Publications by authors named "Simona Fiorentini"

The rise of Vancomycin-resistant enterococci (VRE) strains among cellular therapy recipients raises concerns due to increased morbidity, mortality, and hospitalization costs, particularly impacting transplanted patients with diminished survival expectations. Recent research linking lactose to Enterococcus growth and graft-versus-host disease (GVHD) emphasizes the need for data on reducing lactose in the diets of VRE-carrying patients, especially in cellular therapy contexts like CAR-T or allogeneic hematopoietic stem cell transplantation. Responding to elevated VRE positivity rates in rectal swabs among patients in our BMT Unit, a unique nutritional strategy was implemented, introducing lactose-free milk and strictly enforcing lactose-free diets.

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  • Prisons have a higher prevalence of communicable diseases like hepatitis C virus (HCV), necessitating routine testing and direct treatment access for inmates.
  • In a study of 5,378 admissions in two prisons in Brescia, 54.5% underwent HCV screening, revealing a 9.2% positivity rate with a significant number showing detectable virus levels.
  • Despite 77 treatments being administered, follow-up care for released prisoners was low, indicating a need for better education and improved test-and-treat programs to reduce HCV by 2030 through collaborative efforts with local healthcare services.
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Matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry systems are designed for rapid and reliable microbial identification. VITEK MS PRIME is the bioMérieux's new generation instrument equipped with a continuous load-and-go sample loading system, urgent slide prioritization for critical patient samples and new internal components for faster identification. The aim of this study was to assess the performance of VITEK MS PRIME and to compare it to that of the VITEK MS system.

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  • - SARS-CoV-2 variants of concern (VOCs) are evolving to enhance their ability to spread among humans, with mutations in the spike protein contributing significantly to this adaptation, particularly in immunocompromised patients where long-term virus replication occurs.
  • - Researchers discovered minor viral mutants coexisting with a dominant variant in an immunocompromised patient over a 222-day infection period; these mutations led to changes in how the virus entered cells and interacted with immune responses.
  • - The dominant variant (MB61) showed a faster replication rate and evaded certain immune defenses by using a specific entry method (membrane fusion), unlike the minor variant which used endocytosis and was more susceptible to antiviral responses.
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  • SARS-CoV-2 can infect human lung microvascular endothelial cells without causing cell death or releasing new viral particles, suggesting a unique method of infection.
  • The infection triggers these endothelial cells to produce various pro-inflammatory and pro-angiogenic molecules, leading to changes that promote inflammation and vascular dysfunction.
  • Understanding the interactions between the virus and host cells may reveal new therapeutic targets to combat the inflammation and complications associated with COVID-19.
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  • Human herpesvirus 6 (HHV-6) is a common β-herpesvirus with two species, HHV-6A and HHV-6B, that have similar genetic features yet different effects on health.
  • The U94 gene, unique to HHV-6, plays crucial roles in the virus’s life cycle and disease mechanisms, influencing things like virus replication and immune responses.
  • U94 also possesses properties that could be harnessed in medical applications, such as countering cancer development through its effects on angiogenesis, making it a focus of ongoing research.
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  • The study investigates the evolution of SARS-CoV-2 strains in Italy, focusing on the differences between early and late strains during the COVID-19 epidemic.
  • Nasopharyngeal swabs from March and May 2020 were analyzed, revealing that the GZ69 strain from May showed high replication capacity without causing cell damage, unlike the earlier strain AP66.
  • Genetic analysis indicated that GZ69 possesses 9 nucleotide mutations leading to several changes in key viral proteins, emphasizing the importance of monitoring viral variants, especially those found in asymptomatic individuals.
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  • HMPV (Human Metapneumovirus) is identified as a significant cause of lower respiratory infections and may change the immune response in dendritic cells within the lungs.
  • The study found that HMPV infects human lung microvascular endothelial cells, allowing for prolonged virus release without noticeable cell damage, which influences immune responses in nearby immune cells (monocyte-derived dendritic cells).
  • The research indicates that the secretome from HMPV-infected cells promotes a pro-Th2 immune environment, with specific attention to the mechanisms involving OX40L expression, suggesting a role for HMPV in shifting lung inflammation towards a Th2-dominant response.
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The original version of this article unfortunately contained a mistake. Arnaldo Caruso was not listed among the authors.

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S. typhi infection rarely involves the genitourinary system. We report the first described case of acute epididymo-orchitis due to S.

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Despite antiretroviral therapy, HIV+ individuals still have increased risk to develop lymphomas, including marginal zone lymphomas, suggesting that factors other than HIV-related immunosuppression are probably acting as lymphomagenic factors in the HIV setting. The possible pathogenic involvement of HIV p17 protein variants was investigated in a particularly informative case of HIV-related splenic marginal zone lymphoma, which was negative for oncogenic virus infections, thus allowing us to assess the possible direct contribution of these HIV-encoded proteins to lymphomagenesis. The presence of p17 protein was analyzed by immunohistochemistry in lymphoma tissue.

