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Toxoplasma gondii is a master manipulator capable of effectively siphoning the resources from the host cell for its intracellular subsistence. However, the molecular underpinnings of how the parasite gains resources from its host remain largely unknown. Residing within a non-fusogenic parasitophorous vacuole (PV), the parasite must acquire resources across the limiting membrane of its replicative niche, which is decorated with parasite proteins including those secreted from dense granules. We discovered a role for the host Endosomal Sorting Complex Required for Transport (ESCRT) machinery in host cytosolic protein uptake by T. gondii by disrupting host ESCRT function. We identified the transmembrane dense granule protein TgGRA14, which contains motifs homologous to the late domain motifs of HIV-1 Gag, as a candidate for the recruitment of the host ESCRT machinery to the PV membrane. Using an HIV-1 virus-like particle (VLP) release assay, we found that the motif-containing portion of TgGRA14 is sufficient to substitute for HIV-1 Gag late domain to mediate ESCRT-dependent VLP budding. We also show that TgGRA14 is proximal to and interacts with host ESCRT components and other dense granule proteins during infection. Furthermore, analysis of TgGRA14-deficient parasites revealed a marked reduction in ingestion of a host cytosolic protein compared to WT parasites. Thus, we propose a model in which T. gondii recruits the host ESCRT machinery to the PV where it can interact with TgGRA14 for the internalization of host cytosolic proteins across the PV membrane (PVM). These findings provide new insight into how T. gondii accesses contents of the host cytosol by exploiting a key pathway for vesicular budding and membrane scission.
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http://dx.doi.org/10.1371/journal.ppat.1010138 | DOI Listing |
FEMS Microbiol Rev
September 2025
Department of Life Sciences, School of Basic Sciences and Research, Sharda University, Knowledge Park III, Greater Noida, Uttar Pradesh 201306.
Mtb subverts host immune surveillance by damaging phagolysosomal membranes, exploiting them as replication niches. In response, host cells initiate a coordinated LDR, integrating membrane repair, selective autophagy, and de novo biogenesis. This review delineates a systems-level model of lysosomal quality control governed by three critical regulatory axes: LGALS3/8/9, TRIM E3 ubiquitin ligases, and the AMPK-TFEB signaling pathway.
View Article and Find Full Text PDFFEBS J
September 2025
Jiangsu Key Laboratory of Infection and Immunity, The Fourth Affiliated Hospital of Soochow University, Institutes of Biology and Medical Sciences, Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Degradative autophagy supplies a source of nutrients and energy by digesting cytoplasmic components. Additionally, it eliminates toxic protein aggregates and defective organelles from cells. Exosomes are small vesicles that are released by cells into the extracellular environment and are also involved in maintenance of homeostasis by removing unwanted materials and intracellular pathogens.
View Article and Find Full Text PDFJ Virol
August 2025
Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan.
Herpesviruses replicate their genomes and package them into capsids within the host cell nucleus. These capsids must then translocate from the nucleus to the cytoplasm through a process designated nuclear egress. The virus-encoded nuclear egress complex (NEC), consisting of a nuclear matrix protein and a nuclear membrane protein, plays a crucial role in this process.
View Article and Find Full Text PDFbioRxiv
July 2025
Department of Microbiology, University of Georgia, Athens, GA.
Human pathogenic filarial nematodes of the family Onchocercidae, including and cause debilitating filarial diseases such as lymphatic filariasis and river blindness. These mosquito-borne pathogens are obligately colonized by the gram-negative intracellular alphaproteobacterium, which is essential for nematode sexual reproduction, long-term survival, and pathogenicity in the mammalian host. Like many intracellular bacteria, likely uses numerous surface-exposed and secreted effector proteins to regulate its ability to persist and replicate within nematode host cells.
View Article and Find Full Text PDFInt Rev Immunol
July 2025
Department of Biotechnology, School of Chemical and Life Sciences, New Delhi, India.
() employs diverse virulence factors to evade immune defenses and persist intracellularly. The ESAT-6 secretion system-1 (ESX-1) type VII secretion system (T7SS) releases EsxA, EspA, and EspB, inducing phagosomal rupture and cytosolic access while triggering host defenses, including galectin recruitment and stress granule formation. To counteract host responses, utilizes phthiocerol dimycocerosates (PDIMs) to inhibit autophagy and LC3-associated phagocytosis (LAP) by suppressing NADPH oxidase (NOX2) recruitment and reactive oxygen species (ROS) production.
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