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Antonella Farina,
Roberta Santarelli,
Rossella Bloise,
Roberta Gonnella,
Marisa Granato,
Roberto Bei,
Andrea Modesti,
Mara Cirone,
Luiza Bengtsson,
Antonio Angeloni, Alberto Faggioni
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ABSTRACT: p29, a newly identified Kaposi's sarcoma-associated herpesvirus (KSHV) protein, is the product of ORF67, the positional homolog of the conserved herpesvirus protein UL34. Like its homologues in other herpesviruses, p29 is expressed early during viral lytic cycle, and is localized on the nuclear rim. Upon chemical induction of viral replication in primary effusion lymphoma cells, p29 interacts with p33, encoded by ORF69, the positional homolog of the conserved herpesvirus protein UL31, and both proteins colocalize on the nuclear membrane. IFA and biochemical analysis of infected or transfected cells showed that p29 expression resulted in delocalization and hyperphosphorylation of emerin, whereas other nuclear lamin associated proteins, such as LUMA, LB1 and LBR were not affected. Mislocalization of emerin was robustly increased upon combined expression of p29 and p33, suggesting that emerin destabilization might represent the first step in nuclear lamina disassembling, a process necessary for nucleocapsid maturation.
Virus Research 04/2013; · 2.94 Impact Factor
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ABSTRACT: A growing number of studies indicate that cell death can be either immunogenic or not, depending on its modalities, the type and the activation state of the cells, and finally, the environment where it happens. Increased understanding of the immunogenicity of cancer cell death will significantly improve the outcome of chemotherapeutic treatments.
Oncoimmunology. 10/2012; 1(7):1218-1219.
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ABSTRACT: For an efficient immune response against viral infection, dendritic cells (DCs) must express a coordinate repertoire of receptors that allow their recruitment to the sites of inflammation and subsequently to the secondary lymphoid organs in response to chemokine gradients.Several pathogens are able to subvert the chemokine receptor expression and alter the migration properties of DCs as strategy to escape from the immune control.
Here we report the inhibitory effect of Human Herpesvirus 8 (HHV-8) on the migratory behavior of immature and mature DCs. We found that the virus altered the DC chemokine receptor expression and chemokine induced migration. Moreover HHV-8 was also able to interfere with basal motility of DCs by inducing cytoskeleton modifications.
Based on our findings, we suggest that HHV-8 is able to subvert the DC migration capacity and this represents an additional mechanism which interferes with their immune-functions.
Virology Journal 05/2012; 9:92. · 2.34 Impact Factor
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ABSTRACT: The study was performed to determine if there is an association between the genotype and transmission of HHV-8 types A and C. These HHV-8 subtypes are prevalent in the area of North of Sardinia, which is an island off west Italy's mainland that has a high HHV-8 seroprevalence (35%). Blood and saliva samples from 30 patients with classic Kaposi's sarcoma who were lifetime residents of North Sardinia were analyzed to identify the HHV-8 genotype and quantitate the viral load. Genotype A, especially A1 subtype, was found more frequently (9/30 patients) and had a significantly higher viral load in saliva compared to blood (P = 0.029), where type C was found more frequently but with a viral load lower than 10(3) copies/ml. To determine if there is a correlation between the viral genotype and cellular tropism, type A1 and C3 HHV-8 viral particles were obtained from cell lines BCBL1 and BC3 infected chronically with HHV-8 A1 and C3 genotypes respectively and used to infect HEK293 epithelial origin cells and PBMCs in vitro. The data indicate that the A1 HHV-8 genotype is tropic and replicates at higher levels in the epithelial cell lines.
Journal of Medical Virology 05/2012; 84(5):786-91. · 2.82 Impact Factor
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ABSTRACT: To understand how cytotoxic agent-induced cancer cell death affects the immune system is of fundamental importance to stimulate immune response to counteract the high mortality due to cancer. Here we compared the immunogenicity of Primary Effusion Lymphoma (PEL) cell death induced by anticancer drug Bortezomib (Velcade) and Tyrphostin AG 490, a Janus Activated Kinase 2/signal trasducer and activator of transcription-3 (JAK2/STAT3) inhibitor. We show that both treatments were able to induce PEL apoptosis with similar kinetics and promote dendritic cells (DC) maturation. The surface expression of molecules involved in immune activation, namely calreticulin (CRT), heat shock proteins (HSP) 90 and 70 increased in dying cells. This was correlated with DC activation. We found that PEL cell death induced by Bortezomib was more effective in inducing uptake by DC compared to AG 490 or combination of both drugs. However the DC activation induced by all treatments was completely inhibited when these cells were pretreated with a neutralizing antiboby directed against the HSP90/70 and CRT common receptor, CD91. The activation of DC by Bortezomib and AG 490 treated PEL cells, as seen in the present study, might have important implications for a combined chemo and immunotherapy in such patients.
