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Retrovirus infections. --- Retroviral infections --- Virus diseases
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HIV Infections. --- Retrovirus infections. --- Nervous system --- Diseases --- Diseases.
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Medicine --- Immunology --- virus --- evolution --- human immunity --- endogenous retrovirus
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ARTHRITIS INFECTIOUS --- RHEUMATIC DISEASES --- OSTEITIS --- LYME DISEASE --- RETROVIRUS INFECTIONS
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Retroviridae Infections. --- Infections, Retroviridae --- Infections, Retrovirus --- Retrovirus Infections --- Infection, Retroviridae --- Infection, Retrovirus --- Retroviridae Infection --- Retrovirus Infection --- XMRV Infection --- Xenotropic MuLV-related Virus Infection --- Xenotropic Murine Leukemia Virus-related Virus Infection --- Infection, XMRV --- Infections, XMRV --- XMRV Infections --- Xenotropic MuLV related Virus Infection --- Xenotropic Murine Leukemia Virus related Virus Infection --- Retroviridae Infections --- Retrovirus --- Maladies a virus --- Evolution
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Enzymology --- Enzymes protéolytiques --- Peptide hydrolases --- Peptidohydrolases --- Proteases --- Proteolytic enzymes --- Proteolytiques [Enzymes ] --- Proteolytische enzymen --- Enzymes proteolytiques. --- Retrovirus --- Virus de l'immunodeficience humaine --- Enzymes proteolytiques --- Enzymes. --- Enzymes --- Retroviruses --- Retrovirus - Enzymes. --- Retrovirus - Enzymes --- Proteinases --- Virus, bacterial
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Retrotransposons are present in essentially all eukaryotic genomes and come in two basic flavors: those that are bracketed by long terminal repeats (LTRs) and share a common ancestor with retroviruses, and non-LTR retrotransposons that have a distinct lineage and remain transpositionally active in humans. Both types of retrotransposons replicate through an RNA intermediate, stably integrate into the host genome and have accumulated to a very high copy number in mammals and certain plant species. Autonomous elements produce transcripts capable of undergoing reverse transcription, and minimally encode proteins with reverse transcriptase, integrase/endonucleolytic, and nucleic acid chaperone activities. Retrotransposons are currently distinguished from viruses, since the process of retrotransposition is not infectious. However, this boundary may prove to be provisional as we learn more about these mobile genetic elements. The goal of this Special Issue of Viruses is to highlight progress in understanding the mechanism and consequences of retrotransposon movement. Several active research areas may be covered in reviews and research articles, including the roles of cellular modulators and defense systems, retrotransposon expression and replication, retrotransposon-induced mutations and their association with human diseases, and how these widely disseminated elements mold eukaryotic genomes.
Non-LTR retrotransposon --- Integration --- Human disease --- Endogenous retrovirus --- Reverse transcription --- Host factors --- Genome evolution --- LTR retrotransposon
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Human retroviruses, HIV and HTLV have been recognized as important pathogens because of their association with lethal diseases such as AIDS and ATL. Considerable resources and efforts have been directed at understanding the interaction between these retroviruses and their host which may provide clues as to how the infection can be controlled or prevented. Among the key scientific successes is the identification of intracellular “restriction factors” that have evolved as obstacles to the replication of pathogens including infectious retroviruses. The discovery of APOBEC, which are strong mutagens of retroviral genomes and intracellular retroelements, began a new era of intense research activities into the spectrum of intrinsic anti-HIV activity, leading to the identification of TRIM5a, BST2/Tetherin, and SAMHD1. In response, HIV has evolved several accessory genes as weaponries to evade these intracellular restriction activities. The intracellular antiretroviral defenses evolved in response to endogenous retroelements that make up more than 40% of the entire mammalian genome, and which are regarded as ancestors of infectious retroviruses. LTR-type retroelements are present in all higher eukaryotes, representing about 8% of the human genome. Non-LTR retroelements can be found at extremely high copy numbers also, with a significant portion of mammalin genomes consisting of LINEs. Mammalian genomes are modified by LINEs through insertions, but also by the indirect replication of non-autonomous retrotransposons such as SINEs. LINEs insertion was shown to have played, and continue to play important roles in genomic evolution and somatic genome mosaicism-mediated physiology. And, because retrotransposition can confer genetic diversity that is beneficial to the host, the vertebrate intrinsic immunity has evolved to support a balance between retroelement insertions that confer beneficial and those that cause deleterious gene disruptions. The articles published in this Research Topic should serve not only as valuable references for the field, but provide future topics of research for investigators that should further our understanding of the retrovirus, retroelements and their restrictions.
