Ring finger protein 39 genetic variants associate with HIV-1 plasma viral loads and its replication in cell culture.

The human immunodeficiency virus (HIV-1) exploits host proteins to complete its life cycle. Genome-wide siRNA approaches suggested that host proteins affect HIV-1 replication. However, the results barely overlapped. RING finger protein 39 (RNF39) has been identified from genome-wide association studies. However, its function during HIV-1 replication remains unclear. We investigated the relationship between common RNF39 genetic variants and HIV-1 viral loads. The effect of RNF39 protein knockdown or overexpression on HIV-1 replication was then investigated in different cell lines. Two genetic variants were associated with HIV-1 viral loads. Patients with the ht1-GG/GG haplotype presented lower RNF39 expression levels and lower HIV-1 viral load. RNF39 knockdown inhibited HIV-1 expression. RNF39 protein may be involved in HIV-1 replication as observed in genetic studies on patients with HIV-1 and in in vitro cell cultures.

Citation

Ying-Ju Lin, Chia-Yen Chen, Kuan-Teh Jeang, Xiang Liu, Jen-Hsien Wang, Chien-Hui Hung, Hsinyi Tsang, Ting-Hsu Lin, Chiu-Chu Liao, Shao-Mei Huang, Cheng-Wen Lin, Mao-Wang Ho, Wen-Kuei Chien, Jin-Hua Chen, Tsung-Jung Ho, Fuu-Jen Tsai. Ring finger protein 39 genetic variants associate with HIV-1 plasma viral loads and its replication in cell culture. Cell & bioscience. 2014;4:40

PMID: 25126410

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