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

Vaccines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 354
Author(s):  
Chia-Ming Su ◽  
Raymond Robert Richard Rowland ◽  
Dongwan Yoo

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, CD163, 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.

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Hongfang Ma ◽  
Rui Li ◽  
Longguang Jiang ◽  
Songlin Qiao ◽  
Xin-xin Chen ◽  
...  

AbstractPorcine reproductive and respiratory syndrome (PRRS) is a serious disease burdening global swine industry. Infection by its etiological agent, PRRS virus (PRRSV), shows a highly restricted tropism of host cells and has been demonstrated to be mediated by an essential scavenger receptor (SR) CD163. CD163 fifth SR cysteine-rich domain (SRCR5) is further proven to play a crucial role during viral infection. Despite intense research, the involvement of CD163 SRCR5 in PRRSV infection remains to be elucidated. In the current study, we prepared recombinant monkey CD163 (moCD163) SRCR5 and human CD163-like homolog (hCD163L1) SRCR8, and determined their crystal structures. After comparison with the previously reported crystal structure of porcine CD163 (pCD163) SRCR5, these structures showed almost identical structural folds but significantly different surface electrostatic potentials. Based on these differences, we carried out mutational research to identify that the charged residue at position 534 in association with the one at position 561 were important for PRRSV-2 infection in vitro. Altogether the current work sheds some light on CD163-mediated PRRSV-2 infection and deepens our understanding of the viral pathogenesis, which will provide clues for prevention and control of PRRS.


Author(s):  
Fengyu Zhang ◽  
Michael Waters

Coronavirus disease 19 (COVID-19) caused by infection with a novel severe acute respiratory syndrome virus -2 (SARS-CoV2) has evolved into a pandemic and a global public health emergency. The viral genomics, host cellular factors, and interactions are critical for establishing a viral infection and developing a related disease. This paper aims to provide an overview of viral genomics and discuss host cellular factors so far identified to be involved with the disease susceptibility. The novel pathogen is a beta coronavirus and one of seven that cause diseases to humans. It is a single strand positive-sense RNA genome virus that encodes 27 proteins, including the structural Spike protein that binds to host cell surface receptors and is a key for viral entry, and 16 nonstructural proteins play a critical role in viral replication and virulence. While the angiotensin-converting enzyme, ACE2 receptor, and the proteases TMPRSS2 and furin are established as necessary for viral entry, host factors CD147, Cathepsins, DPP4, GRP78, L-SIGN, DC-SIGN, Sialic acid, and Plasmin(ogen) may also play a role in the viral entry. The Spike protein and nonstructural proteins, and various host factors working together may contribute to the infection kinetics, high infectivity, rapid transmission, and a spectrum of clinical manifestations of COVID-19. More importantly, they can serve as potential targets in developing strategies for therapeutical prevention and intervention.


2019 ◽  
Vol 2019 (1) ◽  
Author(s):  
Phithakdet Phoo-ngurn ◽  
Chanakarn Kiataramkul ◽  
Farida Chamchod

Abstract Porcine reproductive and respiratory syndrome (PRRS) is an important swine disease that affects many swine industries worldwide. The disease can cause reproductive failure and respiratory problems in a swine population. As vaccination is an important tool to control the spread of PRRS virus (PRRSV), we employ a mathematical model to investigate the transmission dynamics of PRRSV and the effects of immunity information, as well as vaccination control strategies. We also explore optimal vaccination coverage and vaccination rate to minimize the number of infected swines and vaccination efforts. Our results suggest that: (i) higher vaccination coverage and vaccination rate together with prior knowledge about immunity may help reduce the prevalence of PRRSV, and (ii) longer maximum vaccination efforts are required when swines stay longer in a population and it takes them longer time to recover from PRRS infections.


2020 ◽  
Vol 6 (12) ◽  
pp. eaaz3367 ◽  
Author(s):  
DongXu He ◽  
AiQin Mao ◽  
YouRan Li ◽  
SiuCheung Tam ◽  
YongTang Zheng ◽  
...  

Mammalian transient receptor potential (TRP) channels are major components of Ca2+ signaling pathways and control a diversity of physiological functions. Here, we report a specific role for TRPC1 in the entry of herpes simplex virus type 1 (HSV-1) into cells. HSV-1–induced Ca2+ release and entry were dependent on Orai1, STIM1, and TRPC1. Inhibition of Ca2+ entry or knockdown of these proteins attenuated viral entry and infection. HSV-1 glycoprotein D interacted with the third ectodomain of TRPC1, and this interaction facilitated viral entry. Knockout of TRPC1 attenuated HSV-1–induced ocular abnormality and morbidity in vivo in TRPC1−/− mice. There was a strong correlation between HSV-1 infection and plasma membrane localization of TRPC1 in epithelial cells within oral lesions in buccal biopsies from HSV-1–infected patients. Together, our findings demonstrate a critical role for TRPC1 in HSV-1 infection and suggest the channel as a potential target for anti-HSV therapy.


