Dear Colleagues,

Although a link between infectious agents and neoplasia has been suggested for a long time, only in recent years has clear-cut evidence of such a close correlation been provided. In view of the relevance of the immune system in controlling infections as well as the role of (chronic) inflammation in the pathogenesis of neoplasias, lymphoproliferative disorders have been claimed to represent an intriguing model to exemplify the relationship with several infectious agents. Mechanisms involved in favoring neoplastic transformation can be either indirect, for instance, the role of Helicobacter Pylori in the pathogenesis of MALT lymphoma, or rather direct, such as the role of Human T Lymphotropic Virus I in Adult T Cell Leukemia. Among these two ends of the spectrum, a plethora of lymphoproliferative disorders underlying a pathogenetic role of infectious agents is reported in the literature. Both viral (either RNA viruses including HTLV, HCV or HIV or DNA viruses, such as Epstein–Barr Virus) and bacterial agents (H. Pylori or Chlamydia species) are included in this growing list. Interestingly, even a putative role for human endogenous retroviral (HERV) sharing has been recently advocated. A common feature of all these disorders is that an initial indolent coexistence, i.e., when several mechanisms are devised by agents to keep their status, at some point strongly impacts with further autonomous proliferation of lymphoid cells, ultimately leading to neoplastic growth and cancer development.

In this Special Issue, we are focusing on the updated definition of mechanisms of different infectious agents as lymphoid cancer makers and the possibility to counteract their action before overt lymphoproliferative transformation, thus blocking their ability to lead to an autonomous cell growth.

Prof. Dr. Renato Zambello
Guest Editor

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