markers (CD45RA, CD45RO), activation markers (HLA-DR), adhesion molecules (LFA-3), costimulatory proteins (B7-2), lymph-node homing receptors (CD62L) and pro-apoptosis molecules (FasL). This analysis was repeated after one cycle of HAART + IL-2, after virus rebound. ResultsLFA-3, followed by CD45RO and HLA-DR, are the most represented CMP on the surface of circulating virions in naive asymptomatic patients; CD45RA, CD62L, B7-2 and FasL are detected only occasionally. After rebound, a significant reduction of CD45RO and HLA-DR, but not of LFA-3, is observed on virions, whereas CD45RA and CD62L, as well as other molecules, are not affected, remaining almost undetectable. ConclusionsAssuming that CMP on HIV-1 reflect the cellular origin of virions, activated T cells expressing CD45RO, HLA-DR, and LFA-3 may be the main source of HIV-1 in asymptomatic patients. After a cycle of HAART + IL-2, followed by therapy interruption, CD45RA and CD62L are detected on virions rarely, indicating that even during virus rebound, expanded naive T cells do not become a major target of virus replication. Furthermore, the presence of HLA-DR on rebound HIV-1 is decreased, consistent with decreased activation of the HIV-producing cells. More extensive investigation may clarify the significance of these findings with respect to pathogenesis.


AIDS Research and Human Retroviruses | 1999

The benign cystic lymphoepithelial lesion of the parotid gland is a viral reservoir in HIV type 1-infected patients

Stefania Uccini; E. Riva; Guido Antonelli; Giampiero D'Offizi; Alessandra Prozzo; Alberto Angelici; Alberto Faggioni; Antonio Angeloni; Maria Rosaria Torrisi; Massimo Gentile; Carlo D. Baroni; Luigi Ruco

The presence of HIV-1 in cystic fluid aspirates from six cases of benign cystic lymphoepithelial lesion (BLL) of the parotid gland, a rare disorder affecting HIV-1-infected patients, has been investigated. HIV-1 p24 protein was present at a concentration ranging from 3 to 15 ng/ml, while it was undetectable in the peripheral blood of the same patients. The number of RNA copies of HIV-1 in the cystic fluids was high, ranging from 0.5 x 10(7) to 7.2 x 10(7) RNA copies/ml. BLL cystic fluid aspirates, despite the high level of HIV-1 RNA, were found to contain only a few infectious virions. The low infectivity correlated with the infrequent detection by electron microscopy of complete HIV-1 particles. The pathogenic mechanism leading to virus accumulation in the cystic fluid was studied by immunohistochemistry of tissue sections. p24 protein was associated with DRC-1+/S-100+ follicular dendritic reticulum cells, which were also present within the cystic cavities. Our findings are consistent with the possibility that the large amounts of virus present in the fluid derive from continuous shedding of HIV-1-infected cells from the surrounding lymphoid tissue.


Aids Patient Care and Stds | 2000

Cystic lymphoepithelial lesions of the parotid gland in HIV-1 infection.

Stefania Uccini; Giampiero D'Offizi; Alberto Angelici; Alessandra Prozzo; E. Riva; Guido Antonelli; Carlo D. Baroni; Luigi Ruco

The benign cystic lymphoepithelial lesion (BLL) of the parotid gland is a rare disorder affecting HIV-1-infected patients. Here we describe the clinical and histopathological features of 10 cases of BLL, who presented to our observation between November 1992 and December 1996, before the combination antiretroviral therapy was introduced.


Clinical Immunology and Immunopathology | 1987

Peripheral and intestinal lymphocyte activation after in vitro exposure to cow's milk antigens in normal subjects and in patients with Crohn's disease

L. Biancone; Roberto Paganelli; Stefano Fais; Ottorino Squarcia; Giampiero D'Offizi; Francesco Pallone

We studied in Crohns disease and controls the in vitro activation of either peripheral (PBMNC) or intestinal (LPMNC) mononuclear cells in response to the cows milk antigen beta-lactoglobulin (Blg). The activation of mononuclear cells was investigated by analyzing the kinetics of the transferrin receptor (T9 antigen) and interleukin 2 receptor (Tac antigen) expression. In both controls and Crohns disease patients Blg (1 microgram/ml) induced a significant (P less than 0.01) increase of T9 and Tac expression by both PBMNC and LPMNC cultured for 3 days. After Blg exposure the counts of T9- and Tac-bearing cells were significantly (P less than 0.05) higher in PBMNC cultures from healthy controls than in those from patients with Crohns disease. In both groups peripheral T-enriched cell suspensions did not express T9 and Tac when stimulated with Blg but were restored to express either antigen by the addition of 10% autologous adherent cells. In LPMNC cultures from patients with Crohns disease the Tac expression after 3 days of Blg stimulation was significantly (P less than 0.05) higher than in the autologous PBMNC. Data from this study indicate that in both controls and patients with Crohns disease lymphocytes sensitized to Blg occur in the circulation as well as in the gut lamina propria. Our data also suggest that in Crohns disease an increased proportion of lymphocytes sensitized to Blg are recruited from the circulation into the site of the intestinal lesion.


