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Expanded protocadherin-1 usage reveals a broader hantavirus entry landscape.

Cierra Word1, Nahomi Guerra-Pilaquinga1, Ezgi Kasikci2

  • 1Department of Microbiology and Immunology, Center for Applied Immunology and Pathological Processes, Center for Cardiovascular Diseases and Sciences, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, USA.

Biorxiv : the Preprint Server for Biology
|July 3, 2026
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Summary

Mammalian hantaviruses can infect human endothelial cells via their glycoproteins, with some using protocadherin-1 (PCDH1) for entry. This research expands understanding of hantavirus tropism and potential therapeutic targets.

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Area of Science:

  • Virology
  • Cellular Biology
  • Immunology

Background:

  • Mammalian hantaviruses cause severe diseases like hantavirus cardiopulmonary syndrome and hemorrhagic fever with renal syndrome.
  • Cellular entry mechanisms for many hantaviruses are not well understood.
  • Protocadherin-1 (PCDH1) has been identified as a receptor for some hantaviruses.

Purpose of the Study:

  • To investigate the ability of diverse hantavirus glycoproteins to mediate cellular entry into human endothelial cells.
  • To determine the role of PCDH1 in the entry of various hantaviruses.
  • To evaluate the efficacy of a broadly reactive anti-Gn/Gc antibody against different hantaviruses.

Main Methods:

  • Generation of replication-competent recombinant vesicular stomatitis viruses (rVSVs) expressing Gn/Gc glycoproteins from multiple hantavirus species.
  • Infection assays using primary human endothelial cells and human cells lacking PCDH1.
  • Binding assays with soluble PCDH1 and neutralization assays using a PCDH1-targeting monoclonal antibody and the anti-Gn/Gc antibody ADI-42898.
  • Infection studies with authentic Tula virus in PCDH1 knockout endothelial cells.

Main Results:

  • Gn/Gc proteins from Necoclí, Sangassou, Thottapalayam, Nova, and Tula viruses supported infection of human endothelial cells, broadening the known range of permissive hantaviruses.
  • Necoclí, Tula, and Nova viruses utilize PCDH1 for efficient entry, demonstrating broader but heterogeneous receptor usage.
  • The anti-Gn/Gc antibody ADI-42898 showed differential neutralization activity against the tested rVSVs, with potent activity against some but not others.
  • Authentic Tula virus infection was confirmed to be PCDH1-dependent.

Conclusions:

  • Endothelial cell entry is permissive for a wider array of hantaviruses than previously recognized.
  • PCDH1 serves as an entry receptor for several divergent hantaviruses, expanding its known phylogenetic scope.
  • Targeted strategies against viral glycoproteins and host cell receptors show differential efficacy, highlighting the complexity of hantavirus countermeasures.