Anita De Rossi has long been involved in oncogenic retroviruses research. Her early efforts were directed towards investigating virus-host interactions in the murine system, including the role of endogenous retroviruses on leukemia development. Since 1983, her research has shifted from murine to human retroviruses (HTLV/HIV) in both experimental models and clinical settings. In the experimental model, she demonstrated that CD4 T cells are not the only target of HIV infection (PNAS 1986). She has been involved in several European projects concerning pediatric HIV/AIDS; her studies in this field addressed the virological and immunological correlates of pediatric disease outcome and are some of the first to indicate that HIV infection from mother-to-child HIV mainly occurs during intrapartum period (AIDS 1992; J Clin Invest 1996) and that host factors may restrict HIV infection (AIDS 1995; J Inf Dis 2001). Her interest has expanded to studying tumors in immunocompromised patients, with particular regard to EBV-related lymphomagenesis in HIV-infected or transplant patients, and more recently to studying cellular replicative potential driven by telomere/telomerase in virus-driven and virus-independent malignancies. Her studies are some of the first demonstrating that LMP1 of EBV activates at transcriptional level the expression of TERT, the catalytic component of telomerase, which in turn contributes to preserving the expression of EBV latency proteins, a prerequisite for EBV-driven transformation (J Virol 2008). The consequence is that inhibition of TERT triggers the activation of the viral lytic cycle with death of the infected cells (Clin Cancer Res 2013).
Lastly, her studies demonstrated that quantification of TERT in plasma may represent a minimally invasive tool for monitoring malignancies (Clin Cancer Res 2008) and response to therapy (Br J Cancer 2018). In addition, her studies provide the rationale for considering inhibition of TERT a useful approach for setting up new therapeutic strategies for virus-dependent and virus-independent malignancies (Clin Cancer Res 2013; Cell Death Dis 2016).