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

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

doi:10.1186/2045-3701-4-40

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

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

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

Background: 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. Methods and results: 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. Conclusions: 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.

Original language	English
Article number	40
Journal	Cell and Bioscience
Volume	4
Issue number	1
DOIs	https://doi.org/10.1186/2045-3701-4-40
Publication status	Published - Aug 5 2014

Keywords

HIV-1 viral load
RNF39
Single nucleotide polymorphism
Viral replication

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/2045-3701-4-40

Cite this

Lin, Y. J., Chen, C. Y., Jeang, K. T., Liu, X., Wang, J. H., Hung, C. H., Tsang, H., Lin, T. H., Liao, C. C., Huang, S. M., Lin, C. W., Ho, M. W., Chien, W. K., Chen, J. H., Ho, T. J., & Tsai, F. J. (2014). Ring finger protein 39 genetic variants associate with HIV-1 plasma viral loads and its replication in cell culture. Cell and Bioscience, 4(1), [40]. https://doi.org/10.1186/2045-3701-4-40

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

abstract = "Background: 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. Methods and results: 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. Conclusions: 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.",

keywords = "HIV-1 viral load, RNF39, Single nucleotide polymorphism, Viral replication",

author = "Lin, {Ying Ju} and Chen, {Chia Yen} and Jeang, {Kuan Teh} and Xiang Liu and Wang, {Jen Hsien} and Hung, {Chien Hui} and Hsinyi Tsang and Lin, {Ting Hsu} and Liao, {Chiu Chu} and Huang, {Shao Mei} and Lin, {Cheng Wen} and Ho, {Mao Wang} and Chien, {Wen Kuei} and Chen, {Jin Hua} and Ho, {Tsung Jung} and Tsai, {Fuu Jen}",

year = "2014",

month = aug,

day = "5",

doi = "10.1186/2045-3701-4-40",

language = "English",

volume = "4",

journal = "Cell and Bioscience",

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publisher = "Society of Chinese Bioscientists in America",

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TY - JOUR

T1 - Ring finger protein 39 genetic variants associate with HIV-1 plasma viral loads and its replication in cell culture

AU - Lin, Ying Ju

AU - Chen, Chia Yen

AU - Jeang, Kuan Teh

AU - Liu, Xiang

AU - Wang, Jen Hsien

AU - Hung, Chien Hui

AU - Tsang, Hsinyi

AU - Lin, Ting Hsu

AU - Liao, Chiu Chu

AU - Huang, Shao Mei

AU - Lin, Cheng Wen

AU - Ho, Mao Wang

AU - Chien, Wen Kuei

AU - Chen, Jin Hua

AU - Ho, Tsung Jung

AU - Tsai, Fuu Jen

PY - 2014/8/5

Y1 - 2014/8/5

N2 - Background: 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. Methods and results: 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. Conclusions: 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.

AB - Background: 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. Methods and results: 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. Conclusions: 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.

KW - HIV-1 viral load

KW - RNF39

KW - Single nucleotide polymorphism

KW - Viral replication

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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