PLoS ONE 01/2012; 7(3):e31732. · 4.09 Impact Factor
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ABSTRACT: BACKGROUND: Homeodomain-interacting protein kinase 2 (HIPK2) is a multifunctional protein that exploits its kinase activity to modulate key molecular pathways in cancer to restrain tumor growth and induce response to therapies. For instance, HIPK2 knockdown induces upregulation of oncogenic hypoxia-inducible factor-1 (HIF-1) activity leading to a constitutive hypoxic and angiogenic phenotype with increased tumor growth in vivo. HIPK2 inhibition, therefore, releases pathways leading to production of pro-inflammatory molecules such as vascular endothelial growth factor (VEGF) or prostaglandin E2 (PGE(2)). Tumor-produced inflammatory mediators other than promote tumour growth and vascular development may permit evasion of anti-tumour immune responses. Thus, dendritic cells (DCs) dysfunction induced by tumor-produced molecules, may allow tumor cells to escape immunosurveillance. Here we evaluated the molecular mechanism of PGE(2) production after HIPK2 depletion and how to modulate it. METHODOLOGY/PRINCIPAL FINDINGS: We show that HIPK2 knockdown in colon cancer cells resulted in cyclooxygenase-2 (COX-2) upregulation and COX-2-derived PGE(2) generation. At molecular level, COX-2 upregulation depended on HIF-1 activity. We previously reported that zinc treatment inhibits HIF-1 activity. Here, zinc supplementation to HIPK2 depleted cells inhibited HIF-1-induced COX-2 expression and PGE(2)/VEGF production. At translational level, while conditioned media of both siRNA control and HIPK2 depleted cells inhibited DCs maturation, conditioned media of only zinc-treated HIPK2 depleted cells efficiently restored DCs maturation, seen as the expression of co-stimulatory molecules CD80 and CD86, cytokine IL-10 release, and STAT3 phosphorylation. CONCLUSION/SIGNIFICANCE: THESE FINDINGS SHOW THAT: 1) HIPK2 knockdown induced COX-2 upregulation, mostly depending on HIF-1 activity; 2) zinc treatment downregulated HIF-1-induced COX-2 and inhibited PGE(2)/VEGF production; and 3) zinc treatment of HIPK2 depleted cells restored DCs maturation.
PLoS ONE 01/2012; 7(11):e48342. · 4.09 Impact Factor
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Jochen Imig,
Natalie Motsch,
Jia Yun Zhu,
Stephanie Barth,
Michal Okoniewski,
Tanja Reineke,
Marianne Tinguely, Alberto Faggioni,
Pankaj Trivedi,
Gunter Meister,
Christoph Renner,
Friedrich A Grässer
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ABSTRACT: The Epstein-Barr virus (EBV) is an oncogenic human Herpes virus found in ∼15% of diffuse large B-cell lymphoma (DLBCL). EBV encodes miRNAs and induces changes in the cellular miRNA profile of infected cells. MiRNAs are small, non-coding RNAs of ∼19-26 nt which suppress protein synthesis by inducing translational arrest or mRNA degradation. Here, we report a comprehensive miRNA-profiling study and show that hsa-miR-424, -223, -199a-3p, -199a-5p, -27b, -378, -26b, -23a, -23b were upregulated and hsa-miR-155, -20b, -221, -151-3p, -222, -29b/c, -106a were downregulated more than 2-fold due to EBV-infection of DLBCL. All known EBV miRNAs with the exception of the BHRF1 cluster as well as EBV-miR-BART15 and -20 were present. A computational analysis indicated potential targets such as c-MYB, LATS2, c-SKI and SIAH1. We show that c-MYB is targeted by miR-155 and miR-424, that the tumor suppressor SIAH1 is targeted by miR-424, and that c-SKI is potentially regulated by miR-155. Downregulation of SIAH1 protein in DLBCL was demonstrated by immunohistochemistry. The inhibition of SIAH1 is in line with the notion that EBV impedes various pro-apoptotic pathways during tumorigenesis. The down-modulation of the oncogenic c-MYB protein, although counter-intuitive, might be explained by its tight regulation in developmental processes.
