About: TIM-1 serves as a receptor for Ebola virus in vivo, enhancing viremia and pathogenesis

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About: TIM-1 serves as a receptor for Ebola virus in vivo, enhancing viremia and pathogenesis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	TIM-1 serves as a receptor for Ebola virus in vivo, enhancing viremia and pathogenesis
Creator	Brunton, Bethany Rogers, Kai Butler, Noah Boulsid, Ruayda Brouillette, Rachel Mauryid, Wendy Phillips, Elisabeth
Source	PMC
abstract	BACKGROUND: T cell immunoglobulin mucin domain-1 (TIM-1) is a phosphatidylserine (PS) receptor, mediating filovirus entry into cells through interactions with PS on virions. TIM-1 expression has been implicated in Ebola virus (EBOV) pathogenesis; however, it remains unclear whether this is due to TIM-1 serving as a filovirus receptor in vivo or, as others have suggested, TIM-1 induces a cytokine storm elicited by T cell/virion interactions. Here, we use a BSL2 model virus that expresses EBOV glycoprotein to demonstrate the importance of TIM-1 as a virus receptor late during in vivo infection. METHODOLOGY/PRINCIPAL FINDINGS: Infectious, GFP-expressing recombinant vesicular stomatitis virus encoding either full length EBOV glycoprotein (EBOV GP/rVSV) or mucin domain deleted EBOV glycoprotein (EBOV GPΔO/rVSV) was used to assess the role of TIM-1 during in vivo infection. GFP-expressing rVSV encoding its native glycoprotein G (G/rVSV) served as a control. TIM-1-sufficient or TIM-1-deficient BALB/c interferon α/β receptor(-/-) mice were challenged with these viruses. While G/rVSV caused profound morbidity and mortality in both mouse strains, TIM-1-deficient mice had significantly better survival than TIM-1-expressing mice following EBOV GP/rVSV or EBOV GPΔO/rVSV challenge. EBOV GP/rVSV or EBOV GPΔO/rVSV in spleen of infected animals was high and unaffected by expression of TIM-1. However, infectious virus in serum, liver, kidney and adrenal gland was reduced late in infection in the TIM-1-deficient mice, suggesting that virus entry via this receptor contributes to virus load. Consistent with higher virus loads, proinflammatory chemokines trended higher in organs from infected TIM-1-sufficient mice compared to the TIM-1-deficient mice, but proinflammatory cytokines were more modestly affected. To assess the role of T cells in EBOV GP/rVSV pathogenesis, T cells were depleted in TIM-1-sufficient and -deficient mice and the mice were challenged with virus. Depletion of T cells did not alter the pathogenic consequences of virus infection. CONCLUSIONS: Our studies provide evidence that at late times during EBOV GP/rVSV infection, TIM-1 increased virus load and associated mortality, consistent with an important role of this receptor in virus entry. This work suggests that inhibitors which block TIM-1/virus interaction may serve as effective antivirals, reducing virus load at late times during EBOV infection.
has issue date	2019-06-26(xsd:dateTime)
bibo:doi	10.1371/journal.pntd.0006983
bibo:pmid	31242184
has license	cc-by
sha1sum (hex)	61aa22d85170a908912fd1f0c0f86ea251b4e311
schema:url	https://doi.org/10.1371/journal.pntd.0006983
resource representing a document's title	TIM-1 serves as a receptor for Ebola virus in vivo, enhancing viremia and pathogenesis
has PubMed Central identifier	PMC6615641
has PubMed identifier	31242184
schema:publication	PLoS Negl Trop Dis
resource representing a document's body	covid:61aa22d85170a908912fd1f0c0f86ea251b4e311#body_text
is schema:about of	named entity 'immunoglobulin' named entity 'receptor' named entity 'viremia' covid:arg/61aa22d85170a908912fd1f0c0f86ea251b4e311 named entity 'vivo' named entity 'infection' named entity 'virions' named entity 'mucin' named entity 'phosphatidylserine' named entity 'immunoglobulin' named entity 'virus receptor' named entity 'EBOV' named entity 'pathogenesis' named entity 'TIM-1' named entity 'Ebola virus' named entity 'viremia' named entity 'apical surface' named entity 'GFP' named entity 'exons' named entity 'GFP' named entity 'Thermo Scientific' named entity 'TIM-1' named entity 'virus' named entity 'deficient mice' named entity 'IP-10' named entity 'clone' named entity 'TIM-1' named entity 'immunomodulatory' named entity 'enveloped virus' named entity 'Reverse Transcription' named entity 'mice' named entity 'infection' named entity 'viral burden' named entity 'HPRT' named entity 'infection' named entity 'TIM-1' named entity 'VSV' named entity 'lymph nodes' named entity 'MCP-1' named entity 'genome' named entity 'mice' named entity 'pathogenesis' named entity 'EBOV' named entity 'cytokine' named entity 'infection' named entity 'Havcr1' named entity 'mice' named entity 'baculovirus' named entity 'C-type lectins' named entity 'proinflammatory' named entity 'TIM-1' named entity 'TIM-1' named entity 'interact' named entity 'mucin domain' named entity 'IgV' named entity 'cDNA' named entity 'clone' named entity 'chemokines' named entity 'Ifnar' named entity 'deficient mice' named entity 'chemokines' named entity 'TIM-4' named entity 'TIM-1' named entity 'EBOV' named entity 'viral entry' named entity 'mice' named entity 'chemokines' named entity 'TIM-1' named entity 'genotype' named entity 'infection' named entity 'EBOV' named entity 'chemokines' named entity 'Homozygous' named entity 'enveloped viruses' named entity 'phosphatidylinositol'

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