Asset Details
Do you wish to reserve the book?
Generation of a genetically double-attenuated Plasmodium berghei parasite that fully arrests growth during late liver stage development
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Generation of a genetically double-attenuated Plasmodium berghei parasite that fully arrests growth during late liver stage development
Do you wish to request the book?
Generation of a genetically double-attenuated Plasmodium berghei parasite that fully arrests growth during late liver stage development
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Generation of a genetically double-attenuated Plasmodium berghei parasite that fully arrests growth during late liver stage development
2024
Overview
Malaria caused by Plasmodium parasites remains a large health burden. One approach to combat this disease involves vaccinating individuals with whole sporozoites that have been genetically modified to arrest their development at a specific stage in the liver by targeted gene deletion, resulting in a genetically attenuated parasite (GAP). Through a comprehensive phenotyping screen, we identified the hscb gene, encoding a putative iron-sulfur protein assembly chaperone, as crucial for liver stage development, making it a suitable candidate gene for GAP generation. Parasites lacking Plasmodium berghei HscB ( Pb HscB) exhibited normal sporozoite production in mosquitoes, but their liver stage development was severely impaired, characterized by slow growth and delayed expression of merozoite surface protein 1 (MSP1). In vivo experiments demonstrated that Pb HscB-deficient parasites exhibited a delay in prepatency of 2–4 days, emphasizing the significance of Pb HscB for exo-erythrocytic development. Although knockout of Pb HscB alone allowed breakthrough infections, it is a potent candidate for a dual gene deletion strategy. PlasMei2, an RNA-binding protein, was previously found to be crucial for the completion of liver stage development. We generated a Pb HscB- Pb Mei2-double attenuated parasite line, serving as a late liver stage-arresting replication-competent (LARC) GAP, providing a solid block of liver-to-blood stage transition.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Arrests
/ Control
/ Female
/ Genes
/ Genetically modified organisms
/ Growth
/ Liver
/ Malaria
/ Medicine and Health Sciences
/ Merozoite Surface Protein 1 - genetics
/ Merozoite Surface Protein 1 - metabolism
/ Mice
/ Plasmodium berghei - genetics
/ Plasmodium berghei - growth & development
/ Proteins
/ Protozoan Proteins - genetics
/ Protozoan Proteins - metabolism
/ RNA
/ Sporozoites - growth & development
/ Sulfur
/ Vaccines
