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Special Issue: Cell Biology of Host-Pathogen Interactions




Summary: Malaria parasite egress from its host cell is a key step in the life cycle of this important pathogen. The article summarises current knowledge of malarial egress and highlights major questions in the field.


Summary:Trypanosoma cruzi, the causative agent of Chagas disease, subverts cell signaling mechanisms to survive in the host. Here, we explain the various cellular mechanisms that T. cruzi hijacks.

Summary: This Review focuses on the structure of 3C and the molecular mechanisms through which it executes both viral and host physiological processes.

Summary: This Review at the intersection of membrane trafficking and virology discusses how viruses hijack the organisation and function of cellular membranes to accomplish their replication, assembly and egress.

Summary: This Review discusses the selection and use of various epithelial cell culture methods and microscopy techniques that can be used to image host–pathogen interactions in vitro.

Summary: This Review highlights diverse strategies through which cellular metabolic processes are rewired to execute defense against microbes.

Summary: A review on the versatile regulations of vimentin in the key steps during the infection of various viruses, including binding, entry, trafficking, replication, assembly, and egress.

Summary: A review on the important role of non-coding RNAs in the interaction between vertebrate host cells, arthropod vectors and vector-borne pathogens.

Summary: A review of common mechanisms of how intracellular pathogens escape from the lumen of vacuoles in infected host cells. A new mechanism based on oxidation of vacuolar membranes is proposed.


Summary: Remodeling of incipient septin structures within fungal infection cells requires the pressure-dependent formation of a contractile F-actin ring and is promoted by the actin-modulating protein coronin.

Summary: The placenta-specific microRNA miR-517a attenuates viral infection. Here we have identified that miR-517a directly targets UNC13D as a part of its antiviral function.

Summary: High-content real-time imaging of L. amazonensis-infected pyroptotic macrophages reveals surface exposure of virulent amastigotes that are retained through attachment to the parasitophorous vacuole membrane.


Summary: TAP110 is a novel mitochondrial genome segregation factor in Trypanosoma brucei that associates with the previously described TAC component TAC102. Ultrastructure expansion microscopy reveals its proximal position to the kDNA.

Summary: CRAMP is a critical component in autophagy-mediated clearance of phagocytosed E. coli by mouse macrophages.

Summary: Characterization of the molecular and ultrastructural pathological effects of Encephalitozoon intestinalis infection in human intestinal epithelial cells.

Summary: Interactions between human neonatal low-density granulocytes and bacteria drive production of extracellular DNA that impairs clearance of bacteria by monocytes and may compromise protective immunity.

Summary:Leishmania donovani redirects macrophage–T cell crosstalk to maintain anti-inflammatory cytokine response via the Jagged–Notch signaling pathway, resulting in immunosuppression during experimental visceral leishmaniasis.

Summary: Development of a novel, enhanced Staphylococcus aureus infection model through humanisation of zebrafish enabled us to show the important contribution of S. aureus virulence factors PVL and HlgCB to infection.

Summary: BPIFB3 is a regulator of a non-canonical cellular autophagy pathway that impacts the replication of enteroviruses and flaviviruses. Here, we define ARFGAP1 and TMED9 as essential components of this pathway.

Summary: Analysis of the interaction between MakA and mammalian host cells reveals that the Vibrio cholerae cytotoxin MakA induces endolysosomal aggregate formation in host cells to modulate autophagy.

Summary: Interaction of borreliae with human macrophages is visualized by high-resolution tomography, revealing the contribution of membrane tunnels, phagosomes and ER to intracellular processing of spirochetes.

Summary: The mechanisms dictating CMV reactivation from latency are incompletely understood. Here, we show the viral-encoded GPCR pUL33 is involved in CREB activation, thus aiding in successful reactivation.

Summary: Crosstalk between endophilin-A2 and caveolin-1, proteins implicated in clathrin-independent endocytosis, regulates a tubular endocytic pathway important for plasma membrane repair and trypanosome invasion.

Summary: Following phagosome membrane damage, Mycobacterium tuberculosis induces the formation of, and escapes from, tubulovesicular autophagosomes in human induced pluripotent stem cell-derived macrophages.

Summary: Single-cell and single-transcript analyses indicate that the cell cycle state at the time of infection tunes the cell-to-cell variability of immediate early gene transcription of human adenovirus.

Summary: Foot-and-mouth disease virus infection induces ER stress and the PERK-mediated UPR, which activates autophagic flux to promote virus multiplication by affecting antiviral interferon production.

Summary: Through ribosome isolation and mass spectrometry approaches, we characterize novel modifications to ribosomal proteins during poxvirus infection.

Summary: Dynamic localisation of the NDC80 protein complex, a kinetochore marker, during proliferative stages of the malaria parasite life cycle reveals unique modes of chromosome segregation.

Summary: PTP1B specifically promotes the secretion of type I IFNs independently of its phosphatase activity, but requiring its proper localization to the ER membrane.

Summary: The parasite T. gondii hijacks the Ras–Erk, Met and Ca2+ signaling machinery to control the migration of immune cells and promote its own dissemination.

Summary: Biochemical, computational, reverse genetic and biophysical approaches show that a divergent motif of profilin has a role in Plasmodium sporozoite migration, which is important for malaria transmission.


Summary: 3D endometrial organoids are used to model Chlamydia infection and the role of secreted virulence factors in reprogramming host epithelial cells and immune cell recruitment.

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