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The Phosphatidylserine Receptor TIM-1 Enhances Authentic Chikungunya Virus Cell Entry
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi. Umeå universitet, Medicinska fakulteten, Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM).ORCID-id: 0000-0002-1612-7247
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi. 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 universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
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2021 (engelsk)Inngår i: Cells, E-ISSN 2073-4409, Vol. 10, nr 7, artikkel-id 1828Artikkel i tidsskrift (Fagfellevurdert) 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.

sted, utgiver, år, opplag, sider
MDPI, 2021. Vol. 10, nr 7, artikkel-id 1828
Emneord [en]
Chikungunya virus, CHIKV, alphavirus, enveloped virus, phosphatidylserine, T-cell immunoglobulin and mucin domain 1, TIM-1, Axl receptor tyrosine kinase, Axl, entry
HSV kategori
Identifikatorer
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
Forskningsfinansiär
Knut and Alice Wallenberg FoundationSwedish Research Council, 2017-05607Tilgjengelig fra: 2021-09-09 Laget: 2021-09-09 Sist oppdatert: 2021-09-09bibliografisk kontrollert

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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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