The following are the supplementary data related

The following are the supplementary data related to this article.
Author Contributions
Role of the Funding Source This work is supported by a grant from the National Institutes of Health/NIDDK to J.V.B. (R37 DK39773, RO1 DK072381). S.K. is the recipient of a Research Fellowship (Sumitomo Life Welfare and Culture Foundation, Japan and NOVARTIS Foundation for Gerontological Research, Japan) for the Promotion of Science.
Conflicts of Interest
Introduction The immune system of individuals infected with ion channel is gradually compromised and when untreated ultimately leads to advanced acquired immunodeficiency syndrome (AIDS), making patients vulnerable to opportunistic infections, malignancies, and other pathologies. Several different types of cancer are observed at an increased incidence in HIV-infected persons compared to the general population (Boshoff and Weiss, 2002; Cesarman, 2013). For example, primary effusion lymphoma (PEL) is a very aggressive non-Hodgkin Lymphoma (NHL) that most regularly appears in patients with major immunodeficiency, primarily in the context of HIV infection and advanced stages of AIDS. PEL is by definition associated with Kaposi\'s sarcoma-associated herpesvirus (KSHV, HHV-8) and most HIV-positive cases also show evidence of Epstein–Barr virus (EBV) infection (Cesarman, 2014). It originates within major body cavities such as the pleural, peritoneal spaces, or the pericardium. PEL has very poor prognosis with a survival time of two to three months after diagnosis without treatment and only six months with aggressive chemotherapy (Chen et al., 2007). There is no standard therapy for the treatment of PEL and combination chemotherapy is considered first-line therapy (Chen et al., 2007; Kaplan, 2013). The use of anti-HIV drugs is associated with better prognosis suggesting antiretroviral therapy as part of the supportive treatment (Lim et al., 2005a; Boulanger et al., 2005). Other approaches outside traditional chemotherapy have been investigated, including the addition of anti-herpes therapy such as cidofovir (Halfdanarson et al., 2006) or the use of NF-κB inhibitors (Keller et al., 2006; An et al., 2004). Very recently, brentuximab vedotin (Bhatt et al., 2013a), which is an anti-CD30 monoclonal antibody conjugated to the microtubule-disrupting agent monomethyl auristatin E, and a proteasome-HDAC inhibitor combination (Bhatt et al., 2013b) have been demonstrated to be effective against PEL. Although patients display response to therapy, remissions are often short-term and current chemotherapy approaches still result in poor outcome (Kaplan, 2012, 2013) warranting investigation of original therapeutic strategies for PEL. Successful HIV replication relies on different cellular factors and processes, and one such cellular co-factor is XPO1. In fact, the HIV protein Rev was first characterized as the prototype cargo protein substrate for XPO1. Rev highjacks the XPO1-mediated nuclear export pathway to transport the late viral RNA species to the cytoplasm (Malim et al., 1989b; Felber et al., 1989; Pollard and Malim, 1998). These late RNA species are produced by alternative splicing from a single, full-length proviral transcript and still contain introns. Importantly, effective replication requires the nuclear export and translation of these intron-containing RNAs. Under normal circumstances, intron-containing pre-RNAs are retained in the nucleus by the interaction of splicing factors until they are either spliced to completion or degraded. In order to overcome the nuclear retention of intron-containing RNAs by host cell factors, the early viral gene product Rev forms a multimeric complex on a secondary structured RNA element (the Rev response element, RRE) present in all unspliced and partially spliced viral mRNAs. Hence prior to the onset of splicing, Rev directs their transport to the cytoplasm via interaction with XPO1. The nuclear export of these late viral messengers is required for both the expression of late viral genes (gag, pol and env) and packaging of genomic RNA.