Evolutionary biology of human hepatitis viruses.
Ontology highlight
ABSTRACT:
SUBMITTER: Rasche A
PROVIDER: S-EPMC7114834 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The enterically transmitted hepatitis A (HAV) and hepatitis E viruses (HEV) are the leading causes of acute viral hepatitis in humans. Despite the discovery of HAV and HEV 40-50 years ago, their evolutionary origins remain unclear. Recent discoveries of numerous nonprimate hepatoviruses and hepeviruses allow revisiting the evolutionary history of these viruses. In this review, we provide detailed phylogenomic analyses of primate and nonprimate hepatoviruses and hepeviruses. We identify conserved and divergent genomic properties and corroborate historical interspecies transmissions by phylogenetic comparisons and recombination analyses. We discuss the likely non-recent origins of human HAV and HEV precursors carried by mammals other than primates, and detail current zoonotic HEV infections. The novel nonprimate hepatoviruses and hepeviruses offer exciting new possibilities for future research focusing on host range and the unique biological properties of HAV and HEV.
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Project description:We provide the first analysis and synthesis of the evolutionary and mechanistic bases for risk of endometriosis in humans, structured around Niko Tinbergen's four questions about phenotypes: phylogenetic history, development, mechanism and adaptive significance. Endometriosis, which is characterized by the proliferation of endometrial tissue outside of the uterus, has its phylogenetic roots in the evolution of three causally linked traits: (1) highly invasive placentation, (2) spontaneous rather than implantation-driven endometrial decidualization and (3) frequent extensive estrogen-driven endometrial proliferation and inflammation, followed by heavy menstrual bleeding. Endometriosis is potentiated by these traits and appears to be driven, proximately, by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic-pituitary-ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that in extreme cases can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known from previous work to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis. The hypothesis that endometriosis risk is driven by low prenatal testosterone, and involves extreme expression of some reproductive phenotypes, is supported by a suite of evidence from genetics, development, endocrinology, morphology and life history. The hypothesis also provides insights into why these two diametric, fitness-reducing disorders are maintained at such high frequencies in human populations. Finally, the hypotheses described and evaluated here lead to numerous testable predictions and have direct implications for the treatment and study of endometriosis. Lay summary: Endometriosis is caused by endometrial tissue outside of the uterus. We explain why and how humans are vulnerable to this disease, and new perspectives on understanding and treating it. Endometriosis shows evidence of being caused in part by relatively low testosterone during fetal development, that 'programs' female reproductive development. By contrast, polycystic ovary syndrome is associated with relatively high testosterone in prenatal development. These two disorders can thus be seen as 'opposite' to one another in their major causes and correlates. Important new insights regarding diagnosis, study and treatment of endometriosis follow from these considerations.
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Project description:With genome sequence and composition highly analogous to human, rhesus macaque represents a unique reference for evolutionary studies of human biology. Here, we developed a comprehensive genomic framework of rhesus macaque, the RhesusBase2, for evolutionary interrogation of human genes and the associated regulations. A total of 1,667 next-generation sequencing (NGS) data sets were processed, integrated, and evaluated, generating 51.2 million new functional annotation records. With extensive NGS annotations, RhesusBase2 refined the fine-scale structures in 30% of the macaque Ensembl transcripts, reporting an accurate, up-to-date set of macaque gene models. On the basis of these annotations and accurate macaque gene models, we further developed an NGS-oriented Molecular Evolution Gateway to access and visualize macaque annotations in reference to human orthologous genes and associated regulations (www.rhesusbase.org/molEvo). We highlighted the application of this well-annotated genomic framework in generating hypothetical link of human-biased regulations to human-specific traits, by using mechanistic characterization of the DIEXF gene as an example that provides novel clues to the understanding of digestive system reduction in human evolution. On a global scale, we also identified a catalog of 9,295 human-biased regulatory events, which may represent novel elements that have a substantial impact on shaping human transcriptome and possibly underpin recent human phenotypic evolution. Taken together, we provide an NGS data-driven, information-rich framework that will broadly benefit genomics research in general and serves as an important resource for in-depth evolutionary studies of human biology.
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Project description:BackgroundHepatitis D Virus (HDV) is classified into eight genotypes with distinct clinical outcomes. Despite the maintenance of highly conserved functional motifs, it is unknown whether sequence divergence between genotypes, such as HDV-1 and HDV-3, or viral interference mechanisms may affect co-infection in the same host and cell, thus hindering the development of HDV inter-genotypic recombinants. We aimed to investigate virological differences of HDV-1 and HDV-3 and assessed their capacity to infect and replicate within the same liver and human hepatocyte in vivo.MethodsHuman liver chimeric mice were infected with hepatitis B virus (HBV) and with one of the two HDV genotypes or with HDV-1 and HDV-3 simultaneously. In a second set of experiments, HBV-infected mice were first infected with HDV-1 and after 9 weeks with HDV-3, or vice versa. Also two distinct HDV-1 strains were used to infect mice simultaneously and sequentially. Virological parameters were determined by strain-specific qRT-PCR, RNA in situ hybridization and immunofluorescence staining.ResultsHBV/HDV co-infection studies indicated faster spreading kinetics and higher intrahepatic levels of HDV-3 compared to HDV-1. In mice that simultaneously received both HDV strains, HDV-3 became the dominant genotype. Interestingly, antigenomic HDV-1 and HDV-3 RNA were detected within the same liver but hardly within the same cell. Surprisingly, sequential super-infection experiments revealed a clear dominance of the HDV strain that was inoculated first, indicating that HDV-infected cells may acquire resistance to super-infection.ConclusionInfection with two largely divergent HDV genotypes could be established in the same liver, but rarely within the same hepatocyte. Sequential super-infection with distinct HDV genotypes and even with two HDV-1 isolates was strongly impaired, suggesting that virus interference mechanisms hamper productive replication in the same cell and hence recombination events even in a system lacking adaptive immune responses.
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