<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Vivax Sporozoite Consortium</submitter><funding>ARC</funding><funding>NIAID NIH HHS</funding><funding>Australian Government National Health and Medical Research Council Independent Research Institute Infrastructure Support Scheme</funding><funding>National Institute of Health</funding><funding>NHMRC</funding><funding>Victorian State Government Operational Infrastructure Support</funding><funding>Bill and Melinda Gates Foundation</funding><funding>Ian Potter Foundation</funding><pagination>501-513</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9973533</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>49(7)</volume><pubmed_abstract>Plasmodium vivax is the key obstacle to malaria elimination in Asia and Latin America, largely attributed to its ability to form resilient hypnozoites (sleeper cells) in the host liver that escape treatment and cause relapsing infections. The decision to form hypnozoites is made early in the liver infection and may already be set in sporozoites prior to invasion. To better understand these early stages of infection, we undertook a comprehensive transcriptomic and histone epigenetic characterization of P. vivax sporozoites. Through comparisons with recently published proteomic data for the P. vivax sporozoite, our study found that although highly transcribed, transcripts associated with functions needed for early infection of the vertebrate host are not detectable as proteins and may be reg</pubmed_abstract><journal>International journal for parasitology</journal><pubmed_title>Transcriptome and histone epigenome of Plasmodium vivax salivary-gland sporozoites point to tight regulatory control and mechanisms for liver-stage differentiation in relapsing malaria.</pubmed_title><pmcid>PMC9973533</pmcid><funding_grant_id>1092789</funding_grant_id><funding_grant_id>1043345</funding_grant_id><funding_grant_id>K25 AI119229</funding_grant_id><funding_grant_id>APP1021544</funding_grant_id><pubmed_authors>Koepfli C</pubmed_authors><pubmed_authors>Emery-Corbin SJ</pubmed_authors><pubmed_authors>Swearingen KE</pubmed_authors><pubmed_authors>Lindner S</pubmed_authors><pubmed_authors>Charnaud S</pubmed_authors><pubmed_authors>Flannery EL</pubmed_authors><pubmed_authors>Smith J</pubmed_authors><pubmed_authors>Vivax Sporozoite Consortium</pubmed_authors><pubmed_authors>Patrapuvich R</pubmed_authors><pubmed_authors>Merrienne N</pubmed_authors><pubmed_authors>Kappe SHI</pubmed_authors><pubmed_authors>Lerch A</pubmed_authors><pubmed_authors>Jex AR</pubmed_authors><pubmed_authors>Ansell B</pubmed_authors><pubmed_authors>Petter M</pubmed_authors><pubmed_authors>Mikolajczak SA</pubmed_authors><pubmed_authors>Duffy MF</pubmed_authors><pubmed_authors>Muller I</pubmed_authors><pubmed_authors>Sattabongkot J</pubmed_authors><pubmed_authors>Moritz RL</pubmed_authors><pubmed_authors>Chuenchob V</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcriptome and histone epigenome of Plasmodium vivax salivary-gland sporozoites point to tight regulatory control and mechanisms for liver-stage differentiation in relapsing malaria.</name><description>Plasmodium vivax is the key obstacle to malaria elimination in Asia and Latin America, largely attributed to its ability to form resilient hypnozoites (sleeper cells) in the host liver that escape treatment and cause relapsing infections. The decision to form hypnozoites is made early in the liver infection and may already be set in sporozoites prior to invasion. To better understand these early stages of infection, we undertook a comprehensive transcriptomic and histone epigenetic characterization of P. vivax sporozoites. Through comparisons with recently published proteomic data for the P. vivax sporozoite, our study found that although highly transcribed, transcripts associated with functions needed for early infection of the vertebrate host are not detectable as proteins and may be reg</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jun</publication><modification>2026-05-28T17:57:55.733Z</modification><creation>2025-04-04T14:30:00.904Z</creation></dates><accession>S-EPMC9973533</accession><cross_references><pubmed>31071319</pubmed><doi>10.1016/j.ijpara.2019.02.007</doi></cross_references></HashMap>