About this Research Topic
Several viruses have the ability for lifelong persistence in the infected host. In some cases, this persistence is achieved by integration of the virus in the host genome. If this integration occurs in the germ line, the virus can be transmitted to the offspring and if the presence of these viruses has no detrimental effects on the fitness of the host, they can become stable genetic elements of the host species. In this way, several virus families have entered genomes and today endogenous viral elements (EVE) are an integral part of all eukaryotic genomes. Endogenous retroviruses (ERV) are the largest group of EVE and compose at least 8% of the human genome.
Most EVE are not able to replicate and form virus particles autonomously. In addition to genetic inactivation, epigenetic control of EVE transcription plays an important role for EVE regulation. Epigenetic mechanisms are reversible and, therefore, reactivation of EVE can occur under physiological and pathological conditions. Such reactivation cannot only affect EVE with complete open reading frames but also EVE with disrupted genomes that are not encoding functionally intact proteins.
Activation of EVE loci can have varying consequences for the host. Some EVE proteins (syncytins, supressyn) are involved in cell-cell fusion events, e.g. during placenta development. Other EVE proteins can act as (super-)antigens and can activate the immune system. In addition, reactivated EVE loci can induce or repress expression of adjacent genes. Finally, EVE are a major source for short and long non-coding RNA as well as double-stranded DNA with potential functions for gene regulation and innate immunity.
Increased EVE transcription has been observed in certain cancer types as well as autoimmune diseases. In some of these cases, release of EVE-derived virus particles from cells has been observed. Reactivation of EVE under such diverse conditions might indicate common pathways in cancer and autoimmunity.
This Research Topic is calling for submission of original research papers and review articles about all aspects of EVE reactivation in the context of cancer and autoimmune diseases.
Most EVE are not able to replicate and form virus particles autonomously. In addition to genetic inactivation, epigenetic control of EVE transcription plays an important role for EVE regulation. Epigenetic mechanisms are reversible and, therefore, reactivation of EVE can occur under physiological and pathological conditions. Such reactivation cannot only affect EVE with complete open reading frames but also EVE with disrupted genomes that are not encoding functionally intact proteins.
Activation of EVE loci can have varying consequences for the host. Some EVE proteins (syncytins, supressyn) are involved in cell-cell fusion events, e.g. during placenta development. Other EVE proteins can act as (super-)antigens and can activate the immune system. In addition, reactivated EVE loci can induce or repress expression of adjacent genes. Finally, EVE are a major source for short and long non-coding RNA as well as double-stranded DNA with potential functions for gene regulation and innate immunity.
Increased EVE transcription has been observed in certain cancer types as well as autoimmune diseases. In some of these cases, release of EVE-derived virus particles from cells has been observed. Reactivation of EVE under such diverse conditions might indicate common pathways in cancer and autoimmunity.
This Research Topic is calling for submission of original research papers and review articles about all aspects of EVE reactivation in the context of cancer and autoimmune diseases.
Keywords: Endogenous Viral Elements (EVE), Endogenous Retroviruses (ERV), Cancer, Autoimmunity
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