2009 ◽  
Vol 84 (6) ◽  
pp. 3101-3105 ◽  
Author(s):  
Hanne Van Gorp ◽  
Wander Van Breedam ◽  
Jan Van Doorsselaere ◽  
Peter L. Delputte ◽  
Hans J. Nauwynck

ABSTRACT Scavenger receptor CD163 is a key entry mediator for porcine reproductive and respiratory syndrome virus (PRRSV). To identify the CD163 protein domains involved in PRRSV infection, deletion mutants and chimeric mutants were created. Infection experiments revealed that scavenger receptor cysteine-rich (SRCR) domain 5 (SRCR 5) is essential for PRRSV infection, while the four N-terminal SRCR domains and the cytoplasmic tail are not required. The remaining CD163 protein domains need to be present but can be replaced by corresponding SRCR domains from CD163-L1, resulting in reduced (SRCR 6 and interdomain regions) or unchanged (SRCR 7 to SRCR 9) infection efficiency. In addition, CD163-specific antibodies recognizing SRCR 5 are able to reduce PRRSV infection.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Yingmei Feng ◽  
Miranda van Eck ◽  
Eline Van Craeyveld ◽  
Frank Jacobs ◽  
Sophie Van Linthout ◽  
...  

Background: Accelerated endothelial regeneration mediated by enhanced endothelial progenitor cell (EPC) incorporation may attenuate the development of allograft vasculopathy. Hypothesis: We investigated the hypothesis that modulation of EPC biology and attenuation of allograft vasculopathy by increased HDL cholesterol following human apo A-I (AdA-I) transfer requires scavenger receptor (SR)-BI expression in bone marrow-derived EPCs. Methods: Bone marrow transplantations with SR-BI+/+ or SR-BI−/− bone marrow were performed 4 weeks before gene transfer or saline injection. E1E3E4-deleted vectors containing a hepatocyte-specific human apo A-I expression cassette or containing no expression cassette were injected via the tail vein. Two weeks later, a common carotid artery of a female Balb/c donor mouse was transplanted paratopically into male recipient C57BL/6 mice. To analyse EPC incorporation, sex mismatch bone marrow transplantations were performed in female C57BL/6 mice and incorporated EPCs were quantified by in situ hybridization for the murine Y-chromosome. Results: Following AdA-I transfer, the number of circulating EPCs increased 2.0-fold (p<0.0001) at different time-points in C57BL/6 mice transplanted with SR-BI+/+ bone marrow but was unaltered in mice with SR-BI−/− bone marrow. The effect of HDL on EPC migration in vitro requires signaling via SR-BI and extracellular signal-regulated kinases (ERK) and is dependent on increased NO production in EPCs. Human apo A-I transfer 2 weeks before paratopic artery transplantation reduced intimal area at day 21 3.7-fold (p<0.001) in mice with SR-BI+/+ bone marrow but had no effect in mice with SR-BI−/− bone marrow. The number of CD31 positive endothelial cells lining the lumen and the number of incorporated EPCs was increased 3.0-fold (p<0.001) and 9.7-fold (p<0.001), respectively, in AdA-I treated chimeric SR-BI+/+ mice compared to control mice with SR-BI+/+ bone marrow. Endothelial regeneration and EPC incorporation was not increased after AdA-I transfer in chimeric SR-BI−/−mice. Conclusion: Human apo A-I transfer-mediated endothelial regeneration to prevent allograft vasculopathy is strictly dependent on SR-BI expressing bone marrow-derived EPCs.


2022 ◽  
Author(s):  
Wenbin Sun ◽  
Jiechen Li ◽  
Wen Gao ◽  
Luyao Kang ◽  
Fengcai Lei ◽  
...  

The electrocatalytic urea oxidation reaction (UOR) has attracted substantial research interests during the past few years owing to its critical role in coupled electrochemical systems for energy conversion, for example,...


Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 154
Author(s):  
Fengling Feng ◽  
Jin Zhao ◽  
Pingchao Li ◽  
Ruiting Li ◽  
Ling Chen ◽  
...  

Antigen-specific T lymphocytes play a critical role in controlling viral infections. However, we report here that preexisting virus-specific T cell responses also contribute to promoting adenovirus (Ad) infection. Previously, we found that CD14+ monocytes from Ad-seropositive individuals exhibited an increased susceptibility to Ad infection, when compared with that of Ad-seronegative individuals. But the underlying mechanisms for this enhancement of viral infection are not completely clarified. In this study, we found that the efficacy of Ad infection into CD14+ monocytes was significantly decreased after CD3+ T lymphocytes depletion from PBMC samples of Ad-seropositive individuals. In contrast, adding virus-specific CD3+ T lymphocytes into PBMC samples of Ad-seronegative individuals resulted in a significant increase of infection efficacy. CD3+ T lymphocytes in PBMC samples from Ad-seropositive individuals were more sensitive to be activated by adenovirus stimulus, characterized by upregulation of multiple cytokines and activation markers and also enhancement of cell proliferation. Further studies demonstrated that GM-CSF and IL-4 can promote Ad infection by up-regulating the expression of scavenger receptor 1 (SR-A) and integrins αVβ5 receptor of CD14+ cells. And taken together, these results suggest a novel role of virus-specific T cells in mediating enhancement of viral infection, and provide insights to understand the pathogenesis and complicated interactions between viruses and host immune cells.


Blood ◽  
2008 ◽  
Vol 111 (4) ◽  
pp. 1749-1750 ◽  
Author(s):  
Meinrad Gawaz

Scavenger receptors are increasingly recognized as playing a critical role in atherothrombosis.1 A new study presented by Valiyaveettil and colleagues in this issue of Blood demonstrates that oxidatively modified high-density lipoprotein (OxHDL) exhibits potent antiplatelet activity via the platelet scavenger receptor B type I (SR-BI).


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