Molecular and cellular interplay in virus-induced tumors in solid organ recipients

Alessia Gallo, Monica Miele, Ester Badami, Pier Giulio Conaldi

Research output: Contribution to journalArticlepeer-review


Patients following solid organ transplantation show a higher risk of developing cancer compared to the general population. Elevated risk is likely due to the interplay of a combination of factors, such as chronic inflammation, coexisting medical conditions, immunosuppressive regimen and persistent infection with oncogenic viruses. In addition, the tumor microenvironment plays a pivotal role in cancer progression, by driving recruitment and in situ differentiation of anti-inflammatory cells of the adaptive and innate immune system such as regulatory T cells, Th17, Dendritic Cells, Myeloid Derived Suppressor Cells, Type 2 Macrophages. Here we discuss the molecular role and the contribution to oncogenesis of Epstein–Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV/HHV8) and Hepatitis C virus (HCV) in immunocompromised patients and describe how these viruses may contribute to oncogenesis both directly and indirectly.

Original languageEnglish
JournalCellular Immunology
Publication statusAccepted/In press - Jan 1 2018


  • Epstein-Barr virus
  • Hepatitis C virus (HCV)
  • Kaposi's sarcoma-associated herpesvirus
  • Oncogenic viruses
  • Solid organ transplantation

ASJC Scopus subject areas

  • Immunology


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