In immunology, all parameters are assigned to either innate or adaptive immunity. However, by documenting adaptive traits executed by cells traditionally classified as part of the innate immune system (e.g., adaptive NK cells and trained macrophage responses), state-of-the-art research increasingly blurs this distinction. To recognize an infection, coordinate different layers of response, and eliminate the intruder, the immune system relies on an arsenal of specific receptors and their downstream signaling pathways. Upon first encounter of the pathogen, one type of receptors - including B and T cell receptors - need to be specifically tailored by somatic mutation and selection processes, while another type of receptors - including pattern-recognition receptors (PPRs) as well as receptors for interferons (IFN), cytokines, and tumor necrosis factor (TNF) - are immediately responsive in their inherited genetic layout. Accordingly, monozygotic twins share the genetic information of the latter but not of the first class of receptors. This research topic aims to address the functional interplay between such germline-encoded receptors (GERs) and DNA viruses.
Over the last couple of years, the ongoing COVID-19 pandemic has forced the research community to focus almost exclusively on the RNA virus SARS-CoV-2. However, it is important to bear in mind that various other viruses also cause morbidity and mortality. DNA viruses such as parvo-, circo-, polyoma-, papilloma-, adeno-, hepadna-, herpes-, and poxviruses affect large parts of the global population by various means. Some DNA viruses such as polyoma-, papilloma-, hepadna-, and ?-herpesviruses predispose or even cause different types of malignancies. Infections with opportunistic DNA viruses such as adenoviruses and herpesviruses can progress self-limiting and subclinical in healthy adults, but can become life-threatening during periods of immature, compromised, or senescent immunity. Furthermore, emerging viruses such as the monkey poxvirus are also among DNA viruses. Since DNA viruses apply fundamentally different adaptation strategies compared to RNA viruses, this research topic aims to address the mutual interplay between DNA viruses and all immune functions regulated by GERs. In particular, we hope that this Research Topic will shed new light on how DNA viruses modulate GERs as well as GER-induced signaling, and how GER-regulated immunity in turn restricts DNA virus replication, dissemination, and diseases.
We welcome the submission of original research, and review articles that cover, but are not limited to, the following sub-topics:
• PRRs and their signaling (including toll-like receptors [TLRs], RIG-like receptors [RLRs], NOD-like receptors [NLRs], and the cGAS-STING pathway)
• Death receptors and their signaling
• Alarmin receptors and their signaling
• C-type lectin receptors and their signaling
• IFN receptors and JAK-STAT signaling
• TNF receptor superfamily members and NF?B signaling
• “Eat-me” and “Do-not-eat-me” receptors and their signaling
• Cytokine and chemokine receptors and their signaling (e.g., G protein, JAK-STAT, NF?B, and MAP kinase signaling)
• NK cell receptors and their signaling
In immunology, all parameters are assigned to either innate or adaptive immunity. However, by documenting adaptive traits executed by cells traditionally classified as part of the innate immune system (e.g., adaptive NK cells and trained macrophage responses), state-of-the-art research increasingly blurs this distinction. To recognize an infection, coordinate different layers of response, and eliminate the intruder, the immune system relies on an arsenal of specific receptors and their downstream signaling pathways. Upon first encounter of the pathogen, one type of receptors - including B and T cell receptors - need to be specifically tailored by somatic mutation and selection processes, while another type of receptors - including pattern-recognition receptors (PPRs) as well as receptors for interferons (IFN), cytokines, and tumor necrosis factor (TNF) - are immediately responsive in their inherited genetic layout. Accordingly, monozygotic twins share the genetic information of the latter but not of the first class of receptors. This research topic aims to address the functional interplay between such germline-encoded receptors (GERs) and DNA viruses.
Over the last couple of years, the ongoing COVID-19 pandemic has forced the research community to focus almost exclusively on the RNA virus SARS-CoV-2. However, it is important to bear in mind that various other viruses also cause morbidity and mortality. DNA viruses such as parvo-, circo-, polyoma-, papilloma-, adeno-, hepadna-, herpes-, and poxviruses affect large parts of the global population by various means. Some DNA viruses such as polyoma-, papilloma-, hepadna-, and ?-herpesviruses predispose or even cause different types of malignancies. Infections with opportunistic DNA viruses such as adenoviruses and herpesviruses can progress self-limiting and subclinical in healthy adults, but can become life-threatening during periods of immature, compromised, or senescent immunity. Furthermore, emerging viruses such as the monkey poxvirus are also among DNA viruses. Since DNA viruses apply fundamentally different adaptation strategies compared to RNA viruses, this research topic aims to address the mutual interplay between DNA viruses and all immune functions regulated by GERs. In particular, we hope that this Research Topic will shed new light on how DNA viruses modulate GERs as well as GER-induced signaling, and how GER-regulated immunity in turn restricts DNA virus replication, dissemination, and diseases.
We welcome the submission of original research, and review articles that cover, but are not limited to, the following sub-topics:
• PRRs and their signaling (including toll-like receptors [TLRs], RIG-like receptors [RLRs], NOD-like receptors [NLRs], and the cGAS-STING pathway)
• Death receptors and their signaling
• Alarmin receptors and their signaling
• C-type lectin receptors and their signaling
• IFN receptors and JAK-STAT signaling
• TNF receptor superfamily members and NF?B signaling
• “Eat-me” and “Do-not-eat-me” receptors and their signaling
• Cytokine and chemokine receptors and their signaling (e.g., G protein, JAK-STAT, NF?B, and MAP kinase signaling)
• NK cell receptors and their signaling