Nucleic Acids Research 11/2010; 39(5):1880-93. · 8.03 Impact Factor
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Eleni Anastasiadou,
Signe Vaeth,
Laura Cuomo,
Francesco Boccellato,
Sara Vincenti,
Mara Cirone,
Carlo Presutti,
Steffen Junker,
Gösta Winberg,
Luigi Frati,
Paul A Wade, Alberto Faggioni,
Pankaj Trivedi
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ABSTRACT: The B cell lymphomas associated with Epstein-Barr virus (EBV) are not limited to any specific stage of B cell differentiation but covers widely different B cell phenotypes. In vitro infection of the virus negative tumors with a recombinant EBV strain has provided important insights into virus-tumor interaction. Here, we investigated the interaction between EBV and terminally differentiated tumor derived B cells, namely multiple myeloma (MM). The in vitro EBV infected MM expressed restricted viral latency. Acquisition of the virus was accompanied by a partial reprogramming to a mature B cell phenotype. Thus, the plasma cell markers syndecan-1 (CD138), Blimp1 and MUM1 were downregulated, while expression of HLADR, CIITA and TCL1, which are normally not expressed in plasmacytoid cells, was upregulated. The silenced transcription factor gene encoding Pax5 and its target BLNK were activated. Significantly, the free lambda light chains secreted in the medium were reduced in EBV infected MM clones. Collectively, these results suggest that the restricted EBV latency can cause at least partial phenotypic reversion of terminally differentiated B tumor cells. We suggest that the restricted EBV latent gene expression may not only be the consequence but the cause of the mature B cell phenotype, actively participating in the virus persistence.
Cancer letters 06/2009; 284(2):165-74. · 4.86 Impact Factor
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ABSTRACT: Functional impairment of dendritic cells (DC) appears to be one of the mechanisms responsible for tumor escape from the control of the immune system. DC isolated from tumor-bearing animals and cancer patients with solid or with hematological malignancies have phenotypic and functional abnormalities. In addition, supernatants from in vitro cultured tumor cells have been shown to interfere with DC differentiation from CD34+ and monocyte precursors. Primary effusion lymphoma (PEL) is a Human Herpesvirus-8 (HHV-8)-associated tumor, which releases several cytokines such as IL-6, IL-10 and VEGF and its growth seems to be dependent on them in vitro or in vivo. In the present study, we found that these cytokines released by PELs have also an important role in interfering with the in vitro differentiation of immature DC (iDC) from CD14+ monocytes. The iDC obtained in the presence of PEL supernatants showed reduction of FITC-dextran uptake, reduction of MLR allostimulatory activity and altered expression of surface molecules, suggesting that cytokines released by PEL adversely affect DC differentiation.
Immunology Letters 10/2008; 120(1-2):37-41. · 2.53 Impact Factor
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ABSTRACT: Previous genetic and biochemical studies performed with several members of the Alphaherpesvirus subfamily have shown that the UL31 and UL34 proteins are essential components of the molecular machinery that mediates the primary egress of newly assembled capsids across the nuclear membrane. Further, there is substantial evidence that BFLF2 and BFRF1, the respective positional homologs of UL31 and UL34 in the Epstein-Barr virus (EBV) genome, are also their functional homologs, i.e., that the UL31/UL34 pathway is common to distant herpesviruses. However, the low degree of protein sequence identity between UL31 and BFLF2 would argue against such a hypothesis. To further clarify this issue, we have constructed a recombinant EBV strain devoid of BFLF2 (DeltaBFLF2) and show that BFLF2 is crucial for efficient virus production but not for lytic DNA replication or B-cell transformation. This defective phenotype could be efficiently restored by trans complementation with a BFLF2 expression plasmid. Detailed analysis of replicating cells by electron microscopy revealed that, as expected, DeltaBFLF2 viruses not only failed to egress from the nucleus but also showed defective DNA packaging. Nonfunctional primary egress did not, however, impair the production and extracellular release of enveloped but empty viral particles that comprised L particles containing tegument-like structures and a few virus-like particles carrying empty capsids. The DeltaBFLF2 and DeltaUL31 phenotypes therefore only partly overlap, from which we infer that BFLF2 and UL31 have substantially diverged during evolution to fulfil related but distinct functions.