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  • Human metapneumovirus (hMPV) is a significant cause of lower respiratory infections in children and has been linked to the development of chronic lung diseases like asthma.
  • Research using human alveolar epithelial A549 cells shows that hMPV can initially trigger cell death (apoptosis) but eventually allows the cells to survive and keep producing the virus.
  • The study sheds light on the mechanisms by which hMPV can persist in lung cells, indicating its potential role in ongoing respiratory issues in children.
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Recent data highlight the presence, in HIV-1-seropositive patients with lymphoma, of p17 variants (vp17s) endowed with B-cell clonogenicity, suggesting a role of vp17s in lymphomagenesis. We investigated the mechanisms responsible for the functional disparity on B cells between a wild-type p17 (refp17) and a vp17 named S75X. Here, we show that a single Arginine (R) to Glycine (G) mutation at position 76 in the refp17 backbone (p17R76G), as in the S75X variant, is per se sufficient to confer a B-cell clonogenic potential to the viral protein and modulate, through activation of the PTEN/PI3K/Akt signaling pathway, different molecules involved in apoptosis inhibition (CASP-9, CASP-7, DFF-45, NPM, YWHAZ, Src, PAX2, MAPK8), cell cycle promotion and cancer progression (CDK1, CDK2, CDK8, CHEK1, CHEK2, GSK-3 beta, NPM, PAK1, PP2C-alpha).

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HIV-1 p17 plays an important role in the virus life-cycle and disease pathogenesis. Recent studies indicated a high heterogeneity of p17. A high number of insertions in the p17 carboxy-terminal region have been more frequently detected in patients with non-Hodgkin lymphoma (NHL), suggesting a role of altered p17 in lymphomagenesis.

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The human immune deficiency virus type 1 (HIV-1) matrix protein p17 (p17), although devoid of a signal sequence, is released by infected cells and detected in blood and in different organs and tissues even in HIV-1-infected patients undergoing successful combined antiretroviral therapy (cART). Extracellularly, p17 deregulates the function of different cells involved in AIDS pathogenesis. The mechanism of p17 secretion, particularly during HIV-1 latency, still remains to be elucidated.

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Although in decline after successful anti-HIV therapy, B-cell lymphomas are still elevated in HIV-1-seropositive (HIV+) persons, and the mechanisms are obscure. The HIV-1 matrix protein p17 persists in germinal centers long after HIV-1 drug suppression, and some p17 variants (vp17s) activate Akt signaling and promote growth of transformed B cells. Here we show that vp17s derived from four of five non-Hodgkin lymphoma (NHL) tissues from HIV+ subjects display potent B-cell growth-promoting activity.

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The rapid diagnosis of tuberculosis (TB) and the detection of drug-resistant Mycobacterium tuberculosis strains are critical for successful public health interventions. Therefore, TB diagnosis requires the availability of diagnostic tools that allow the rapid detection of M. tuberculosis and drug resistance in clinical samples.

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The HIV-1 matrix protein p17 (p17) plays a crucial role in the virus life cycle. It is released in the extracellular space from HIV-1-infected cells and accumulates in the tissues of patients, even in those successfully treated with highly active antiretroviral therapy. Extracellular p17 deregulates the biological functions of many different cells that are directly or indirectly implicated in AIDS pathogenesis.

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Objective: A therapeutic vaccination based on a synthetic peptide (AT20) representative of the HIV-1 matrix protein p17 (p17) functional region, coupled to keyhole limpet hemocyanin (KLH) AT20-KLH was capable of inducing the production of high-avidity antibodies (Abs) toward a previous untargeted p17 hotspot of functional activity in highly active antiretroviral therapy (HAART)-treated HIV-1-infected patients. Since avidity of Abs after immunization and the retention of antigens are important in sustaining the long-lasting production of specific humoral responses, we asked whether AT20-KLH vaccination would result in development of a long-lived immune response.

Methods: The long-term duration of Ab response to AT20-KLH has been evaluated in 10 patients previously enrolled for the AT20-KLH vaccination trial at day 898 post-immunization.

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Human immunodeficiency virus p17 matrix protein is released by infected cells and may accumulate within lymphoid tissues where it may deregulate the biological activities of different cell populations by binding to CXCR1 and CXCR2 cellular receptors. S75X, a natural p17 variant, was recently shown to enhance the malignant properties of lymphoma cells. We investigated a reference p17 protein and the S75X variant for their ability to bind to Epstein-Barr virus (EBV)-infected primary and fully transformed B-lymphocytes and trigger downstream effects of potential pathogenic relevance.

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Objective: Monocyte inflammatory processes are fundamental events in AIDS pathogenesis. HIV-1 matrix protein p17, released from infected cells, was found to exert an interleukin (IL)-8 chemokine-like activity on human monocytes, promoting their trafficking and sustaining inflammatory processes, after binding to CXCR1. A haplotype of the CXCR1 gene (CXCR1_300_142) has been associated with slow HIV disease progression.

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Carbapenem-resistant K. pneumoniae has recently been reported as a new multidrug-resistant nosocomial pathogen. This study reports the emergence of carbapenem-resistant K.

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Background: The HIV-1 matrix protein p17 (p17MA) is a pleiotropic protein that plays a key role in the HIV-1 life cycle. It has been long believed to have a highly conserved primary amino acid sequence and a well-preserved structural integrity to avoid severe fitness consequences. However, recent data revealed that the carboxy (COOH)-terminus of p17MA possesses high levels of predicted intrinsic disorder, which would subtend to at least partially unfolded status of this region.

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