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Article

The Phosphatidylserine Receptor TIM-1 Enhances Authentic Chikungunya Virus Cell Entry

1
Centre for Experimental and Clinical Infection Research, TWINCORE, Institute for Experimental Virology, a Joint Venture between the Medical School Hannover and the Helmholtz Centre for Infection Research, 30625 Hannover, Germany
2
Department of Biochemistry & Research Center for Emerging Infections and Zoonoses (RIZ), University of Veterinary Medicine Hannover, 30559 Hannover, Germany
3
Department of Clinical Microbiology, Umeå University, 90185 Umeå, Sweden
4
Wallenberg Centre for Molecular Medicine (WCMM), Umeå University, 90185 Umeå, Sweden
*
Author to whom correspondence should be addressed.
Academic Editors: Thomas Hoenen and Allison Groseth
Cells 2021, 10(7), 1828; https://doi.org/10.3390/cells10071828
Received: 2 June 2021 / Revised: 12 July 2021 / Accepted: 15 July 2021 / Published: 20 July 2021
(This article belongs to the Special Issue Virus — Host Cell Interactions)
Chikungunya virus (CHIKV) is a re-emerging, mosquito-transmitted, enveloped positive stranded RNA virus. Chikungunya fever is characterized by acute and chronic debilitating arthritis. Although multiple host factors have been shown to enhance CHIKV infection, the molecular mechanisms of cell entry and entry factors remain poorly understood. The phosphatidylserine-dependent receptors, T-cell immunoglobulin and mucin domain 1 (TIM-1) and Axl receptor tyrosine kinase (Axl), are transmembrane proteins that can serve as entry factors for enveloped viruses. Previous studies used pseudoviruses to delineate the role of TIM-1 and Axl in CHIKV entry. Conversely, here, we use the authentic CHIKV and cells ectopically expressing TIM-1 or Axl and demonstrate a role for TIM-1 in CHIKV infection. To further characterize TIM-1-dependent CHIKV infection, we generated cells expressing domain mutants of TIM-1. We show that point mutations in the phosphatidylserine binding site of TIM-1 lead to reduced cell binding, entry, and infection of CHIKV. Ectopic expression of TIM-1 renders immortalized keratinocytes permissive to CHIKV, whereas silencing of endogenously expressed TIM-1 in human hepatoma cells reduces CHIKV infection. Altogether, our findings indicate that, unlike Axl, TIM-1 readily promotes the productive entry of authentic CHIKV into target cells. View Full-Text
Keywords: Chikungunya virus; CHIKV; alphavirus; enveloped virus; phosphatidylserine; T-cell immunoglobulin and mucin domain 1; TIM-1; Axl receptor tyrosine kinase; Axl; entry Chikungunya virus; CHIKV; alphavirus; enveloped virus; phosphatidylserine; T-cell immunoglobulin and mucin domain 1; TIM-1; Axl receptor tyrosine kinase; Axl; entry
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MDPI and ACS Style

Kirui, J.; Abidine, Y.; Lenman, A.; Islam, K.; Gwon, Y.-D.; Lasswitz, L.; Evander, M.; Bally, M.; Gerold, G. The Phosphatidylserine Receptor TIM-1 Enhances Authentic Chikungunya Virus Cell Entry. Cells 2021, 10, 1828. https://doi.org/10.3390/cells10071828

AMA Style

Kirui J, Abidine Y, Lenman A, Islam K, Gwon Y-D, Lasswitz L, Evander M, Bally M, Gerold G. The Phosphatidylserine Receptor TIM-1 Enhances Authentic Chikungunya Virus Cell Entry. Cells. 2021; 10(7):1828. https://doi.org/10.3390/cells10071828

Chicago/Turabian Style

Kirui, Jared, Yara Abidine, Annasara Lenman, Koushikul Islam, Yong-Dae Gwon, Lisa Lasswitz, Magnus Evander, Marta Bally, and Gisa Gerold. 2021. "The Phosphatidylserine Receptor TIM-1 Enhances Authentic Chikungunya Virus Cell Entry" Cells 10, no. 7: 1828. https://doi.org/10.3390/cells10071828

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