# Hijacking the neonatal Fc receptor: the novel biology of arterivirus entry, transmission, and persistence

> **NIH AI R01** · UNIVERSITY OF WISCONSIN-MADISON · 2026 · $615,446

## Abstract

PROJECT SUMMARY/ABSTRACT
Understanding novel mechanisms by which animal viruses enter cells, evade immunity, and cause disease has
scientific and public health importance. Arteriviruses are an understudied family of RNA viruses (related to
coronaviruses) that infect a wide variety of mammals. The host and viral factors that determine arterivirus
disease, persistence, and cross-species transmission remain unknown and unpredictable. This lack of
understanding has implications for predicting/thwarting arterivirus emergence in humans, as some arteriviruses
have been shown to infect human cells. Macrophages are exclusively infected by most arteriviruses, but the
subpopulation(s) of macrophages that support arterivirus replication remain poorly defined. The process by
which arteriviruses enter cells is highly novel and also poorly understood. Each virion displays an unusually
large set of surface glycoproteins (7-11 depending on the virus) that are unlike any known viral fusion
machinery. The macrophage-specific molecule CD163 is a required arterivirus receptor, yet CD163 by itself is
insufficient to mediate arterivirus entry. We recently identified the neonatal Fc receptor (FcRn) as an important
entry factor that arteriviruses use together with CD163 to gain entry into cells. Aim 1 of this project builds upon
this discovery to define the molecular details of the arterivirus:FcRn interaction. In Aim 1a, we will map the
site(s) on FcRn that are critical for arterivirus engagement by creating chimeric FcRn molecules that
incorporate features of arterivirus-permissive and -resistant FcRn orthologs, with the goal of defining the
domains, motifs, and residues involved in arterivirus/FcRn interactions. In Aim 1b, we will generate chimeric
arteriviruses that contain combinations of glycoproteins from different arteriviruses, seeking to define the viral
glycoproteins, domains, motifs, and residues involved in FcRn engagement. In Aim 1c, we will continue to
develop our understandi

## Key facts

- **NIH application ID:** 11266824
- **Project number:** 1R01AI195454-01
- **Recipient organization:** UNIVERSITY OF WISCONSIN-MADISON
- **Principal Investigator:** Adam Lee Bailey
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** AI
- **Fiscal year:** 2026
- **Award amount:** $615,446
- **Award type:** 1
- **Project period:** 2026-04-03T00:00:00 → 2031-03-31T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11266824

## Citation

> US National Institutes of Health, RePORTER application 11266824, Hijacking the neonatal Fc receptor: the novel biology of arterivirus entry, transmission, and persistence (1R01AI195454-01). Retrieved via AI Analytics 2026-07-03 from https://api.ai-analytics.org/grant/nih/11266824. Licensed CC0.

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