J
James E. K. Hildreth
Researcher at Meharry Medical College
Publications - 124
Citations - 8654
James E. K. Hildreth is an academic researcher from Meharry Medical College. The author has contributed to research in topics: Virus & Antibody. The author has an hindex of 46, co-authored 119 publications receiving 8226 citations. Previous affiliations of James E. K. Hildreth include Johns Hopkins University & Icahn School of Medicine at Mount Sinai.
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Journal ArticleDOI
Evidence for Budding of Human Immunodeficiency Virus Type 1 Selectively from Glycolipid-Enriched Membrane Lipid Rafts
TL;DR: A model for the budding of HIV virions through lipid rafts is proposed whereby host cell cholesterol, sphingolipids, and GPI-linked proteins within these domains are incorporated into the viral envelope, perhaps as a result of preferential sorting of HIV Gag to lipid rafting.
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The Trojan exosome hypothesis.
TL;DR: The Trojan exosomal origin hypothesis predicts that retroviruses pose an unsolvable paradox for adaptive immune responses, that retroviral antigen vaccines are unlikely to provide prophylactic protection, and that alloimmunity is a central component of antiretroviral immunity.
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Exosomes and HIV Gag bud from endosome-like domains of the T cell plasma membrane
TL;DR: This article showed that Jurkat T cells possess discrete domains of plasma membrane that are enriched for exosomal and endosomal proteins and serve as sites of immediate exosome biogenesis.
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Lipid rafts and HIV pathogenesis: host membrane cholesterol is required for infection by HIV type 1.
TL;DR: The results show that removal of cellular cholesterol rendered primary cells and cell lines highly resistant to HIV-1-mediated syncytium formation and to infection by both CXCR4- and CCR5-specific viruses.
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Evidence that HIV budding in primary macrophages occurs through the exosome release pathway.
TL;DR: The first test designed to differentiate between the lipid raft hypothesis of retroviral biogenesis and the Trojan exosome hypothesis is performed, showing significant differences in the abundance of host proteins on the cell surface and in HIV.