Journal of Virology 05/2008; 82(8):4042-51. · 5.40 Impact Factor
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Barbara Serafini,
Barbara Rosicarelli,
Diego Franciotta,
Roberta Magliozzi,
Richard Reynolds,
Paola Cinque,
Laura Andreoni,
Pankaj Trivedi,
Marco Salvetti, Alberto Faggioni,
Francesca Aloisi
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ABSTRACT: Epstein-Barr virus (EBV), a ubiquitous B-lymphotropic herpesvirus, has been associated with multiple sclerosis (MS), an inflammatory disease of the central nervous system (CNS), but direct proof of its involvement in the disease is still missing. To test the idea that MS might result from perturbed EBV infection in the CNS, we investigated expression of EBV markers in postmortem brain tissue from MS cases with different clinical courses. Contrary to previous studies, we found evidence of EBV infection in a substantial proportion of brain-infiltrating B cells and plasma cells in nearly 100% of the MS cases examined (21 of 22), but not in other inflammatory neurological diseases. Ectopic B cell follicles forming in the cerebral meninges of some cases with secondary progressive MS were identified as major sites of EBV persistence. Expression of viral latent proteins was regularly observed in MS brains, whereas viral reactivation appeared restricted to ectopic B cell follicles and acute lesions. Activation of CD8+ T cells with signs of cytotoxicity toward plasma cells was also noted at sites of major accumulations of EBV-infected cells. Whether homing of EBV-infected B cells to the CNS is a primary event in MS development or the consequence of a still unknown disease-related process, we interpret these findings as evidence that EBV persistence and reactivation in the CNS play an important role in MS immunopathology.
Journal of Experimental Medicine 12/2007; 204(12):2899-912. · 13.85 Impact Factor
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ABSTRACT: Several viruses interfere with the host immune response by infecting dendritic cells and by altering their functional activity. Here, we report that exposure to Human herpesvirus 8 (HHV-8) of human dendritic cell (DC) monocyte precursors resulted in impaired immature DC (iDC) formation as indicated by a reduced CD1a expression. In accordance, the immunostimulatory ability of such iDC was significantly reduced, as indicated by mixed lymphocyte culture (MLR) assays. The immunostimulatory functions of DCs were similarly inhibited by the UV inactivated viral stocks, suggesting that the virus binding is sufficient to determine the observed effect. Furthermore, HHV8 mediated inhibition of the DC allostimulatory function was present in lipopolysaccharide (LPS) matured DCs. A strong reduction of the expression of the costimulatory molecule CD80 on the surface of the virus-exposed cells was observed as well. Impairment of dendritic cell development and function might represent an important strategy used by HHV-8 to escape from the host defense mechanisms.
Immunology Letters 11/2007; 113(1):40-6. · 2.53 Impact Factor
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ABSTRACT: Epstein-Barr virus (EBV)-negative diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma-derived cell lines infected in vitro with a recombinant EBV expressed type II/III latency. High expression of EBNA2 inversely correlated with expression of germinal center (GC)-associated genes, BCL6 and TCL1. The decreased expression of BCL6 appeared to be dose dependent, with almost complete abrogation in highly EBNA2-expressing clones. The role of EBNA2 in negative regulation of these genes was confirmed by transfection and in a hormone-inducible EBNA2 cell system. LMP1 transfection reduced expression of TCL1, but not of BCL6, in DLBCLs. The GC-associated gene repression was at the transcriptional level and CBF1 independent. A decrease in HLA-DR, surface immunoglobulin M, and class II transactivator expression and an increase in CCL3, a BCL6 repression target, was observed in EBNA2-expressing clones. Since BCL6 is indispensable for GC formation and somatic hypermutations (SHM), we suggest that the previously reported lack of SHM seen in EBNA2-expressing GC cells from infectious mononucleosis tonsils could be due to negative regulation of BCL6 by EBNA2. These findings suggest that EBNA2 interferes with the GC phenotype.
Journal of Virology 04/2007; 81(5):2274-82. · 5.40 Impact Factor
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ABSTRACT: High prevalence of human herpesvirus type 8 (HHV-8) infection has been reported on the island of Sardinia. Among emigrants from Sardinia, rates of HHV-8 infection are lower than they are in Sardinia and are similar to those observed in the local population. Thus, environmental factors seem to play a relevant role in affecting the prevalence of HHV-8 infection.
