The ability of microorganisms to infect and cause disease in higher organisms depends on (i) the nature of the infecting organism(s), (ii) the route of infection, (iii) virulence factors, which enable long-term survival within the organism, and (iv) the immune defense mechanisms of the given host. Molecular epidemiological investigations provide evidence regarding the etiology and mechanisms by which micro-organisms cause disease in order to develop strategies for their prevention. While classic immunogenetic biomarkers (single nucleotide polymorphisms - SNPs) have been shown to be related to resistance or susceptibility to infectious disease, new studies have highlighted alterations in the epigenetic landscape of immune cells as an equally important means of detecting and understanding the progression of infectious diseases.
There is mounting evidence that micro-organisms can influence various epigenetic factors that are essential for the regulation of chromatin structure and of transcription in immune cells. These factors include DNA methylation, histone modifications and miRNAs. These highly evolved epigenetic mechanisms enable the host to alter and reprogram gene expression in response to environmental stimuli, including microbial agents. DNA methylation and histone modifications within the chromatin of various immune cell types has been reported in instances of infection with various gut bacterial species (e.g. Helicobacter pylori, Clostridium coccoide and Listeria monocytogenes), in bacterial sepsis, in tuberculosis (TB), and in infections with Entamoeba histolytica, Malaria, Herpes virus and Dengue virus.
MicroRNAs (miRNAs), defined as short non-coding RNAs, function to regulate the expression of protein coding genes in viruses and eukaryotes at the post-transcriptional level. In recent years, several miRNAs have been reported as molecular biomarkers and immunological modulators in a large array of infectious diseases, including Hepatitis B and C, TB, Malaria and those caused by HIV-1, Dengue virus, Helicobacter pylori, Toxoplasma, Leishmania, and Trypanosoma and parasitic helminths.
In this Research Topic, we aim to discuss the molecular basis of the regulation of epigenetic markers in immune cells and how the epigenome of immune cells is altered in infectious diseases. We also aim to discuss the potential effects of epigenetic alterations in immune cells in the context of human disease and their therapeutic targeting potential in the context of clinical applications.
We welcome the submission of Original Research, Review, Method, Clinical Trial and Case Reports that cover, but are not limited to, the following topics:
1. Immuno-epigenetic markers, e.g. DNA methylation, histone modifications and miRNAs, including polymorphisms in their corresponding genes and binding sites.
2. Epigenetic-mediated modulation of immunological processes in infectious disease.
3. The role of immune-epigenetics in determining disease susceptibility, pathogenesis and evolution.
4. Therapeutic targeting of epigenetic markers for the treatment of infectious diseases.
The ability of microorganisms to infect and cause disease in higher organisms depends on (i) the nature of the infecting organism(s), (ii) the route of infection, (iii) virulence factors, which enable long-term survival within the organism, and (iv) the immune defense mechanisms of the given host. Molecular epidemiological investigations provide evidence regarding the etiology and mechanisms by which micro-organisms cause disease in order to develop strategies for their prevention. While classic immunogenetic biomarkers (single nucleotide polymorphisms - SNPs) have been shown to be related to resistance or susceptibility to infectious disease, new studies have highlighted alterations in the epigenetic landscape of immune cells as an equally important means of detecting and understanding the progression of infectious diseases.
There is mounting evidence that micro-organisms can influence various epigenetic factors that are essential for the regulation of chromatin structure and of transcription in immune cells. These factors include DNA methylation, histone modifications and miRNAs. These highly evolved epigenetic mechanisms enable the host to alter and reprogram gene expression in response to environmental stimuli, including microbial agents. DNA methylation and histone modifications within the chromatin of various immune cell types has been reported in instances of infection with various gut bacterial species (e.g. Helicobacter pylori, Clostridium coccoide and Listeria monocytogenes), in bacterial sepsis, in tuberculosis (TB), and in infections with Entamoeba histolytica, Malaria, Herpes virus and Dengue virus.
MicroRNAs (miRNAs), defined as short non-coding RNAs, function to regulate the expression of protein coding genes in viruses and eukaryotes at the post-transcriptional level. In recent years, several miRNAs have been reported as molecular biomarkers and immunological modulators in a large array of infectious diseases, including Hepatitis B and C, TB, Malaria and those caused by HIV-1, Dengue virus, Helicobacter pylori, Toxoplasma, Leishmania, and Trypanosoma and parasitic helminths.
In this Research Topic, we aim to discuss the molecular basis of the regulation of epigenetic markers in immune cells and how the epigenome of immune cells is altered in infectious diseases. We also aim to discuss the potential effects of epigenetic alterations in immune cells in the context of human disease and their therapeutic targeting potential in the context of clinical applications.
We welcome the submission of Original Research, Review, Method, Clinical Trial and Case Reports that cover, but are not limited to, the following topics:
1. Immuno-epigenetic markers, e.g. DNA methylation, histone modifications and miRNAs, including polymorphisms in their corresponding genes and binding sites.
2. Epigenetic-mediated modulation of immunological processes in infectious disease.
3. The role of immune-epigenetics in determining disease susceptibility, pathogenesis and evolution.
4. Therapeutic targeting of epigenetic markers for the treatment of infectious diseases.