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Current Opinion in Virology Aug 2018Viruses are ubiquitous parasites of cellular life forms and the most abundant biological entities on earth. The relationships between viruses and their hosts involve the... (Review)
Review
Viruses are ubiquitous parasites of cellular life forms and the most abundant biological entities on earth. The relationships between viruses and their hosts involve the continuous arms race but are by no account limited to it. Growing evidence shows that, in the course of evolution, viruses and their components are repeatedly recruited (exapted) for host functions. The functions of exapted viruses typically involve either defense from other viruses or cellular competitors or transfer of nucleic acids between cells, or storage functions. Virus exaptation can reach different depths, from recruitment of a fully functional virus to exploitation of defective, partially degraded viruses, to utilization of individual virus proteins.
Topics: Animals; DNA Viruses; Evolution, Molecular; Genome, Viral; Host Microbial Interactions; Host-Pathogen Interactions; Humans; Proviruses; Viral Proteins; Virophages; Viruses
PubMed: 30071360
DOI: 10.1016/j.coviro.2018.07.011 -
Current Issues in Molecular Biology 2020Polydnaviruses (PDVs) were originally viewed as large DNA viruses that are beneficial symbionts of parasitoid wasps. Two groups of PDVs were also recognized:... (Review)
Review
Polydnaviruses (PDVs) were originally viewed as large DNA viruses that are beneficial symbionts of parasitoid wasps. Two groups of PDVs were also recognized: bracoviruses (BVs), which are associated with wasps in the family Braconidae, and ichnoviruses (IVs), which are associated with wasps in the family Ichneumonidae. Results to date indicate that BVs are endogenous virus elements (EVEs) that evolved from an ancient betanudivirus. IVs are also likely EVEs but are unrelated to BVs. BVs and IVs are very unusual relative to most known EVEs because they retain many viral functions that benefit wasps in parasitizing hosts. However, BVs and IVs cannot be considered beneficial symbionts because all components of their genomes are fixed in wasps. Recent studies indicate that other nudiviruses have endogenized in insects. Each exhibits a different functional fate from BVs but shares certain architectural features. We discuss options for classifying BVs and other endogenized nudiviruses. We also discuss future directions.
Topics: Biological Evolution; DNA Viruses; Genes, Viral; Genome, Viral; Genomics; Phylogeny; Symbiosis; Virus Physiological Phenomena
PubMed: 31167960
DOI: 10.21775/cimb.034.163 -
Viruses Nov 2017It is increasingly clear that DNA viruses exploit cellular epigenetic processes to control their life cycles during infection. This review will address epigenetic... (Review)
Review
It is increasingly clear that DNA viruses exploit cellular epigenetic processes to control their life cycles during infection. This review will address epigenetic regulation in members of the polyomaviruses, adenoviruses, human papillomaviruses, hepatitis B, and herpes viruses. For each type of virus, what is known about the roles of DNA methylation, histone modifications, nucleosome positioning, and regulatory RNA in epigenetic regulation of the virus infection will be discussed. The mechanisms used by certain viruses to dysregulate the host cell through manipulation of epigenetic processes and the role of cellular cofactors such as BRD4 that are known to be involved in epigenetic regulation of host cell pathways will also be covered. Specifically, this review will focus on the role of epigenetic regulation in maintaining viral episomes through the generation of chromatin, temporally controlling transcription from viral genes during the course of an infection, regulating latency and the switch to a lytic infection, and global dysregulation of cellular function.
Topics: DNA Methylation; DNA Viruses; Epigenesis, Genetic; Gene Expression Regulation, Viral; Herpesvirus 4, Human; Histone Code; Host-Pathogen Interactions; Humans; Nucleosomes; Plasmids; Protein Processing, Post-Translational; Virus Latency; Virus Physiological Phenomena; Viruses
PubMed: 29149060
DOI: 10.3390/v9110346 -
Cell Host & Microbe May 2016Viral latency can be considered a metastable, nonproductive infection state that is capable of subsequent reactivation to repeat the infection cycle. Viral latent... (Review)
Review
Viral latency can be considered a metastable, nonproductive infection state that is capable of subsequent reactivation to repeat the infection cycle. Viral latent infections have numerous associated pathologies, including cancer, birth defects, neuropathy, cardiovascular disease, chronic inflammation, and immunological dysfunctions. The mechanisms controlling the establishment, maintenance, and reactivation from latency are complex and diversified among virus families, species, and strains. Yet, as examined in this review, common properties of latent viral infections can be defined. Eradicating latent virus has become an important but elusive challenge and will require a more complete understanding of the mechanisms controlling these processes.
