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mBio2025; 16(7); e0062325; doi: 10.1128/mbio.00623-25

CD81 is a receptor for equine arteritis virus (family: Arteriviridae).

Abstract: Arteriviruses are a family of single-stranded, positive-sense RNA (+ssRNA) viruses that infect diverse animal hosts. Many arteriviruses are macrophage-tropic, consistent with their utilization of the macrophage-specific molecule CD163 as a receptor. However, the horse arterivirus (equine arteritis virus, EAV), which infects additional cell types beyond macrophages, does not utilize CD163 in its entry mechanism. Here, we use a genome-wide CRISPR knockout screen to identify alternative receptors that could explain this discrepancy in arterivirus receptor utilization and tropism, identifying the plasma membrane tetraspanin CD81 as a required host factor for EAV infection. Genetic knockout of CD81 or pre-incubation with soluble CD81 protected cells from infection with EAV, but had no impact on susceptibility to other arteriviruses. Bypassing the entry step of the viral life cycle by transfecting the EAV genome into CD81-knockout cells produced infectious EAV, implicating CD81 in the EAV entry process. Screening of CD81 orthologs from natural arterivirus hosts identified the brushtail possum CD81 as unsupportive of EAV entry, indicating that CD81 incompatibility can serve as a barrier to cross-species infection. Horse/possum CD81 chimeras were then used to map the structural domains of CD81 engaged by EAV, identifying alpha helix "D" on the large extracellular loop of CD81 as critical for EAV entry. This study identifies the first example of receptor switching in the Arteriviridae family and, given the broad tissue distribution of CD81 expression, suggests that the adoption of CD81 enabled an expansion of EAV tropism.IMPORTANCEArteriviruses are a family of diverse positive-sense RNA viruses that can infect a wide range of animal hosts, but many details regarding how arteriviruses gain entry into cells remain unclear. Most arteriviruses are thought to utilize the macrophage-specific molecule CD163 as a receptor; however, the horse arterivirus (equine arteritis virus, EAV) infects additional cell types beyond macrophages and does not utilize CD163. In this study, we identified the host factor CD81 as a significant player in EAV entry. Beyond the implications that this discovery holds for equine health, this study adds to the increasingly complex picture of arterivirus entry and demonstrates that these viruses are capable of adopting new host molecules as receptors, with consequences for the types of cells these viruses infect, the disease they cause, and their mode(s) of transmission.
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Publication Date: 2025-05-27 PubMed ID: 40422661PubMed Central: PMC12239600DOI: 10.1128/mbio.00623-25Google Scholar: Lookup
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  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This study demonstrates that the equine arteritis virus (EAV), which belongs to the arterivirus family, uses an alternative receptor, CD81, to enter its host cells, unlike other arteriviruses commonly known to use the CD163 receptor.

Understanding the Research

The research aims to unravel the infection mechanism of horse arterivirus (Equine Arteritis Virus), which is distinct from other arteriviruses in terms of receptor utilization and increased tropism. Arteriviruses are a group of single-stranded RNA viruses known to infect a variety of animal hosts, primarily through the macrophage-specific molecule CD163 as a receptor. However, EAV diverges from this receptor utilization trend, prompting researchers to investigate alternative receptors.

  • The researchers used a genome-wide CRISPR knockout screen to discover alternative receptors. This method led to the identification of CD81, a plasma membrane tetraspanin, as a critical host factor in EAV infection.
  • Evidence was found that either genetic knockout of CD81, or its pre-incubation with a soluble form, could protect cells from EAV infection. However, this had no effect on susceptibility to other arteriviruses, indicating CD81’s specificity as an EAV receptor.
  • To further implicate CD81 in the EAV entry process, an experiment was conducted in which the EAV genome was transfected into CD81-knockout cells. This process resulted in the creation of infectious EAV, asserting CD81’s role in EAV entry.
  • Testing of CD81 orthologs from arterivirus hosts revealed that CD81 in some species, such as the brushtail possum, was incompatible with EAV entry. This suggests a biological barrier against cross-species EAV infection.
  • The study also identified alpha helix “D”, located on the large extracellular loop of CD81, as vital for EAV entry. This was determined using horse/possum CD81 chimeras.

Significance of the Research

This study is of importance as it highlights the adaptability of arteriviruses, such as the equine arteritis virus, in choosing alternate host cell entry points. This is a significant finding for equine health, as it augments the understanding of how the EAV obtains entry into the host cell, a knowledge that may influence future treatment and prevention strategies. Additionally, it adds a fresh dimension to the understanding of arteriviruses, establishing that they can adopt new host molecules as receptors, which in turn impacts the types of cells they can infect, the diseases they induce, and their modes of transmission.

Cite This Article

APA
Maloney SM, Shaw TM, Nennig KM, Larsen MS, Shah A, Kumar A, Marcotrigiano J, Grove J, Snijder EJ, Kirchdoerfer RN, Bailey AL. (2025). CD81 is a receptor for equine arteritis virus (family: Arteriviridae). mBio, 16(7), e0062325. https://doi.org/10.1128/mbio.00623-25

Publication

mBio
ISSN: 2150-7511
NlmUniqueID: 101519231
Country: United States
Language: English
Volume: 16
Issue: 7
Pages: e0062325

Researcher Affiliations

Maloney, Sara M
  • Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
  • University of Wisconsin-Madison Cellular and Molecular Pathology Graduate Program, Madison, Wisconsin, USA.
Shaw, Teressa M
  • Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
Nennig, Kylie M
  • Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
Larsen, Malorie S
  • Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
Shah, Aadit
  • Stanford University School of Medicine, Stanford, California, USA.
Kumar, Ashish
  • Structural Virology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, USA.
Marcotrigiano, Joseph
  • Structural Virology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, USA.
Grove, Joe
  • MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland, United Kingdom.
Snijder, Eric J
  • Molecular Virology Laboratory, Leiden University Center of Infectious Diseases (LUCID), Leiden University Medical Center, Leiden, South Holland, The Netherlands.
Kirchdoerfer, Robert N
  • Department of Biochemistry, Institute for Molecular Virology, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Bailey, Adam L
  • Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.

MeSH Terms

  • Animals
  • Equartevirus / physiology
  • Equartevirus / genetics
  • Receptors, Virus / metabolism
  • Receptors, Virus / genetics
  • Tetraspanin 28 / genetics
  • Tetraspanin 28 / metabolism
  • Horses
  • Virus Internalization
  • Arterivirus Infections / virology
  • Arterivirus Infections / veterinary
  • Humans
  • Cell Line
  • Viral Tropism
  • Antigens, CD / metabolism
  • Gene Knockout Techniques
  • CD163 Antigen

Grant Funding

  • P30 CA014520 / NCI NIH HHS
  • R21 AI180295 / NIAID NIH HHS
  • T32 GM135119 / NIGMS NIH HHS
  • R21AI180295 / National Institute of Allergy and Infectious Diseases

Conflict of Interest Statement

The authors declare no conflict of interest.

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Citations

This article has been cited 1 times.
  1. Thieulent CJ, Sarkar S, Carossino M, Bhowmik M, Zhu H, Balasuriya UBR. Cell Surface Vimentin Is an Attachment Factor That Facilitates Equine Arteritis Virus Infection In Vitro. Viruses 2026 Jan 15;18(1).
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