Viruses constitute mobile genetic elements that require host cell machinery for their replication and spread. In addition, they can take up residence in the host as persistent non-replicating elements or become integrated into the host chromosomes where their genomes are duplicated during cellular ...
Viruses constitute mobile genetic elements that require host cell machinery for their replication and spread. In addition, they can take up residence in the host as persistent non-replicating elements or become integrated into the host chromosomes where their genomes are duplicated during cellular replication. There are clear examples of viruses that cause disease through their direct destruction of cells during the virus replication process or indirectly through activation of the host immune response. However, the most successful viruses appear to have evolved to co-exist with their hosts, and may even provide some level of benefit. They have accomplished this coexistence by multiple means, such as germline integration, infection of hosts prior to immune development, suppression of innate and acquired immune responses, and taking up residence in immune privileged tissue. Transposons, by extension, are mobile genetic elements within eukaryotic genomes, with many parallels to viruses in regards to their structure, duplication and reintegration mechanisms, however, the functional consequences of their retrotransposition are only now emerging. In this call for papers, we are interested in exploring the idea that mobile genetic elements, acting directly within cells of the central nervous system (CNS), serve as modifying agents that affect neurodevelopment and modulate neurophysiology. A strong case is emerging for the role of endogenous retroviral elements as playing a causative role in several neurodegenerative diseases, consistent with more than 50 years of work on related exogenous retroviruses. However, given that mammalian genomes include a large percentage of endogenous viral and retrotransposon elements, it suggests that they also serve to benefit the host, and specifically the nervous system.
Exogenous and endogenous retroviruses provide a good starting point to explore this idea, especially given their implication in motor and cognitive diseases, but appreciate that mobile genetic element-neural cell interactions that alter CNS physiology and development likely extend well beyond retroviruses. Thus we encourage contributions that broadly represent the mammalian “virome”, including long and short interspersed retrotransposons (LINEs and SINEs) as genetic elements modifying CNS development and function. Most studies on virus-CNS interactions to date have concentrated on innate and adaptive immune responses to infection, with many fewer studies dedicated to dissecting the primary virus-neural interactions as critical drivers of neurophysiological change. Therefore, in this call for paper we are primarily interested in studies examining direct viral/transposon-neural cell interactions that modify neural development and/or neural function, rather than examining neurophysiological responses to neuroinflammation. The focus on these interactions will likely prove especially important for understanding whether and how neuro-infectious agents and mobile genetic elements affect
a) CNS function and
b) initiate diseases of unknown origin such as Alzheimer's disease, sporadic amyotrophic lateral sclerosis, multiple sclerosis, and schizophrenia.
This Research Topic will be open to Original Research, Commentaries, Reviews, and Theoretical papers.
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