Intracellular interleukin-32γ mediates antiviral activity of cytokines against hepatitis B virus

Doo Hyun Kim, Eun-Sook Park, Ah Ram Lee, Soree Park, Yong Kwang Park, Sung Hyun Ahn, Hong Seok Kang, Ju Hee Won, Yea Na Ha, ByeongJune Jae, Dong-Sik Kim, Woo-Chang Chung, Moon Jung Song, Kee-Hwan Kim, Seung Hwa Park, Soo-Hyun Kim and Kyun-Hwan Kim ()
Additional contact information
Doo Hyun Kim: Konkuk University
Eun-Sook Park: Konkuk University
Ah Ram Lee: Konkuk University
Soree Park: Konkuk University
Yong Kwang Park: Konkuk University
Sung Hyun Ahn: Konkuk University
Hong Seok Kang: Konkuk University
Ju Hee Won: Konkuk University
Yea Na Ha: Konkuk University
ByeongJune Jae: Konkuk University
Dong-Sik Kim: Korea University College of Medicine
Woo-Chang Chung: Korea University
Moon Jung Song: Korea University
Kee-Hwan Kim: The Catholic University of Korea
Seung Hwa Park: Konkuk University
Soo-Hyun Kim: Konkuk University
Kyun-Hwan Kim: Konkuk University

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract Cytokines are involved in early host defense against pathogen infections. In particular, tumor necrosis factor (TNF) and interferon-gamma (IFN-γ) have critical functions in non-cytopathic elimination of hepatitis B virus (HBV) in hepatocytes. However, the molecular mechanisms and mediator molecules are largely unknown. Here we show that interleukin-32 (IL-32) is induced by TNF and IFN-γ in hepatocytes, and inhibits the replication of HBV by acting intracellularly to suppress HBV transcription and replication. The gamma isoform of IL-32 (IL-32γ) inhibits viral enhancer activities by downregulating liver-enriched transcription factors. Our data are validated in both an in vivo HBV mouse model and primary human hepatocytes. This study thus suggests that IL-32γ functions as intracellular effector in hepatocytes for suppressing HBV replication to implicate a possible mechanism of non-cytopathic viral clearance.

Date: 2018
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DOI: 10.1038/s41467-018-05782-5

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