FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2078967094> ?p ?o ?g. }

• W2078967094 endingPage "359" @default.
• W2078967094 startingPage "359" @default.
• W2078967094 abstract "Every journey has a beginning, and similarly each infection must begin somewhere and somehow. When initiating an infection, the microbe must get to its host; it might need to attach to the host or breach a barrier, engage a particular host pathway to enact virulence mechanisms, or overcome factors that the host immune response sends its way. This themed issue of Trends in Microbiology covers this crucial time at the beginning of an infection including the first steps of how a microbial infection is initiated in the host. The reviews in this issue discuss the initiation of infection from a pathogenesis perspective, including the host response, and the intricate molecular mechanisms and cellular biology that occur during this timeframe.First, a pathogen must be in the same place as its host. In his Science & Society piece, Scott Weaver discusses how the geographical distribution of some zoonotic arboviral diseases, such as dengue and West Nile virus, have been expanding, reaching urban areas and putting them in contact with humans. Weaver explores potential responses that urban societies could take to limit the geographic range of these viruses and their spread to urban areas, and thus their frequency in human populations.Once a pathogen comes in contact with its host, it must recognize and attach to host cells or surfaces. Valle et al. discuss the lifestyle switch that motile bacteria undertake to form chronic biofilm infections, including the signal transduction mechanisms used to recognize and respond to environmental signals that promote adherence. Cyclic di-nucleotide secondary messengers aid the development of biofilms by repressing flagella and increasing the production of the extracellular matrix that envelops biofilms. Similarly, Borrelia spirochetes can produce a variety of surface-attached adhesins that recognize host substrates and promote infection. Coburn et al. discuss how recently developed imaging technologies could help identify the particular mechanistic role of each adhesin during colonization and infection of ticks and vertebrate hosts.In addition to attaching to host cells, many pathogens also enter into host cells and this represents an obligate step for viral pathogenesis. Mercer and Greber examine the different receptors that viruses use to enter macrophages and dendritic cells and the endocytic pathways used for viral entry. Scott Filler examines how fungi use receptors on non-phagocytic host cells to enter and cause infection, and speculates how fungal–receptor interactions could be targeted with therapeutics.We then turn to more specifically examine HIV, which enters into CD4+ T cells, macrophages, and dendritic cells typically via the CCR5 and CXCR4 co-receptors. Earl et al. discuss how 3D electron microscopy can be used to better understand structural aspects of HIV entry and how this can inform vaccine design. Once in macrophages, virus-containing compartments can provide a protective niche for HIV-1. Tan and Sattentau discuss how HIV-1 assembly, budding, and storage can occur in these compartments and the implications of this compartment for pathogenesis.Hosts have evolved a variety of mechanisms including the innate immune system to block the initial stages of infection. Innate immune defenses are activated once the host senses pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs). Gürtler and Bowie discuss how PRRs sense microbial nucleic acids in the endosome, cytosol, and nucleus, thus allowing these cellular receptors to identify and try to counter invading microbes at the early stages of infection.After detection by the host immune response, pathogens need to overcome the host's immune and cell biological barriers in order for a successful infection to ensue. Rajsbaum and García-Sastre review how viruses can evade host antiviral responses by manipulating the ubiquitin system. Several bacterial pathogens secrete effector proteins through a type III secretion system (T3SS) and Raymond et al. examine how T3SS effectors can manipulate signaling pathways involved in endosomal trafficking, phagocytosis, apoptosis, and the host inflammatory response to promote the establishment of an infection.Together, these articles outline the first steps of an infection in the host, despite host responses aimed at quashing the infection. I would like to thank all the authors of these articles for writing such insightful pieces as well as the peer-reviewers for their thoughtful comments on these manuscripts. I hope you enjoy reading the articles from this themed issue of Trends in Microbiology as much as I have and let us put one foot in front of the other and initiate our journey into the issue. Every journey has a beginning, and similarly each infection must begin somewhere and somehow. When initiating an infection, the microbe must get to its host; it might need to attach to the host or breach a barrier, engage a particular host pathway to enact virulence mechanisms, or overcome factors that the host immune response sends its way. This themed issue of Trends in Microbiology covers this crucial time at the beginning of an infection including the first steps of how a microbial infection is initiated in the host. The reviews in this issue discuss the initiation of infection from a pathogenesis perspective, including the host response, and the intricate molecular mechanisms and cellular biology that occur during this timeframe. First, a pathogen must be in the same place as its host. In his Science & Society piece, Scott Weaver discusses how the geographical distribution of some zoonotic arboviral diseases, such