Recombinant adenovirus-delivered soluble CD163 and sialoadhesin receptors protected pigs from porcine reproductive and respiratory syndrome virus infection

Xia, Wenlong; Wu, Zhaojun; Guo, Changming; Zhu, Shanyuan; Zhang, Xinyu; Xia, Xiaoli; Sun, Huaichang

doi:10.1016/j.vetmic.2018.04.006

Cited by 13 publications

(12 citation statements)

References 28 publications

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“…The rAd-Sn4D-Fc-treated pigs exhibited more severe clinical signs than the rAd-SRCR59-Fc-treated pig [116]. The co-expression of soluble CD169 and soluble CD163 provided complete protection against PRRSV infection [116]. These results confirm the hypothesis that CD163 is the core receptor for PRRSV.…”

Section: In Vivo Evidence For Cd163 As the Receptor For Prrsvsupporting

confidence: 68%

“…Pigs were inoculated with rAd-Sn4D-Fc and rAd-SRCR59-Fc followed by infection with PRRSV-2 JXA1. The rAd-Sn4D-Fc-treated pigs exhibited more severe clinical signs than the rAd-SRCR59-Fc-treated pig [116]. The co-expression of soluble CD169 and soluble CD163 provided complete protection against PRRSV infection [116].…”

Section: In Vivo Evidence For Cd163 As the Receptor For Prrsvmentioning

confidence: 95%

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Recent Advances in PRRS Virus Receptors and the Targeting of Receptor–Ligand for Control

Rowland

Yoo

2021

Vaccines

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Cellular receptors play a critical role in viral infection. At least seven cellular molecules have been identified as putative viral entry mediators for porcine reproductive and respiratory syndrome virus (PRRSV). Accumulating data indicate that among these candidates, sialoadhesin (CD)163, a cysteine-rich scavenger receptor on macrophages, is the major receptor for PRRSV. This review discusses the recent advances and understanding of the entry of PRRSV into cells, viral pathogenesis in CD163 gene-edited swine, and CD163 as a potential target of receptor–ligand for the control of PRRS.

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Section: In Vivo Evidence For Cd163 As the Receptor For Prrsvsupporting

confidence: 68%

Section: In Vivo Evidence For Cd163 As the Receptor For Prrsvmentioning

confidence: 95%

Recent Advances in PRRS Virus Receptors and the Targeting of Receptor–Ligand for Control

Rowland

Yoo

2021

Vaccines

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“…Neutralization of PRRSV infectivity for porcine alveolar macrophages was achieved by addition of soluble Siglec-1 and CD163 Fc fusion proteins, or by recombinant adenovirus-or exosome-delivered microRNA that specifically targeted CD163 and Siglec-1 (Chen et al 2014b;Zhu et al 2014). In addition, pigs that received recombinant adenovirus-delivered soluble CD163 plus Siglec-1 had reduced PPRSV viral loads and fecal viral emission, concurrent with improved clinical scores and higher survival rates from the contagious infection (Xia et al 2018). It is notable that an in vivo study conducted in SIGLEC1 knockout pigs found that the absence of Siglec-1 expression does not alter to the clinical course and histopathology of PRRSV infection (Prather et al 2013), implying a potential redundant function of CD163 and Siglec-1 in PRRSV infection and the importance of dual targeting for potential pharmacological interventions.…”

Section: Siglecs In Viral Infectionmentioning

confidence: 95%

Siglecs at the Host–Pathogen Interface

Chang

Nizet

2020

Advances in Experimental Medicine and Biology

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Siglecs are sialic acid (Sia) recognizing immunoglobulin-like receptors expressed on the surface of all the major leukocyte lineages in mammals. Siglecs recognize ubiquitous Sia epitopes on various glycoconjugates in the cell glycocalyx and transduce signals to regulate immunological and inflammatory activities of these cells. The subset known as CD33-related Siglecs is principally inhibitory receptors that suppress leukocyte activation, and recent research has shown that a number of bacterial pathogens use Sia mimicry to engage these Siglecs as an immune evasion strategy. Conversely, Siglec-1 is a macrophage phagocytic receptor that engages GBS and other sialylated bacteria to promote effective phagocytosis and antigen presentation for the adaptive immune response, whereas certain viruses and parasites use Siglec-1 to gain entry to immune cells as a proximal step in the infectious process. Siglecs are positioned in crosstalk with other host innate immune sensing pathways to modulate the immune response to infection in complex ways. This chapter summarizes the current understanding of Siglecs at the host-pathogen interface, a field of study expanding in breadth and medical importance, and which provides potential targets for immune-based anti-infective strategies.