AIDS Research and Human Retroviruses | 2008

Plasma HIV RNA decline and emergence of drug resistance mutations among patients with multiple virologic failures receiving resistance testing-guided HAART.

Valerio Tozzi; Rita Bellagamba; Filippo Castiglione; Alessanda Amendola; Jelena Ivanovic; Emanuele Nicastri; Raffaella Libertone; Giampiero D'Offizi; Giuseppina Liuzzi; Caterina Gori; Federica Forbici; Roberta D'Arrigo; A. Bertoli; Maria Flora Salvatori; Maria Rosaria Capobianchi; Andrea Antinori; Carlo Federico Perno; Pasquale Narciso

Early recognition of virologic failure in patients with extensive drug resistance receiving salvage-HAART is essential to avoid exposure to subinhibitory regimens. We studied plasma viral load (PVL) decline and rates of drug-resistance mutation (DRM) accumulation in such patients. A prospective, 48 week study of 38 heavily pretreated patients receiving genotypic resistance testing (GRT)-guided HAART was conducted. The rate of PVL decline was studied by weekly PVL determinations. To assess DRM accumulation, serial GRTs were performed in all nonresponders (never reaching PVL <50 or two PVLs >50 copies/ml after suppression). Over 48 weeks, 10 patients (26%) were nonresponders. Receiving less then two fully active drugs and having an elevated number of PI and NRTI mutations at baseline were strongly associated with virologic failure. There was no evidence of a difference in the change from baseline PVL to week 1 and 2 between responders and nonresponders. By contrast, PVL reductions from week 2 to week 3 and thereafter were significantly greater for responders (p < 0.01). Among nonresponders, the incidence rates per patient-month (95% CI) of emergent DRM were 0.67 (0.13-1.20), 0.40 (0.00-0.74), and 0.37 (0.00-0.75) at weeks 4, 8, and 24, respectively. Having limited baseline resistance, receiving at least two fully active drugs, and showing constant PVL reductions from week 2 to week 3 and thereafter were predictive of virologic response. In contrast, early changes in PVL levels were not. Virologic failure was associated with detection of emergent DRMs. Virologic rebound in patients on salvage-HAART should be addressed aggressively.


Journal of Experimental Medicine | 1995

CD8+ T lymphocytes provide helper activity for IgE synthesis in human immunodeficiency virus-infected patients with hyper-IgE.

Roberto Paganelli; Enrico Scala; Ignacio J. Ansotegui; Clara M. Ausiello; Eva Halapi; Emanuele Fanales-Belasio; Giampiero D'Offizi; Ivano Mezzaroma; Franco Pandolfi; Massimo Fiorilli; Antonio Cassone; Fernando Aiuti


Human Reproduction | 1996

Semen analysis in HIV seropositive men and in subjects at high risk for HIV infection.

F. Dondero; Tiziana Rossi; Giampiero D'Offizi; Fernando Mazzilli; Rosamaria Rosso; Nadia Sarandrea; Elena Pinter; Fernando Aiuti


Blood | 1997

Death of bystander cells by a novel pathway involving early mitochondrial damage in human immunodeficiency virus-related lymphadenopathy

Maurizio Carbonari; Anna Maria Pesce; Marina Cibati; Alessandro Modica; Lucia Dell'Anna; Giampiero D'Offizi; Alberto Angelici; Stefania Uccini; Andrea Modesti; Massimo Fiorilli

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Fernando Aiuti

Sapienza University of Rome

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Alberto Angelici

Sapienza University of Rome

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Franco Pandolfi

Catholic University of the Sacred Heart

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Massimo Fiorilli

Sapienza University of Rome

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Roberto Paganelli

Sapienza University of Rome

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Stefania Uccini

Sapienza University of Rome

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Pasquale Narciso

National Institutes of Health

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Anna Maria Pesce

Sapienza University of Rome

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Elena Pinter

Sapienza University of Rome

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