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The Phosphatidylserine Receptor TIM-1 Enhances Authentic Chikungunya Virus Cell Entry
Umeå University, Faculty of Medicine, Department of Clinical Microbiology. Umeå University, Faculty of Medicine, Wallenberg Centre for Molecular Medicine at Umeå University (WCMM).ORCID iD: 0000-0002-1612-7247
Umeå University, Faculty of Medicine, Department of Clinical Microbiology. 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, Hannover, Germany.ORCID iD: 0000-0001-5109-9408
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
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2021 (English)In: Cells, E-ISSN 2073-4409, Vol. 10, no 7, article id 1828Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
MDPI, 2021. Vol. 10, no 7, article id 1828
Keywords [en]
Chikungunya virus, CHIKV, alphavirus, enveloped virus, phosphatidylserine, T-cell immunoglobulin and mucin domain 1, TIM-1, Axl receptor tyrosine kinase, Axl, entry
National Category
Microbiology in the medical area
Identifiers
URN: urn:nbn:se:umu:diva-187299DOI: 10.3390/cells10071828ISI: 000676394100001PubMedID: 34359995Scopus ID: 2-s2.0-85114081934OAI: oai:DiVA.org:umu-187299DiVA, id: diva2:1592476
Funder
Knut and Alice Wallenberg FoundationSwedish Research Council, 2017-05607Available from: 2021-09-09 Created: 2021-09-09 Last updated: 2021-09-09Bibliographically approved

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Abidine, YaraLenman, AnnasaraIslam, Md. KoushikulYong-Dae, GwonEvander, MagnusBally, MartaGerold, Gisa

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Kirui, JaredAbidine, YaraLenman, AnnasaraIslam, Md. KoushikulYong-Dae, GwonEvander, MagnusBally, MartaGerold, Gisa
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Department of Clinical MicrobiologyWallenberg Centre for Molecular Medicine at Umeå University (WCMM)Infectious Diseases
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