Sickle Cell Anemia and <i>Babesia</i> Infection

<i>Babesia</i> is an intraerythrocytic, obligate Apicomplexan parasite that has, in the last century, been implicated in human infections via zoonosis and is now widespread, especially in parts of the USA and Europe. It is naturally transmitted by the bite of a tick, but transfused blood...

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Autores principales: Divya Beri, Manpreet Singh, Marilis Rodriguez, Karina Yazdanbakhsh, Cheryl Ann Lobo
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Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/85e8d45af9a54c8a93c34de8890ed9fd
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spelling oai:doaj.org-article:85e8d45af9a54c8a93c34de8890ed9fd2021-11-25T18:38:14ZSickle Cell Anemia and <i>Babesia</i> Infection10.3390/pathogens101114352076-0817https://doaj.org/article/85e8d45af9a54c8a93c34de8890ed9fd2021-11-01T00:00:00Zhttps://www.mdpi.com/2076-0817/10/11/1435https://doaj.org/toc/2076-0817<i>Babesia</i> is an intraerythrocytic, obligate Apicomplexan parasite that has, in the last century, been implicated in human infections via zoonosis and is now widespread, especially in parts of the USA and Europe. It is naturally transmitted by the bite of a tick, but transfused blood from infected donors has also proven to be a major source of transmission. When infected, most humans are clinically asymptomatic, but the parasite can prove to be lethal when it infects immunocompromised individuals. Hemolysis and anemia are two common symptoms that accompany many infectious diseases, and this is particularly true of parasitic diseases that target red cells. Clinically, this becomes an acute problem for subjects who are prone to hemolysis and depend on frequent transfusions, like patients with sickle cell anemia or thalassemia. Little is known about <i>Babesia</i>’s pathogenesis in these hemoglobinopathies, and most parallels are drawn from its evolutionarily related <i>Plasmodium</i> parasite which shares the same environmental niche, the RBCs, in the human host. In vitro as well as in vivo <i>Babesia</i>-infected mouse sickle cell disease (SCD) models support the inhibition of intra-erythrocytic parasite proliferation, but mechanisms driving the protection of such hemoglobinopathies against infection are not fully studied. This review provides an overview of our current knowledge of <i>Babesia</i> infection and hemoglobinopathies, focusing on possible mechanisms behind this parasite resistance and the clinical repercussions faced by <i>Babesia</i>-infected human hosts harboring mutations in their globin gene.Divya BeriManpreet SinghMarilis RodriguezKarina YazdanbakhshCheryl Ann LoboMDPI AGarticle<i>Babesia</i>sickle-cell anemiahemolysishaemoglobinopathiesMedicineRENPathogens, Vol 10, Iss 1435, p 1435 (2021)
institution DOAJ
collection DOAJ
language EN
topic <i>Babesia</i>
sickle-cell anemia
hemolysis
haemoglobinopathies
Medicine
R
spellingShingle <i>Babesia</i>
sickle-cell anemia
hemolysis
haemoglobinopathies
Medicine
R
Divya Beri
Manpreet Singh
Marilis Rodriguez
Karina Yazdanbakhsh
Cheryl Ann Lobo
Sickle Cell Anemia and <i>Babesia</i> Infection
description <i>Babesia</i> is an intraerythrocytic, obligate Apicomplexan parasite that has, in the last century, been implicated in human infections via zoonosis and is now widespread, especially in parts of the USA and Europe. It is naturally transmitted by the bite of a tick, but transfused blood from infected donors has also proven to be a major source of transmission. When infected, most humans are clinically asymptomatic, but the parasite can prove to be lethal when it infects immunocompromised individuals. Hemolysis and anemia are two common symptoms that accompany many infectious diseases, and this is particularly true of parasitic diseases that target red cells. Clinically, this becomes an acute problem for subjects who are prone to hemolysis and depend on frequent transfusions, like patients with sickle cell anemia or thalassemia. Little is known about <i>Babesia</i>’s pathogenesis in these hemoglobinopathies, and most parallels are drawn from its evolutionarily related <i>Plasmodium</i> parasite which shares the same environmental niche, the RBCs, in the human host. In vitro as well as in vivo <i>Babesia</i>-infected mouse sickle cell disease (SCD) models support the inhibition of intra-erythrocytic parasite proliferation, but mechanisms driving the protection of such hemoglobinopathies against infection are not fully studied. This review provides an overview of our current knowledge of <i>Babesia</i> infection and hemoglobinopathies, focusing on possible mechanisms behind this parasite resistance and the clinical repercussions faced by <i>Babesia</i>-infected human hosts harboring mutations in their globin gene.
format article
author Divya Beri
Manpreet Singh
Marilis Rodriguez
Karina Yazdanbakhsh
Cheryl Ann Lobo
author_facet Divya Beri
Manpreet Singh
Marilis Rodriguez
Karina Yazdanbakhsh
Cheryl Ann Lobo
author_sort Divya Beri
title Sickle Cell Anemia and <i>Babesia</i> Infection
title_short Sickle Cell Anemia and <i>Babesia</i> Infection
title_full Sickle Cell Anemia and <i>Babesia</i> Infection
title_fullStr Sickle Cell Anemia and <i>Babesia</i> Infection
title_full_unstemmed Sickle Cell Anemia and <i>Babesia</i> Infection
title_sort sickle cell anemia and <i>babesia</i> infection
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/85e8d45af9a54c8a93c34de8890ed9fd
work_keys_str_mv AT divyaberi sicklecellanemiaandibabesiaiinfection
AT manpreetsingh sicklecellanemiaandibabesiaiinfection
AT marilisrodriguez sicklecellanemiaandibabesiaiinfection
AT karinayazdanbakhsh sicklecellanemiaandibabesiaiinfection
AT cherylannlobo sicklecellanemiaandibabesiaiinfection
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