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Updated: Jun 4, 2026

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
Published on: August 25, 2017
Expression of DcR3 and its effects in kaposi's sarcoma-associated herpesvirus-infected human endothelial cells
Seungmin Yoo1, Jaehyuk Jang, Sil Kim
1Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon, South Korea.
Objective:
Kaposi's sarcoma-associated herpesvirus (KSHV) is classified as a gamma-herpesvirus and it causes Kaposi's sarcoma in patients infected with the human immunodeficiency virus (HIV). Decoy receptor 3 (DcR3) is known as a decoy receptor for Fas ligand, LIGHT and TL1A and it can neutralize the biological effect of TL1A by inhibiting the TL1A-DR3 interaction in human endothelial cells. The present study examined the expression of DcR3 in human endothelial cells and its effect during the early stages of KSHV infection.
Methods:
The expression of DcR3 was assessed using real-time RT-PCR and ELISA in human umbilical cord vein endothelial cells (HUVECs) infected with KSHV. Cell proliferation and apoptosis of KSHV-infected HUVECs were assessed after treatment of infected cells with an anti-DcR3 antibody or recombinant human TL1A.
Results:
DcR3 expression was induced during the early phase of KSHV infection. Inhibition of DcR3 with anti-DcR3 antibodies or recombinant human TL1A-induced apoptosis in KSHV-infected HUVECs.
Conclusion:
The expression of DcR3 plays an important role in the prevention of apoptosis in HUVECs during the early phases of KSHV infection, thus ensuring the successful establishment and maintenance of the viral infection.
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