as dengue and West Nile virus, have been expanding, reaching urban areas and putting them in contact with humans. Weaver explores potential responses that urban societies could take to limit the geographic range of these viruses and their spread to urban areas, and thus their frequency in human populations. Once a pathogen comes in contact with its host, it must recognize and attach to host cells or surfaces. Valle et al. discuss the lifestyle switch that motile bacteria undertake to form chronic biofilm infections, including the signal transduction mechanisms used to recognize and respond to environmental signals that promote adherence. Cyclic di-nucleotide secondary messengers aid the development of biofilms by repressing flagella and increasing the production of the extracellular matrix that envelops biofilms. Similarly, Borrelia spirochetes can produce a variety of surface-attached adhesins that recognize host substrates and promote infection. Coburn et al. discuss how recently developed imaging technologies could help identify the particular mechanistic role of each adhesin during colonization and infection of ticks and vertebrate hosts. In addition to attaching to host cells, many pathogens also enter into host cells and this represents an obligate step for viral pathogenesis. Mercer and Greber examine the different receptors that viruses use to enter macrophages and dendritic cells and the endocytic pathways used for viral entry. Scott Filler examines how fungi use receptors on non-phagocytic host cells to enter and cause infection, and speculates how fungal–receptor interactions could be targeted with therapeutics. We then turn to more specifically examine HIV, which enters into CD4+ T cells, macrophages, and dendritic cells typically via the CCR5 and CXCR4 co-receptors. Earl et al. discuss how 3D electron microscopy can be used to better understand structural aspects of HIV entry and how this can inform vaccine design. Once in macrophages, virus-containing compartments can provide a protective niche for HIV-1. Tan and Sattentau discuss how HIV-1 assembly, budding, and storage can occur in these compartments and the implications of this compartment for pathogenesis. Hosts have evolved a variety of mechanisms including the innate immune system to block the initial stages of infection. Innate immune defenses are activated once the host senses pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs). Gürtler and Bowie discuss how PRRs sense microbial nucleic acids in the endosome, cytosol, and nucleus, thus allowing these cellular receptors to identify and try to counter invading microbes at the early stages of infection. After detection by the host immune response, pathogens need to overcome the host's immune and cell biological barriers in order for a successful infection to ensue. Rajsbaum and García-Sastre review how viruses can evade host antiviral responses by manipulating the ubiquitin system. Several bacterial pathogens secrete effector proteins through a type III secretion system (T3SS) and Raymond et al. examine how T3SS effectors can manipulate signaling pathways involved in endosomal trafficking, phagocytosis, apoptosis, and the host inflammatory response to promote the establishment of an infection. Together, these articles outline the first steps of an infection in the host, despite host responses aimed at quashing the infection. I would like to thank all the authors of these articles for writing such insightful pieces as well as the peer-reviewers for their thoughtful comments on these manuscripts. I hope you enjoy reading the articles from this themed issue of Trends in Microbiology as much as I have and let us put one foot in front of the other and initiate our journey into the issue." @default.
• W2078967094 created "2016-06-24" @default.
• W2078967094 creator A5064735751 @default.
• W2078967094 date "2013-08-01" @default.
• W2078967094 modified "2023-09-23" @default.
• W2078967094 title "Taking the first steps towards infection" @default.
• W2078967094 doi "https://doi.org/10.1016/j.tim.2013.06.007" @default.
• W2078967094 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23910544" @default.
• W2078967094 hasPublicationYear "2013" @default.
• W2078967094 type Work @default.
• W2078967094 sameAs 2078967094 @default.
• W2078967094 citedByCount "0" @default.
• W2078967094 crossrefType "journal-article" @default.
• W2078967094 hasAuthorship W2078967094A5064735751 @default.
• W2078967094 hasBestOaLocation W20789670941 @default.
• W2078967094 hasConcept C159047783 @default.
• W2078967094 hasConcept C70721500 @default.
• W2078967094 hasConcept C86803240 @default.
• W2078967094 hasConceptScore W2078967094C159047783 @default.
• W2078967094 hasConceptScore W2078967094C70721500 @default.
• W2078967094 hasConceptScore W2078967094C86803240 @default.
• W2078967094 hasIssue "8" @default.
• W2078967094 hasLocation W20789670941 @default.
• W2078967094 hasLocation W20789670942 @default.
• W2078967094 hasOpenAccess W2078967094 @default.
• W2078967094 hasPrimaryLocation W20789670941 @default.
• W2078967094 hasRelatedWork W1487857142 @default.
• W2078967094 hasRelatedWork W1702322095 @default.
• W2078967094 hasRelatedWork W1865764402 @default.
• W2078967094 hasRelatedWork W1975114493 @default.
• W2078967094 hasRelatedWork W1990804418 @default.
• W2078967094 hasRelatedWork W1993764875 @default.
• W2078967094 hasRelatedWork W2082860237 @default.
• W2078967094 hasRelatedWork W2118087741 @default.
• W2078967094 hasRelatedWork W2130076355 @default.
• W2078967094 hasRelatedWork W3029386773 @default.
• W2078967094 hasVolume "21" @default.
• W2078967094 isParatext "false" @default.
• W2078967094 isRetracted "false" @default.
• W2078967094 magId "2078967094" @default.
• W2078967094 workType "article" @default.