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“…Indispensable receptor (Whitworth et al, 2016) Gene-edited pigs (Whitworth et al, 2016;Wells et al, 2017;Burkard et al, 2018;Yang et al, 2018;Chen et al, 2019;Guo et al, 2019a;Wang et al, 2019a;Xu et al, 2020b) MicroRNAs (Gao et al, 2013;Zhu et al, 2014; The recombinant protein (Chen et al, 2014;Xia et al, 2018) MAbs (Xu et al, 2020a;Zhang et al, 2020d;Han et al, 2022) Peptides (Han et al, 2022) Small molecules (Huang et al, 2020) Sn Attachment and entry co-factor? (Prather et al, 2013) Negative regulator of host innate immunity (Liu et al, 2020a;Zhang et al, 2020a) MAbs (Duan et al, 1998) The recombinant protein (Chen et al, 2014;Xia et al, 2018) MicroRNA (Zhu et al, 2014) HS Attachment factor (Delputte et al, 2002) Release factor (Guo et al, 2017a) Heparin (Delputte et al, 2002) Heparinase (Delputte et al, 2002) Heparanase inhibitor (Guo et al, 2017b) Vimentin Attachment factor (Kim et al, 2006;Song et al, 2016) Replication factor (Song et al, 2016;Chang et al, 2018;Zheng et al, 2021) Transport factor (Liang et al, 2020) Antibodies (Kim et al, 2006) Inhibitors…”

Section: Cd163mentioning

confidence: 99%

“…CD163 itself can be exploited to restrict PRRSV infection. On the one hand, the recombinant adenovirus-delivered soluble CD163 SRCR5-9 protein has been shown to suppress PRRSV infection both in vitro and in vivo ( Chen et al, 2014 ; Xia et al, 2018 ). On the other hand, specific monoclonal antibodies (mAbs) targeting CD163 SRCR5, SRCR6, SRCR7, or PST I domain have been recently reported to inhibit PRRSV infection in vitro ( Xu et al, 2020a ; Zhang et al, 2020d ; Han et al, 2022 ).…”

Section: Previously Identified Host Cellular Factorsmentioning

confidence: 99%

Reappraising host cellular factors involved in attachment and entry to develop antiviral strategies against porcine reproductive and respiratory syndrome virus

Qiao

Zhang

2022

Front. Microbiol.

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Porcine reproductive and respiratory syndrome (PRRS), caused by PRRS virus (PRRSV), is a highly contagious disease that brings tremendous economic losses to the global swine industry. As an intracellular obligate pathogen, PRRSV infects specific host cells to complete its replication cycle. PRRSV attachment to and entry into host cells are the first steps to initiate the replication cycle and involve multiple host cellular factors. In this review, we recapitulated recent advances on host cellular factors involved in PRRSV attachment and entry, and reappraised their functions in these two stages, which will deepen the understanding of PRRSV infection and provide insights to develop promising antiviral strategies against the virus.

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Recombinant adenovirus-delivered soluble CD163 and sialoadhesin receptors protected pigs from porcine reproductive and respiratory syndrome virus infection

Cited by 13 publications

References 28 publications

Recent Advances in PRRS Virus Receptors and the Targeting of Receptor–Ligand for Control

Recent Advances in PRRS Virus Receptors and the Targeting of Receptor–Ligand for Control

Siglecs at the Host–Pathogen Interface

Reappraising host cellular factors involved in attachment and entry to develop antiviral strategies against porcine reproductive and respiratory syndrome virus

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