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Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2

Sporozoite forms of the malaria parasite Plasmodium are transmitted by mosquitoes and first infect the liver for an initial round of replication before parasite proliferation in the blood. The molecular mechanisms involved during sporozoite invasion of hepatocytes remain poorly understood. In previo...

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Autores principales: Langlois, Anne-Claire, Marinach, Carine, Manzoni, Giulia, Silvie, Olivier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6033427/
https://www.ncbi.nlm.nih.gov/pubmed/29975762
http://dx.doi.org/10.1371/journal.pone.0200032
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author Langlois, Anne-Claire
Marinach, Carine
Manzoni, Giulia
Silvie, Olivier
author_facet Langlois, Anne-Claire
Marinach, Carine
Manzoni, Giulia
Silvie, Olivier
author_sort Langlois, Anne-Claire
collection PubMed
description Sporozoite forms of the malaria parasite Plasmodium are transmitted by mosquitoes and first infect the liver for an initial round of replication before parasite proliferation in the blood. The molecular mechanisms involved during sporozoite invasion of hepatocytes remain poorly understood. In previous studies, two receptors of the Hepatitis C virus (HCV), the tetraspanin CD81 and the Scavenger Receptor BI (SR-BI), were shown to play an important role during entry of Plasmodium sporozoites into hepatocytic cells. In contrast to HCV entry, which requires both CD81 and SR-BI together with additional host factors, CD81 and SR-BI operate independently during malaria liver infection, as sporozoites can use CD81 and/or SR-BI, depending on the Plasmodium species, to invade hepatocytes. However, the molecular function of CD81 and SR-BI during parasite entry remains unknown. Another HCV entry factor, the Ephrin receptor A2 (EphA2), was recently reported to play a key role as a host cell entry factor during malaria liver infection. Here, we investigated the contribution of EphA2 during CD81-dependent and SR-BI-dependent sporozoite infection. Using small interfering RNA (siRNA) and antibodies against EphA2, combined with direct detection of parasites by flow cytometry or microscopy, we show that blocking EphA2 has no significant impact on P. yoelii or P. berghei host cell infection, irrespective of the entry route. Thus, our findings argue against an important role of EphA2 during malaria liver infection.
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spelling pubmed-60334272018-07-19 Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2 Langlois, Anne-Claire Marinach, Carine Manzoni, Giulia Silvie, Olivier PLoS One Research Article Sporozoite forms of the malaria parasite Plasmodium are transmitted by mosquitoes and first infect the liver for an initial round of replication before parasite proliferation in the blood. The molecular mechanisms involved during sporozoite invasion of hepatocytes remain poorly understood. In previous studies, two receptors of the Hepatitis C virus (HCV), the tetraspanin CD81 and the Scavenger Receptor BI (SR-BI), were shown to play an important role during entry of Plasmodium sporozoites into hepatocytic cells. In contrast to HCV entry, which requires both CD81 and SR-BI together with additional host factors, CD81 and SR-BI operate independently during malaria liver infection, as sporozoites can use CD81 and/or SR-BI, depending on the Plasmodium species, to invade hepatocytes. However, the molecular function of CD81 and SR-BI during parasite entry remains unknown. Another HCV entry factor, the Ephrin receptor A2 (EphA2), was recently reported to play a key role as a host cell entry factor during malaria liver infection. Here, we investigated the contribution of EphA2 during CD81-dependent and SR-BI-dependent sporozoite infection. Using small interfering RNA (siRNA) and antibodies against EphA2, combined with direct detection of parasites by flow cytometry or microscopy, we show that blocking EphA2 has no significant impact on P. yoelii or P. berghei host cell infection, irrespective of the entry route. Thus, our findings argue against an important role of EphA2 during malaria liver infection. Public Library of Science 2018-07-05 /pmc/articles/PMC6033427/ /pubmed/29975762 http://dx.doi.org/10.1371/journal.pone.0200032 Text en © 2018 Langlois et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Langlois, Anne-Claire
Marinach, Carine
Manzoni, Giulia
Silvie, Olivier
Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2
title Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2
title_full Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2
title_fullStr Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2
title_full_unstemmed Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2
title_short Plasmodium sporozoites can invade hepatocytic cells independently of the Ephrin receptor A2
title_sort plasmodium sporozoites can invade hepatocytic cells independently of the ephrin receptor a2
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6033427/
https://www.ncbi.nlm.nih.gov/pubmed/29975762
http://dx.doi.org/10.1371/journal.pone.0200032
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