k1 membrane protein. six types are recognised (a-f). prevention since persons infected with kshv will asymptomatically give the virus, caution should be used by sex partners in having unprotected sex and activities where saliva might be shared during sexual activity. prudent advice is to use condoms when needed and avoid deep kissing with partners with kshv and hiv infections or whose status is unknown. treatment kaposi's sarcoma 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 herpesviruses such as kshv have been used to successfully prevent development of kaposi's sarcoma, 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 kaposi's sarcoma occurrence. although kshv 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 kshv 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. kshv genes kshv encodes for ~90 genes and multiple non-coding rnas, such as micrornas. the "orf" genes are named based on genome position of the homologous genes in the first rhadinovirus described, herpesvirus saimiri. the "k" genes are unique to kshv, some kshv genes have well-characterized functions, while others remain uncharacterized. orf2 – dihydrofolate reductase orf8 – gb – envelope glycoprotein involved in viral entry orf9 – pol8 – dna polymerase required for viral dna replication orf10 – regulates rna export and responses to type i ifns orf16 – vbcl2 orf18, orf24, orf30, orf31, orf34, orf66 – viral transcription factors required for the expression of late genes orf21 – vtk – thymidine kinase orf22 – gh – envelope glycoprotein involved in viral entry orf23 – uncharacterized orf25, orf26 and orf65 – capsid proteins orf33 – involved in viral particle formation orf34 – unclear function orf35 – unclear function, mutant does not express early viral genes orf36 – vpk – viral protein kinase with multiple roles in replication cycle orf37 – sox – dual function protein – dnase activity required for genome packaging and rnase activity regulates host gene expression orf38 – involved in viral particle formation orf39 – gm – envelope glycoprotein orf40 and orf41 – helicase and primase – dna replication orf42 – uncharacterized orf45 - tegument protein, binds and prevents dephosphorylation of p90 ribosomal s6 kinases (rsks) and erk for modulate the erk/rsk mapk signaling pathway orf47 – gl – envelope glycoprotein involved in viral entry orf49 – may be required for viral gene expression orf50 – rta, replication and transcription activator – the major transcription factor driving lytic kshv reactivation orf52 – kicgas – tegument protein required for formation of virions and inhibition of cgas dna sensing orf53 – gn – envelope glycoprotein orf55 – uncharacterized orf57 – mta – regulates rna stability, export and translation of viral genes orf59 – pf–8 – polymerase processivity factor, accessory subunit of viral dna polymerase orf67 and orf69 – nuclear egress orf70 – thymidylate synthase orf72 – vcyclin orf73 – lana, latency-associated nuclear antigen– tethers genome to chromosome during latency, also regulates host gene expression. a cytoplasmic form of lana may inhibit activation of immune responses. orf74 – vgpcr orf75 – fgarat pan, polyadenylated nuclear rna – non–coding linear and circular rnas mirnas (mirks) – viral micrornas expressed during latency to regulate proliferation and cell death k1 – involved in oncogenesis k2 - interleukin 6 homolog, q2hrc7 k3 and k5 – ubiquitin e3 ligases – regulates antigen presentation k4 – vccl2 – chemokine k4.1 – vccl3 – chemokine k8 – transcriptional repressor – modulates chromatin k8.1 – envelope glycoprotein k9 – virf1, viral interferon regulatory factor 1 k10 – virf4. a circular rna (circrna) is also generated from this locus. k10.5 – virf3 (initially designated lana2), is expressed during latency in pel cell lines, but is also a bona fide lytic factor, like all of the virfs. k11 – virf2 k12 – kaposin k13 – vflip