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Updated: Sep 2, 2025

Monitoring Activation of the Antiviral Pattern Recognition Receptors RIG-I And PKR By Limited Protease Digestion and Native PAGE
Published on: July 29, 2014
PRRS virus receptors and an alternative pathway for viral invasion
Abstract:
Porcine reproductive and respiratory syndrome virus (PRRSV) has a highly restricted cell tropism, which is closely related to the specific receptors associated with PRRSV infection. At least nine cellular molecules have been identified as putative receptors for PRRSV, including CD163, a cysteine-rich scavenger receptor. With the participation of the CD163 receptor and other cofactors, PRRSV invades cells via low pH-dependent clathrin-mediated endocytosis. In addition, PRRSV utilizes viral apoptotic mimicry to infect cells though macropinocytosis as an alternative pathway. In this review, we discuss recent advances in the studies on receptors and pathways that play an important role in PRRSV invasion, and simultaneously explore the use of specific antibodies, small molecules, and blockers targeting receptor-ligand interactions, as a potential strategy for controlling PRRSV infection. Novel antiviral strategies against PRRSV could be developed by identifying the interaction between receptors and ligands.
Insights
Porcine reproductive and respiratory syndrome virus (PRRSV) infection relies on specific cell receptors like CD163 and entry pathways such as endocytosis. Targeting these interactions offers potential antiviral strategies for PRRSV control.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Porcine reproductive and respiratory syndrome virus (PRRSV) exhibits restricted cell tropism, crucial for its infectivity.
- Multiple cellular molecules, including the scavenger receptor CD163, act as putative PRRSV receptors.
- PRRSV employs specific entry mechanisms into host cells.
Purpose of the Study:
- To review recent advancements in understanding PRRSV cell invasion mechanisms.
- To explore potential antiviral strategies targeting PRRSV receptors and entry pathways.
- To highlight the significance of receptor-ligand interactions in PRRSV pathogenesis.
Main Methods:
- Literature review of studies on PRRSV receptors and cellular entry pathways.
- Analysis of PRRSV infection mechanisms, including endocytosis and macropinocytosis.
- Discussion of therapeutic strategies targeting receptor-ligand interactions.
Main Results:
- PRRSV utilizes CD163 and other cofactors for cell entry via clathrin-mediated endocytosis.
- Macropinocytosis serves as an alternative PRRSV infection pathway through viral apoptotic mimicry.
- Receptor-ligand interactions are key determinants of PRRSV cell tropism and infection.
Conclusions:
- Understanding PRRSV entry mechanisms is vital for developing effective control strategies.
- Targeting specific receptors and their interactions presents a promising avenue for novel PRRSV antivirals.
- Further research into receptor-ligand dynamics can lead to innovative therapeutic interventions against PRRSV.
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