Research Papers:

Porcine alveolar macrophage CD163 abundance is a pivotal switch for porcine reproductive and respiratory syndrome virus infection

Tong-Yun Wang _, Yong-Gang Liu, Liang Li, Gang Wang, Hai-Ming Wang, Hong-Liang Zhang, Shi-Fei Zhao, Jia-Cong Gao, Tong-Qing An, Zhi-Jun Tian, Xue-Hui Cai and Xue-Hui Cai

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Oncotarget. 2018; 9:12174-12185. https://doi.org/10.18632/oncotarget.24040

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Tong-Yun Wang1,*, Yong-Gang Liu1,*, Liang Li1, Gang Wang1, Hai-Ming Wang1, Hong-Liang Zhang1, Shi-Fei Zhao1, Jia-Cong Gao1, Tong-Qing An1, Zhi-Jun Tian1, Yan-Dong Tang1 and Xue-Hui Cai1

1State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute of Chinese Academy of Agricultural Sciences, Harbin 150001, China

*These authors contributed equally to this work

Correspondence to:

Xue-Hui Cai, email: [email protected]

Yan-Dong Tang, email: [email protected]

Keywords: PRRSV; CD163; infection; switch; abundance

Received: July 07, 2017     Accepted: November 15, 2017     Published: January 06, 2018


Porcine reproductive and respiratory syndrome virus (PRRSV) is a problematic virus that is difficult to control. The principal target cells for PRRSV infection are porcine alveolar macrophages (PAMs). Increasing evidence has demonstrated that CD163 is the determinant receptor for PRRSV infection. However, the relationship between CD163 abundance and PRRSV infection is unclear. In this study, we first generated primary immortalized PAMs (iPAMs) using SV40 large T antigen and demonstrated that CD163 expression is suppressed by the alternative splicing of mRNA in iPAMs. Two forms of CD163 transcripts were discovered, and most iPAMs expressed a short-form CD163 transcript that lacked from scavenger receptor cysteine-rich tandem repeat 1 (SRCR1) to SRCR5 of the functional domain. More importantly, using flow cytometric cell sorting technology, we isolated CD163-positive single-cell-derived clones with varying CD163 abundances to investigate the relationship between CD163 abundance and PRRSV infection. For the first time, we showed that cells with low CD163 abundance (approximately 20%) do not initiate PRRSV infection, while cells with moderate CD163 abundance display limited infection. PRRSV initiated efficient infection only in cells with high CD163 abundances. Our results demonstrate that CD163 abundance is a pivotal switch for PRRSV replication.

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