Do tissue-dwelling trypanosomes sustain transmission populations?
Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasite...
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description | Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission.
Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission. |
doi_str_mv | 10.1016/j.pt.2024.12.001 |
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Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission.</description><identifier>ISSN: 1471-4922</identifier><identifier>ISSN: 1471-5007</identifier><identifier>EISSN: 1471-5007</identifier><identifier>DOI: 10.1016/j.pt.2024.12.001</identifier><identifier>PMID: 39690069</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>antigen diversity ; antigenic variation ; differentiation ; transmission ; trypanosome ; variant surface glycoprotein</subject><ispartof>Trends in parasitology, 2024-12</ispartof><rights>2024 The Authors</rights><rights>Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-7792-2749 ; 0000-0001-6173-046X ; 0000-0001-5739-976X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39690069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Larcombe, Stephen D.</creatorcontrib><creatorcontrib>Munday, Jane C.</creatorcontrib><creatorcontrib>McCulloch, Richard</creatorcontrib><title>Do tissue-dwelling trypanosomes sustain transmission populations?</title><title>Trends in parasitology</title><addtitle>Trends Parasitol</addtitle><description>Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission.
Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission.</description><subject>antigen diversity</subject><subject>antigenic variation</subject><subject>differentiation</subject><subject>transmission</subject><subject>trypanosome</subject><subject>variant surface glycoprotein</subject><issn>1471-4922</issn><issn>1471-5007</issn><issn>1471-5007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNo1kL1PwzAUxC0EoqWwM6GMLAm24zgxC6rKp1SJBWbrxXlBrtI4xA6o_z2uWqZ3evrpdHeEXDOaMcrk3SYbQsYpFxnjGaXshMyZKFlaUFqeHrVQnM_IhfebCBRlqc7JLFdSUSrVnCwfXRKs9xOmzS92ne2_kjDuBuidd1v0iZ98ANvHJ_R-G0nr-mRww9RBiNI_XJKzFjqPV8e7IJ_PTx-r13T9_vK2Wq5TZEKx1AgATquaCyhUXYKRpeGArcwpVMANKlXlUoEqJROFqCspsUKety0waHiVL8jtwXcY3feEPuiYxsTI0KObvM6ZkEpEDxHRmyM61Vts9DDaLYw7_V87AvcHAGPgH4uj9sZib7CxI5qgG2c1o3q_sd7oIej9xppxHSfM_wBl226B</recordid><startdate>20241216</startdate><enddate>20241216</enddate><creator>Larcombe, Stephen D.</creator><creator>Munday, Jane C.</creator><creator>McCulloch, Richard</creator><general>Elsevier Ltd</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7792-2749</orcidid><orcidid>https://orcid.org/0000-0001-6173-046X</orcidid><orcidid>https://orcid.org/0000-0001-5739-976X</orcidid></search><sort><creationdate>20241216</creationdate><title>Do tissue-dwelling trypanosomes sustain transmission populations?</title><author>Larcombe, Stephen D. ; Munday, Jane C. ; McCulloch, Richard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e1491-c4aa208b24a59b7ac67c2aef630a8a2ce998369a9761454b866e8e23ffa1ad283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>antigen diversity</topic><topic>antigenic variation</topic><topic>differentiation</topic><topic>transmission</topic><topic>trypanosome</topic><topic>variant surface glycoprotein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Larcombe, Stephen D.</creatorcontrib><creatorcontrib>Munday, Jane C.</creatorcontrib><creatorcontrib>McCulloch, Richard</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Trends in parasitology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Larcombe, Stephen D.</au><au>Munday, Jane C.</au><au>McCulloch, Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Do tissue-dwelling trypanosomes sustain transmission populations?</atitle><jtitle>Trends in parasitology</jtitle><addtitle>Trends Parasitol</addtitle><date>2024-12-16</date><risdate>2024</risdate><issn>1471-4922</issn><issn>1471-5007</issn><eissn>1471-5007</eissn><abstract>Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission.
Trypanosoma brucei infectious populations are marked by considerable diversity in the parasite’s major antigen, the variant surface glycoprotein (VSG). However, most parasites in the bloodstream are non-replicating, questioning how VSG diversity arises. Beaver et al. show that extravascular parasites in host tissues many explain this paradox and provide insight into trypanosome transmission.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>39690069</pmid><doi>10.1016/j.pt.2024.12.001</doi><orcidid>https://orcid.org/0000-0001-7792-2749</orcidid><orcidid>https://orcid.org/0000-0001-6173-046X</orcidid><orcidid>https://orcid.org/0000-0001-5739-976X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | antigen diversity antigenic variation differentiation transmission trypanosome variant surface glycoprotein |
title | Do tissue-dwelling trypanosomes sustain transmission populations? |
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