李慶雲2006-07-262018-07-112006-07-262018-07-111999http://ntur.lib.ntu.edu.tw//handle/246246/22829Human herpesvirus 8 was discovered through the etiology search of Kaposi¡¦s sarcoma. This virus was soon identified to belong to human herpesviruses. To date, HHV8 has been shown to be highly associated with some malignancies, such as Kaposi’s sarcoma and body cavity lymphoma. The remarkable higher incidence of Kaposi¡¦s sarcoma in HI V-infected patients can be explained in two ays. One is that HIV infection leads to immune disruption and impaired tumor surveillance in the host. The immune dysfunction is the direct reason of occurrence of Kaposi’s sarcoma and HIV plays an indirect role. Another possibility is HIV can turn o: the replication of HHV8. Increased HHV activity in turn leads to the occurrence of Kaposi’s sarcoma. In this aspect, I-IIV plays a more direct role. We have done a series )f cell-fusion experiments and found that H-1V8 could increase the RNA amounts of HIX-l. The reverse was also true. LTR-CAT produced significant more amounts of CAT when transfected into BCBL.1 cells and stimulated with TPA. This result demonstrated that HHV8 could transactivate HIV-l LTR. We are currently exploring the cis-elements on HIV- 1 LTR that is responsive to HHV8. Furthermore, Vpr an I Tat are being tested for their ability to activate the replication of HHV8.application/pdf746988 bytesapplication/pdfzh-TW國立臺灣大學醫學院小兒科HIV-lHHV8VprTat[SDGs]SDG3reporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/22829/1/882314B002139.pdf