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J Biomed 2017; 2:117-119. doi:10.7150/jbm.18610 This volume Cite

Commentary

HSHV-HIV, not just molecular interaction, but also interfere with the fate-Re “Claudin-2 downregulation by KSHV infection is involved in the regulation of endothelial barrier function”

Chunhong Di¹, Xiaobo Wang¹, Yutao Yan^2✉, Lei Yang^2✉

1. Affiliated Hospital, Hangzhou Normal University, 126 Wenzhou St., Hangzhou 310015, Zhejiang, China;
2. School of Medicine, Hangzhou Normal University, 16 Xuelin St. Hangzhou 310018, Zhejiang, China.

✉ Corresponding authors: Yutao Yan, M.D., Ph.D., School of Medicine, Hangzhou Normal University, 16 Xuelin St. Hangzhou Zhejiang 310018. Email: 20130070edu.cn Tel: (86)571-28867302 Lei Yang, M.D., Ph.D., School of Medicine, Hangzhou Normal University, 16 Xuelin St. Hangzhou Zhejiang 310018. Email: yanglei62edu.cn Tel: (86)571-28865010 More

Commentary-article in J Cutan Pathol, Volume 41, 630

Abstract

Co-infection of Kaposi sarcoma-associated herpesvirus (KSHV) and human immunodeficiency virus (HIV) was able to prolong the survival of patients with AIDS, but the underlying mechanisms are still elusive. Different from previous hypothesis such as the role of KSHV on cell transformation, Tan et al (J Cutan Pathol 2014; 41: 630-639. doi:10.1111/cup.12332) pointed out a novel insight that claudin-2 is involved in the prolonged survival of KSHV-HIV infected patients by increasing the transendothelial barrier function. Further, this report identified new model to study molecular interactions, especially DNA-RNA interaction.

Keywords: Kaposi sarcoma-associated herpesvirus, human immunodeficiency virus

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