Annalisa Saracino
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Annalisa Saracino has a total of 28 co-authors. Here are the top co-authors by number of shared publications:
- Aldo Bertoli
Department of Experimental Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
1 shared publication - Alessia Ciancio
A.O.U. Città della Salute e della Scienza di Torino, 10126 Torino, Italy
1 shared publication - Alessia Magnapera
Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy
1 shared publication - Andrea Di Lorenzo
Department of System Medicine, Tor Vergata University, 00133 Rome, Italy
1 shared publication - Antonella Olivero
Department of Medical Sciences, University of Turin, 10126 Turin, Italy
1 shared publication - Caterina Tramontozzi
Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy
1 shared publication
Latest Publications
- Open Access
Chronic HDV Infection Shows Higher HBsAg Isoform Levels than HBV Infection, Paralleling HDV Replicative Activity
Background & Aim: The entry of Hepatitis D Virus (HDV) depends on HBV surface proteins (HBsAg) composed of three isoforms: large-, middle, and small HBsAg. Here, we investigate the levels of total HBsAg and HBsAg isoforms and their correlations with HDV-RNA, HBcrAg, and transaminases in the setting of untreated chronic hepatitis D (CHD). Methods: This study includes 316 HBeAg-negative patients: 192 CHD and 124 with chronic hepatitis B (CHB) as a control group. HBsAg isoforms were quantified by ad hoc-designed ELISAs. Results: The composition of HBsAg isoforms varied between the two groups of patients, with remarkably higher small HBsAg, middle-HBsAg, and large HBsAg in CHD than in CHB. This data was confirmed by multivariable analysis (p < 0.0001). Among CHD, HBsAg isoforms positively correlated with HDV-RNA (p < 0.0001) and HBcrAg (p < 0.0001) but not with HBV-DNA. The results were confirmed by stratifying patients according to HDV-RNA (< or >1000 IU/mL) and HBcrAg (< or >3 logU/mL). Furthermore, CHD patients with ALT > upper limit of normal presented significantly higher S-HBsAg and M-HBsAg levels. Conclusions: CHD is characterized by a more elevated HBsAg isoform production, paralleling HDV-RNA and HBcrAg release. This may suggest a preferential recruitment of HBsAg isoforms in HDV virions at the expense of HBV virions. The association of HBsAg isoforms with higher ALT also suggests their potential contribution in supporting HDV-induced pro-inflammatory stimuli.
Open AccessChronic HDV Infection Shows Higher HBsAg Isoform Levels than HBV Infection, Paralleling HDV Replicative Activity
Background & Aim: The entry of Hepatitis D Virus (HDV) depends on HBV surface proteins (HBsAg) composed of three isoforms: large-, middle, and small HBsAg. Here, we investigate the levels of total HBsAg and HBsAg isoforms and their correlations with HDV-RNA, HBcrAg, and transaminases in the setting of untreated chronic hepatitis D (CHD). Methods: This study includes 316 HBeAg-negative patients: 192 CHD and 124 with chronic hepatitis B (CHB) as a control group. HBsAg isoforms were quantified by ad hoc-designed ELISAs. Results: The composition of HBsAg isoforms varied between the two groups of patients, with remarkably higher small HBsAg, middle-HBsAg, and large HBsAg in CHD than in CHB. This data was confirmed by multivariable analysis (p < 0.0001). Among CHD, HBsAg isoforms positively correlated with HDV-RNA (p < 0.0001) and HBcrAg (p < 0.0001) but not with HBV-DNA. The results were confirmed by stratifying patients according to HDV-RNA (< or >1000 IU/mL) and HBcrAg (< or >3 logU/mL). Furthermore, CHD patients with ALT > upper limit of normal presented significantly higher S-HBsAg and M-HBsAg levels. Conclusions: CHD is characterized by a more elevated HBsAg isoform production, paralleling HDV-RNA and HBcrAg release. This may suggest a preferential recruitment of HBsAg isoforms in HDV virions at the expense of HBV virions. The association of HBsAg isoforms with higher ALT also suggests their potential contribution in supporting HDV-induced pro-inflammatory stimuli.