<unk> 's<unk>  is usually a localized tumor that can be treated either surgically or through local irradiation. Chemotherapy with drugs such as liposomal anthracyclines or paclitaxel may be used, particularly for invasive disease. Antiviral drugs, such as ganciclovir, that target the replication of<unk> es such as<unk>  have been used to successfully prevent development of<unk> 's<unk> , although once the tumor develops these drugs are of little or no use. For patients with AIDS-KS, the most effective therapy is highly active antiretroviral therapy to reduce HIV infection. AIDS patients receiving adequate anti-HIV treatment may have up to a 90% reduction in<unk> 's<unk>  occurrence. Although<unk>  affects the host immune system, there is ample chance for clinical intervention to recover this change. One challenge is overexpression inhibitory of target cell repress immune. Under longtime inflammation stimulation, the target cell becomes unable to respond, which leads to an exhausted phenotype. The activation immunotherapies can revive and enhance immune cell function. Comparing to other immunotherapies, therapies targeting the anti-programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) has been a great success. Because of<unk>  infection, the monocytes increase the expression of PD-1, which is an inhibitory molecule, and cause immune escape in many tumor types. There is high PD-1 expression in NK cells from KS-HIV patients and cause exhausted phenotype. The anti-PD-1 antibody, (nivolumab or pembrolizumab), demonstrated a significant antitumor effect. Nivolumab is currently an ongoing phase I clinical trial, and Pembrolizumab has shown its function in treatment for HIV and KS patients in phase I and is in a phase II trial for treatment. A thalidomide analog medicine - Pomalidomide was also granted by the FDA in 2011. Pomalidomide was shown to recover the expression of MHC-1, which help cell display intracellular proteins to cytotoxic T cells, and it also can repress the expression of PD-L1 and increase the CD8+ T cell killing.
Kaposi's sarcoma-associated herpesvirus
Human T-lymphotropic virus 2
Trichodysplasia spinulosa polyomavirus
Human T-lymphotropic virus 1
SV40 large T antigen
Human T-lymphotropic virus
Subtypes of HIV
Epstein–Barr virus viral-capsid antigen