Clinical Infectious Diseases 05/2006; 42(7):e66-8. · 9.15 Impact Factor
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ABSTRACT: The switch from latency to lytic phase of Epstein-Barr virus (EBV) is coordinated by the expression of two viral transactivators known as ZEBRA and RTA. The BFRF1 gene has been shown to be transcribed during the early phases of EBV lytic cycle. Here, we characterized the BFRF1 promoter showing that ZEBRA transfection stimulated BFRF1 expression, whereas RTA induced BFRF1 only after the transfection of an amount of plasmid largely in excess than that sufficient to stimulate the expression of other RTA-responsive genes. However, a co-operative effect between ZEBRA and RTA in the expression of BFRF1 is evident since the transfection of RTA can rescue the transactivating capacity of a mutant of the ZEBRA protein, known as Z(S186A), that has a substitution affecting the DNA binding region. Moreover, we identified one ZEBRA-responsive element (ZRE) and one RTA-responsive element (RRE) within the BFRF1 promoter region.
Virology 04/2006; 347(1):109-16. · 3.35 Impact Factor
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Luisa Bertolini,
Maria Luisa Aebischer,
Franco Ameglio,
Antonio Angeloni,
Isabella Delaroche, Alberto Faggioni,
Alberto Fruscalzo,
Giovanni Gorini,
Annalucia Serafino,
Giuseppe Starace,
Antonio Tabilio
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ABSTRACT: The present study describes the phenotypic and genotypic features of seven individual growth transformed, euploid-diploid EBV+ human B cell lines arisen spontaneously in vitro. The lines, obtained under general and standard culture conditions (un-manipulated), from seven individual bone marrow samples of 18 healthy young adults, Caucasian, of both sexes, display many traits of normal B cells and represent a mixture of EBV infected latently (latency type III) and producer cells (5-16% VCA+ by immunofluorescence) releasing seven individual different viral strains [Fruscalzo et al., 2001. DNA sequence heterogeneity within the Epstein-Barr virus family of repeats in the latent origin of replication. Gene 265, 165-173] similar to the B95-8 genotype as shown by results of Southern blot of BamHI-digested DNA fragment. These tests were planned to characterize more fully this panel of new bone marrow cell lines sharing normal B cell traits.
Journal of Virological Methods 07/2005; 126(1-2):91-100. · 2.01 Impact Factor
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ABSTRACT: The molecular mechanisms that underlie maturation and egress of Epstein-Barr virus (EBV) virions are only partially characterized. We have recently shown that the BFRF1 gene, the EBV positional homolog of herpes simplex virus type 1 and pseudorabies virus UL34, is expressed early during EBV lytic replication and that it is found predominantly on the nuclear membrane (A. Farina, R. Santarelli, R. Gonnella, R. Bei, R. Muraro, G. Cardinali, S. Uccini, G. Ragona, L. Frati, A. Faggioni, and A. Angeloni, J. Virol. 74:3235-3244, 2000). These data suggest that the BFRF1 protein might be involved in viral primary envelopment. To precisely determine the function of this protein, we have constructed an EBV mutant devoid of the BFRF1 gene (BFRF1-KO). 293 cells carrying BFRF1-KO showed no differences in comparison with wild-type EBV in terms of DNA lytic replication or expression of late viral proteins upon induction of the lytic cycle. However, binding assays and infection experiments using cell lines or human cord blood lymphocytes showed a clear reduction in the viral mutant titers. Complementation experiments with BFRF1-KO and a BFRF1 expression vector restored viral titers to levels similar to those for the wild-type control, showing that the modifications that we introduced were limited to the BFRF1 gene. Electron microscopic observations showed that the reduction in viral titers was due to sequestration of EBV nucleocapsids in the nuclei of lytically induced cells. This suggests that BFRF1 is involved in transport of the maturing virion across the nuclear membrane. This hypothesis was further supported by the observation that BFRF1 is present in maturing intracellular virions but not in their extracellular counterparts. This implies that BFRF1 is a key protein for EBV maturation.
