Following on from the success of the research topic
The pathogenic Yersiniae – advances in the understanding of physiology and virulence, we are pleased to launch a follow-up on the Molecular and Cellular Biology of Yersinia. Within the genus Yersinia exist the prominent human pathogens Y. pestis, Y. enterocolitica, and Y. pseudotuberculosis and the fish pathogen Y. ruckeri. Responsible for the life-threatening zoonotic disease plague that has caused millions of deaths throughout history, Y. pestis is arguably the most notorious of all bacterial pathogens. Facilitated by the ease of in vitro culturing, genetic tractability, and availability of relevant infection models, studies of Y. pestis have revealed a great deal about its flea-rodent life cycle as well as mechanisms facilitating transmission and infection of humans.
Furthermore, understanding human disease caused by Yersinia is enhanced through studies of Y. enterocolitica and Y. pseudotuberculosis pathogenesis. Despite only being responsible for self-limiting gastrointestinal infections in healthy humans, relevant mouse infection models that mirror disseminated Yersinia infection has helped uncover Yersinia virulence determinants that have evolved to overcome host defences. Moreover, complementing studies on Yersinia pathogens of humans are those that investigate Y. ruckeri pathogenesis. Aided by natural infection models, studies of Y. ruckeri are revealing true pathogenic mechanisms used by these bacteria to overcome both non-specific and specific immune responses of infected fish. In combination with assorted genome sequencing analyses, these mechanistic studies are collectively benefitting understanding of Yersinia pathogen evolution as well as Yersinia pathogen adaptation to changing environments both inside and outside of the host.
This includes uncovering novel regulatory mechanisms controlling virulence gene expression in response to prevailing nutrient resources associated with the infected host or in the environment. This Research Topic therefore welcomes new contributions that lead to an improved molecular understanding of Yersinia-host cell interactions and the network of regulatory control mechanisms that define Yersinia survival in the host or when free living in the environment. It also welcomes studies that define potential targets for the design and development of anti-Yersinia therapeutic drugs and vaccines, as well as translational studies that involve unique cooperation between diverse disciplines.
Following on from the success of the research topic
The pathogenic Yersiniae – advances in the understanding of physiology and virulence, we are pleased to launch a follow-up on the Molecular and Cellular Biology of Yersinia. Within the genus Yersinia exist the prominent human pathogens Y. pestis, Y. enterocolitica, and Y. pseudotuberculosis and the fish pathogen Y. ruckeri. Responsible for the life-threatening zoonotic disease plague that has caused millions of deaths throughout history, Y. pestis is arguably the most notorious of all bacterial pathogens. Facilitated by the ease of in vitro culturing, genetic tractability, and availability of relevant infection models, studies of Y. pestis have revealed a great deal about its flea-rodent life cycle as well as mechanisms facilitating transmission and infection of humans.
Furthermore, understanding human disease caused by Yersinia is enhanced through studies of Y. enterocolitica and Y. pseudotuberculosis pathogenesis. Despite only being responsible for self-limiting gastrointestinal infections in healthy humans, relevant mouse infection models that mirror disseminated Yersinia infection has helped uncover Yersinia virulence determinants that have evolved to overcome host defences. Moreover, complementing studies on Yersinia pathogens of humans are those that investigate Y. ruckeri pathogenesis. Aided by natural infection models, studies of Y. ruckeri are revealing true pathogenic mechanisms used by these bacteria to overcome both non-specific and specific immune responses of infected fish. In combination with assorted genome sequencing analyses, these mechanistic studies are collectively benefitting understanding of Yersinia pathogen evolution as well as Yersinia pathogen adaptation to changing environments both inside and outside of the host.
This includes uncovering novel regulatory mechanisms controlling virulence gene expression in response to prevailing nutrient resources associated with the infected host or in the environment. This Research Topic therefore welcomes new contributions that lead to an improved molecular understanding of Yersinia-host cell interactions and the network of regulatory control mechanisms that define Yersinia survival in the host or when free living in the environment. It also welcomes studies that define potential targets for the design and development of anti-Yersinia therapeutic drugs and vaccines, as well as translational studies that involve unique cooperation between diverse disciplines.