Retroviruses. --- HTLV (Viruses) --- HIV (Viruses) --- Retrovirus --- BST2/Tetherin --- HIV --- line --- HTLV --- APOBEC --- restriction factor --- Retroelement --- SAMHD1
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Les rétrovirus font partie d’une famille virale particulière qui intègre leurs informations virales au génome de la cellule hôte sous la forme d’un provirus. Parmi eux, on peut retrouver le virus de la leucose féline, qui provoque une pathologie polysystémique chez le chat. Le virus de la leucose féline, ou FeLV, présente différents sous-types influençant les récepteurs et la pathogénie : le(s) FeLV de type A, B, C, D et T. La leucose féline constitue un cas particulier en médecine vétérinaire, concernant ces rétrovirus endogènes, avec la présence simultanée du virus sous sa forme exogène, responsable des présentations cliniques, mais également sous sa forme endogène, présent chez tous les individus de l’espèce. On retrouve également d’autres rétrovirus endogènes chez le chat dont Mac-1, RD-114 et la famille des ERV-DCs. L’impact des rétrovirus endogènes sur leur hôte a pendant longtemps été négligé, mais de nombreuses études commencent à mettre en évidence leurs multiples rôles, tant évolutifs que sur l’immunité, ainsi que leur impact sur de nouvelles infections virales. Les rétrovirus endogènes du chat ne font pas exception à la règle, avec de nombreuses interactions entre ceux-ci et le virus de la leucose féline. Ils sont à l’origine de l’apparition de deux virus chimériques : le FeLV-D avec les ERV-DCs et le FELV-B avec l’enFeLV. Leurs gènes produisent également deux facteurs anti-viraux : FeLIX pour les segments d’enFeLV et Refrex-1 pour les ERV-DCs. De plus, certaines interactions, bien que démontrées, ne sont pas encore tout à fait comprises, telles que la mise en évidence d’une corrélation inversée entre le nombre de copies d’enFeLV et la tendance à développer une infection progressive lors d’une infection par le FeLV-A. Ces découvertes permettent non seulement une meilleure compréhension globale des différents acteurs interagissant lors de l’infection par le virus de la leucose féline, mais ouvrent également la porte à de nouvelles pistes dans la lutte et la prévention de cette maladie. Retroviruses are a special viral family. During their cycle, they integrate their genome in the host cell as a provirus. Feline Leukemia Virus (FeLV) is part of the retroviruses family and is responsible for a polysystemic disease in cats. Different types of FeLV are described: A, B, C, D and T. They influence the receptor interaction and the outcome of the disease. Feline leukemia is a remarkably interesting disease in veterinary medicine because the virus causing it can the found as an exogenous virus but can also be found in all cats as an endogenous retrovirus (enFeLV). Other endogenous retroviruses are described in the cat species such as Mac-1, RD-114 and the ERV-DCs. During a long time, the impact of endogenous retroviruses on their host has been considered as minor or non-existing. Nowadays, more and more studies highlight their considerable impact on the evolution of mammals but also on their host immunity, including the response against new viral infections. And the recent studies on cat’s endogenous retroviruses are part of them with many interactions between endogenous retroviruses and the infection by the feline leukemia virus. Two variants of FeLV arise from recombination with endogenous segments: FeLV-D from ERV-DCs segments and FeLV-B from enFeLV. Endogenous genes are also responsible for two anti-viral factors: FeLIX from enFeLV segments and Refrex-1 from ERV-DC genes. And more interactions are suspected with recent studies showing an inverted correlation between the number of enFeLV copies and the tendency of an infection by the FeLV-A to become progressive. These recent discoveries are an essential step for a better understanding of the different actors and factors impacting the outcome of an infection by the feline leukemia virus. Moreover, they open up new research fields concerning anti-viral treatments and vaccines.
ERV --- Endogenous retrovirus --- FeLV --- Feline Leukimia Virus --- Sciences du vivant > Médecine vétérinaire & santé animale
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