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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004155naa a2200541 4500
001oai:DiVA.org:umu-170550
003SwePub
008200527s2020 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1705502 URI
0247 a https://doi.org/10.1007/s00430-020-00675-12 DOI
040 a (SwePub)umu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Alberione, Maria Pia4 aut
2451 0a Single-nucleotide variants in human CD81 influence hepatitis C virus infection of hepatoma cells
264 c 2020-04-22
264 1b Springer,c 2020
338 a electronic2 rdacarrier
500 a Special Issue on Tetraspanins in Infection and Immunity.
520 a An estimated number of 71 million people are living with chronic hepatitis C virus (HCV) infection worldwide and 400,000 annual deaths are related to the infection. HCV entry into the hepatocytes is complex and involves several host factors. The tetraspanin human CD81 (hCD81) is one of the four essential entry factors and is composed of one large extracellular loop, one small extracellular loop, four transmembrane domains, one intracellular loop and two intracellular tails. The large extracellular loop interacts with the E2 glycoprotein of HCV. Regions outside the large extracellular loop (backbone) of hCD81 have a critical role in post-binding entry steps and determine susceptibility of hepatocytes to HCV. Here, we investigated the effect of five non-synonymous single-nucleotide variants in the backbone of hCD81 on HCV susceptibility. We generated cell lines that stably express the hCD81 variants and infected the cells using HCV pseudoparticles and cell culture-derived HCV. Our results show that all the tested hCD81 variants support HCV pseudoparticle entry with similar efficiency as wild-type hCD81. In contrast, variants A54V, V211M and M220I are less supportive to cell culture-derived HCV infection. This altered susceptibility is HCV genotype dependent and specifically affected the cell entry step. Our findings identify three hCD81 genetic variants that are impaired in their function as HCV host factors for specific viral genotypes. This study provides additional evidence that genetic host variation contributes to inter-individual differences in HCV infection and outcome.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Infektionsmedicin0 (SwePub)302092 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Infectious Medicine0 (SwePub)302092 hsv//eng
653 a Hepatitis C virus
653 a HCV
653 a Hepatocyte
653 a Tetraspanin
653 a CD81
653 a Receptor
653 a Single-nucleotide variant
653 a Entry
653 a Genetic variant
7001 a Moeller, Rebecca4 aut
7001 a Kirui, Jared4 aut
7001 a Ginkel, Corinne4 aut
7001 a Doepke, Mandy4 aut
7001 a Stroeh, Luisa J.4 aut
7001 a Machtens, Jan-Philipp4 aut
7001 a Pietschmann, Thomas4 aut
7001 a Gerold, Gisa,d 1979-u Umeå universitet,Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM),Avdelningen för virologi,Institute for Experimental Virology, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Medical School Hannover and the Helmholtz Centre for Infection Research, Hannover, Germany4 aut0 (Swepub:umu)gige0003
7102 a Umeå universitetb Wallenberg centrum för molekylär medicin vid Umeå universitet (WCMM)4 org
7730 t Medical Microbiology and Immmunologyd : Springerg 209:4, s. 499-514q 209:4<499-514x 0300-8584x 1432-1831
8564 u https://doi.org/10.1007/s00430-020-00675-1y Fulltext
8564 u https://umu.diva-portal.org/smash/get/diva2:1432513/FULLTEXT02.pdfx primaryx Raw objecty fulltext:print
8564 u https://link.springer.com/content/pdf/10.1007/s00430-020-00675-1.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-170550
8564 8u https://doi.org/10.1007/s00430-020-00675-1

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