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Competing interests The authors hereby declare that they do not have any competing interest in this study. Authors’ contributions PP and VL conceived and NF-��B inhibitor designed the study. CG, AMF, BS, MGP, VL, PP collected and assembled the data, AM performed the ultrasound examinations, VL performed the statistical analysis, VL and PP wrote the manuscript. LS gave support in the statistical analysis and in the final drafting of the paper. All authors read and approved the final manuscript.”
“Introduction Kaposi sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus found in all forms of Kaposi’s sarcoma (KS) and is also highly associated with two lymphoproliferative disorders that are primary effusion lymphoma (PEL) and multicentric Castleman’s disease

(MCD) [1]. KSHV is able to infect a variety of non haematological and haematological cells such as B and T lymphocytes, monocytes, macrophages and dendritic cells (DC) that express the known KSHV receptors [2–6], such as proteoglycan heparan sulphates (HS), GNAT2 DC-SIGN and some integrins [7–10]. THP-1 is a monocytic cell line derived from an acute monocytic leukemia patient whose infection by KSHV has been previously reported [11, 12]. These cells support a latent viral infection that implies the expression of few viral proteins in the majority of the infected cells that is sufficient to subvert the expression of monocyte activation markers and influence the cytokine release [12]. Among the molecular pathways altered in tumor cells harboring KSHV, or following KSHV de-novo infection is phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) [13, 14], which is an ubiquitous pathway that controls cell survival and cell metabolism [15, 16]. PI3Ks are divided into four classes that have different substrate specificities.