Many infections induce over-activity of the immune system. Even an efficiently treated chronic infection, such as HIV, may result in persistent low-level inflammation. This may be the consequence of various mechanisms, including the direct stimulation of receptors of the innate immune system by pathogen-associated molecular patterns (PAMPs), the recognition of danger-associated molecular patterns (DAMPs) released by infected cells, and the specific activation of the adaptive immune system, leading to the deregulation of the whole immune system.
These infections can have indirect effects on immune function through perturbations in the microbiota and/or metabolic disorders favored by the infectious agent. This immune over-activity can result in various comorbidities including the development of tumors, insulin resistance, and metabolic syndrome, or auto-immune diseases.
The main aim of the Research Topic is to elucidate the mechanisms by which infectious agents induce chronic activation of the immune system, for example, via combinations of inhibitory and stimulating strategies used by the pathogens to bypass the immune response. It also aims to understand how the modification of organs, tissues, and cell subpopulations in the course of infections contributes to chronic immune activation, the consequences of antimicrobial treatment on this immune activation, and the ways this immune activation contributes to the onset of long-term non-infectious diseases.
Of note, the topic is not limited to non-acute infections, since acute infections, such as Chikungunya infection, are also proven to provoke chronic disorders.
We welcome the submission of Original Research, Reviews, Hypothesis and Theory, and Case Reports covering, but not limited to, the following topics:
1. Molecular pathways resulting in chronic immune activation in the course of infection
2. The contribution of host and pathogen genetic background to the level of immune activation
3. The role of infectious agent escape strategies in provoking chronic immune activation
4. The relationship between infection-induced changes in metabolism, microbiome, and coagulation, and chronic immune activation
5. Mechanisms linking specific types of immune over-activation to comorbidities, including immune deficiency resulting in poor vaccine response
6. Animal models representing counterexamples, i.e. non-pathogenic SIV infection of primates or various viral infections in bats
7. Novel strategies to prevent/inhibit the pathogenic consequences of infection-induced chronic immune activation
Topic Editor Prof. Pierre Corbeau received financial support from MSD, MSDAvenir, and Gilead. Topic editor Dr. Nicholas Funderburg received financial support from Gilead. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Many infections induce over-activity of the immune system. Even an efficiently treated chronic infection, such as HIV, may result in persistent low-level inflammation. This may be the consequence of various mechanisms, including the direct stimulation of receptors of the innate immune system by pathogen-associated molecular patterns (PAMPs), the recognition of danger-associated molecular patterns (DAMPs) released by infected cells, and the specific activation of the adaptive immune system, leading to the deregulation of the whole immune system.
These infections can have indirect effects on immune function through perturbations in the microbiota and/or metabolic disorders favored by the infectious agent. This immune over-activity can result in various comorbidities including the development of tumors, insulin resistance, and metabolic syndrome, or auto-immune diseases.
The main aim of the Research Topic is to elucidate the mechanisms by which infectious agents induce chronic activation of the immune system, for example, via combinations of inhibitory and stimulating strategies used by the pathogens to bypass the immune response. It also aims to understand how the modification of organs, tissues, and cell subpopulations in the course of infections contributes to chronic immune activation, the consequences of antimicrobial treatment on this immune activation, and the ways this immune activation contributes to the onset of long-term non-infectious diseases.
Of note, the topic is not limited to non-acute infections, since acute infections, such as Chikungunya infection, are also proven to provoke chronic disorders.
We welcome the submission of Original Research, Reviews, Hypothesis and Theory, and Case Reports covering, but not limited to, the following topics:
1. Molecular pathways resulting in chronic immune activation in the course of infection
2. The contribution of host and pathogen genetic background to the level of immune activation
3. The role of infectious agent escape strategies in provoking chronic immune activation
4. The relationship between infection-induced changes in metabolism, microbiome, and coagulation, and chronic immune activation
5. Mechanisms linking specific types of immune over-activation to comorbidities, including immune deficiency resulting in poor vaccine response
6. Animal models representing counterexamples, i.e. non-pathogenic SIV infection of primates or various viral infections in bats
7. Novel strategies to prevent/inhibit the pathogenic consequences of infection-induced chronic immune activation
Topic Editor Prof. Pierre Corbeau received financial support from MSD, MSDAvenir, and Gilead. Topic editor Dr. Nicholas Funderburg received financial support from Gilead. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
