Environmental and social changes intensify human exposure to harmful disease agents. The complexity of this rendezvous is impacted by the diversity of pathogens and the wide array of invasion strategies they use to enter host cells. Intracellular localization provides protection from the host’s immune system, access to its transcription/translation machinery, and a nutrient-rich environment. The invasion routes offered by cells are limited and common to various pathogens. These involve (1) recognition/interaction with host-cell surface components; (2) initiation of signal transduction pathways; (3) rearrangement of the host’s cytoskeleton; and (4) internalization of the pathogen. Often, however, the “citadel” – the nuclear envelope – still has to be seized. The final battle involves overpowering the citadel’s communication channels – the nuclear pore complex (NPC) – to enable the pathogen to modulate host-cell metabolism at the transcriptional level, and highjack its transcriptional machinery for reproduction. Even so, there is another level of complexity – pathogens rarely exist in isolation. Patients may sustain co-infection with multiple disease agents, and the composition of the co-infecting microorganisms dictates dynamic interactions with the host and defines the disease’s path and treatment.
Present worldwide events grimly demonstrate the devastating outcomes that occur when the host endures co-infection with more than one pathogen. It has become a matter of considerable importance to expose similarities between the molecular mechanisms of cellular invasion applied by widely diverse taxonomic groups of pathogens (from viruses and bacteria to eukaryotic intracellular parasites). Systematizing and reviewing the current knowledge, sharing scientific methods, and exploring the synergy or antagonism between co-infecting invaders from similar or distant taxonomic origins, can help in developing efficient therapies for future encounters.
The aim of the current collection is to cover the interactions of a wide variety of pathogens with the host-cell’s plasma membrane and nuclear envelope/NPCs, including molecular interfaces between different co-infecting agents at those cellular locations. This will include original research articles, reviews, mini-reviews, and method papers. We welcome authors to submit manuscripts on the following, or related topics:
– Viral docking to the plasma membrane and internalization of the virus
– Import of viral genomes into the eukaryotic cell nucleus and modulation of NPCs by viral proteins
– Docking and internalization of bacteria by eukaryotic cells
– Manipulation of host-cell nuclear import/export machinery by bacterial proteins and/or nucleic acids
– Unicellular eucaryotic pathogens at the host-cell plasma membrane – from interaction to engulfment
– Effect of the parasite-encoded compounds on nuclear pore function in a host’s cells
– Molecular mechanisms underlying co-infection of cells with more than one type of pathogen
– Synergistic or antagonistic relations between co-infecting pathogens
- Interactions of intracellular pathogens with endosomal and lysosomal host systems
- Pathogen-directed diversion of endoplasmic reticulum and golgi membrane trafficking
- Interactions between pathogen-derived proteins with host intracellular trafficking machinery
- Endoplasmic reticulum and golgi "viral factories"
Environmental and social changes intensify human exposure to harmful disease agents. The complexity of this rendezvous is impacted by the diversity of pathogens and the wide array of invasion strategies they use to enter host cells. Intracellular localization provides protection from the host’s immune system, access to its transcription/translation machinery, and a nutrient-rich environment. The invasion routes offered by cells are limited and common to various pathogens. These involve (1) recognition/interaction with host-cell surface components; (2) initiation of signal transduction pathways; (3) rearrangement of the host’s cytoskeleton; and (4) internalization of the pathogen. Often, however, the “citadel” – the nuclear envelope – still has to be seized. The final battle involves overpowering the citadel’s communication channels – the nuclear pore complex (NPC) – to enable the pathogen to modulate host-cell metabolism at the transcriptional level, and highjack its transcriptional machinery for reproduction. Even so, there is another level of complexity – pathogens rarely exist in isolation. Patients may sustain co-infection with multiple disease agents, and the composition of the co-infecting microorganisms dictates dynamic interactions with the host and defines the disease’s path and treatment.
Present worldwide events grimly demonstrate the devastating outcomes that occur when the host endures co-infection with more than one pathogen. It has become a matter of considerable importance to expose similarities between the molecular mechanisms of cellular invasion applied by widely diverse taxonomic groups of pathogens (from viruses and bacteria to eukaryotic intracellular parasites). Systematizing and reviewing the current knowledge, sharing scientific methods, and exploring the synergy or antagonism between co-infecting invaders from similar or distant taxonomic origins, can help in developing efficient therapies for future encounters.
The aim of the current collection is to cover the interactions of a wide variety of pathogens with the host-cell’s plasma membrane and nuclear envelope/NPCs, including molecular interfaces between different co-infecting agents at those cellular locations. This will include original research articles, reviews, mini-reviews, and method papers. We welcome authors to submit manuscripts on the following, or related topics:
– Viral docking to the plasma membrane and internalization of the virus
– Import of viral genomes into the eukaryotic cell nucleus and modulation of NPCs by viral proteins
– Docking and internalization of bacteria by eukaryotic cells
– Manipulation of host-cell nuclear import/export machinery by bacterial proteins and/or nucleic acids
– Unicellular eucaryotic pathogens at the host-cell plasma membrane – from interaction to engulfment
– Effect of the parasite-encoded compounds on nuclear pore function in a host’s cells
– Molecular mechanisms underlying co-infection of cells with more than one type of pathogen
– Synergistic or antagonistic relations between co-infecting pathogens
- Interactions of intracellular pathogens with endosomal and lysosomal host systems
- Pathogen-directed diversion of endoplasmic reticulum and golgi membrane trafficking
- Interactions between pathogen-derived proteins with host intracellular trafficking machinery
- Endoplasmic reticulum and golgi "viral factories"