Journal of Virology 04/2005; 79(6):3703-12. · 5.40 Impact Factor
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Roberta Gonnella,
Antonella Farina,
Roberta Santarelli,
Salvatore Raffa,
Regina Feederle,
Roberto Bei,
Marisa Granato,
Andrea Modesti,
Luigi Frati,
Henri-Jacques Delecluse,
Maria Rosaria Torrisi,
Antonio Angeloni, Alberto Faggioni
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ABSTRACT: We have reported in the accompanying paper that the BFRF1 protein of Epstein-Barr virus (EBV) is important for efficient primary viral envelopment and egress (A. Farina, R. Feederle, S. Raffa, R. Gonnella, R. Santarelli, L. Frati, A. Angeloni, M. R. Torrisi, A. Faggioni, and H.-J. Delecluse, J. Virol. 79:3703-3712). Here we describe the characterization of the product of the EBV BFLF2 gene, which belongs to a family of conserved herpesviral genes which include the UL31 genes of herpes simplex virus and of pseudorabies virus and whose products are known to interact with UL34, the positional homolog of BFRF1. BFLF2 is an early transcript and is expressed in a variety of cell lines upon EBV lytic cycle activation. Western blotting of purified virion preparations showed that BFLF2 is a component of intracellular virions but is absent from mature extracellular virions. Coimmunoprecipitation experiments indicated that BFLF2 interacts with BFRF1, which was confirmed by immunofluorescence confocal microscopy showing that the two proteins colocalize on the nuclear membrane not only upon cotransfection in epithelial cells but also during viral replication. In cells carrying an EBV mutant with the BFRF1 gene deleted (293-BFRF1-KO cells) BFLF2 expression was low, and it was restored to wild-type levels upon treatment of the cells with the proteasome inhibitor MG132. Furthermore, recomplementing the 293-BFRF1-KO cells by BFRF1 transfection restored BFLF2 expression to the wild-type level. In addition, when expressed alone BFLF2 was localized diffusely inside the nucleus, whereas in the presence of BFRF1 the two proteins colocalized at the nuclear rim. Finally, 293 epithelial cells transfected with either protein or cotransfected were analyzed by electron microscopy to investigate potential alterations in the morphology of the nuclear membrane. The ultrastructural analysis revealed that (i) BFRF1 caused duplications of the nuclear membrane, similar to those reported to occur during the course of herpesviral replication, and (ii) while BFLF2 alone did not cause any apparent alteration, coexpression of the two proteins dramatically induced profound convolutions of the duplicated nuclear membrane. Both biochemical and morphological analysis showed association of the BFRF1-BFLF2 complex with a component of the nuclear lamina, lamin B. Taken together, these results and those of the accompanying paper (Farina et al., J. Virol. 79:3703-3712) indicate an important role of BFRF1 and BFLF2 in the early steps of EBV maturation at the nuclear membrane.
Journal of Virology 04/2005; 79(6):3713-27. · 5.40 Impact Factor
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Journal of Clinical Virology 10/2004; 31(1):78-80. · 3.97 Impact Factor
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Francesca Cottoni,
Roberta Santarelli,
Giuseppe Gentile,
Domenico Gallisai,
Angela Capobianchi,
Maria Vittoria Masala,
Maria Antonietta Montesu,
Marisa Coinu,
Daniela Piras,
Pietro Martino,
Gabriella Girelli,
Rosanna Satta,
Decio Cerimele,
Luigi Frati, Alberto Faggioni,
Antonio Angeloni
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ABSTRACT: The potential risk of acquiring infection by the novel human herpesvirus-8 (HHV-8) through blood derivatives is still debated.
In the present study, we determined HHV-8 seroprevalence in beta-thalassemic patients living in Italy.
We have analysed 86 patients from Sardinia, an island characterised by a high diffusion of HHV-8, as well as 33 thalassemics from the area of Rome, where a lower rate of HHV-8 infection has been reported. These data have been compared with HHV-8 seroprevalence found in healthy controls living in the same areas of the assayed patients.
A three-fold increase in HHV-8 seroprevalence was found among thalassemic patients when compared to control groups taken from the same regions (17.6% versus 5.1%). This risk factor was statistically significant when considering the Sardinians alone (P = 0.01) and the entire population analysed in the present survey (P = 0.0006). In the Roman area also an increased seroprevalence in thalassemic subjects was found (12.1% versus 4.6%) but it was not statistically significant (P = 0.2). HHV-8 is sporadically present in the blood of healthy individuals and it is unknown whether the virus eventually present in donors' blood is completely cleared by the treatments which blood undergoes before red cells are transfused. Based on these considerations, we hypothesise that multiply transfused subjects living in areas at high HHV-8 prevalence present an increased risk of being infected.
Journal of Clinical Virology 06/2004; 30(1):106-9. · 3.97 Impact Factor