Topics: Animals; DNA Viruses; Epigenesis, Genetic; Genes, Viral; Herpesvirus 1, Human; Humans; Virus Diseases; Virus Integration; Virus Latency; Virus Physiological Phenomena; Virus Replication
PubMed: 27173930
DOI: 10.1016/j.chom.2016.04.008 -
Virology Oct 2014The family Marseilleviridae encompasses giant viruses that replicate in free-living Acanthamoeba amoebae. Since the discovery of the founding member Marseillevirus in... (Review)
Review
The family Marseilleviridae encompasses giant viruses that replicate in free-living Acanthamoeba amoebae. Since the discovery of the founding member Marseillevirus in 2007, 7 new marseilleviruses have been observed, including 3 from environmental freshwater, one from a dipteran, and two from symptom-free humans. Marseilleviruses have ≈250-nm-large icosahedral capsids and 346-386-kb-long mosaic genomes that encode 444-497 predicted proteins. They share a small set of core genes with Mimivirus and other large and giant DNA viruses that compose a monophyletic group, first described in 2001. Comparative genomics analyses indicate that the family Marseilleviridae currently includes three lineages and a pan-genome composed of ≈600 genes. Antibodies against marseilleviruses and viral DNA have been observed in a significant proportion of asymptomatic individuals and in the blood and lymph nodes of a child with adenitis; these observations suggest that these giant viruses may be blood borne and question if they may be pathogenic in humans.
Topics: Acanthamoeba; Animals; DNA Viruses; DNA, Viral; Fresh Water; Genome, Viral; Genomics; Humans; Insecta; Phylogeny; Virus Replication
PubMed: 25104553
DOI: 10.1016/j.virol.2014.07.014 -
Journal of Medical Virology Jan 2023Cellular infections by DNA viruses trigger innate immune responses mediated by DNA sensors. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon gene (STING)...
Cellular infections by DNA viruses trigger innate immune responses mediated by DNA sensors. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon gene (STING) signaling pathway has been identified as a DNA-sensing pathway that activates interferons in response to viral infection and, thus, mediates host defense against viruses. Previous studies have identified oncogenes E7 and E1A of the DNA tumor viruses, human papillomavirus 18 (HPV18) and adenovirus, respectively, as inhibitors of the cGAS-STING pathway. However, the function of STING in infected cells and the mechanism by which HPV18 E7 antagonizes STING-induced Interferon beta production remain unknown. We report that HPV18 E7 selectively antagonizes STING-triggered nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation but not IRF3 activation. HPV18 E7 binds to STING in a region critical for NF-κB activation and blocks the nuclear accumulation of p65. Moreover, E7 inhibition of STING-triggered NF-κB activation is related to HPV pathogenicity but not E7-Rb binding. HPV18 E7, severe acute respiratory syndrome coronavirus-2 open reading frame 3a, human immunodeficiency virus-2 viral protein X, and Kaposi's sarcoma-associated herpesvirus KSHV viral interferon regulatory factor 1 selectively inhibited STING-triggered NF-κB or IRF3 activation, suggesting a convergent evolution among these viruses toward antagonizing host innate immunity. Collectively, selective suppression of the cGAS-STING pathway by viral proteins is likely to be a key pathogenic determinant, making it a promising target for treating oncogenic virus-induced tumor diseases.
Topics: Humans; NF-kappa B; Interferon-beta; Human papillomavirus 18; Nucleotidyltransferases; COVID-19; Immunity, Innate; DNA; DNA Viruses; Oncogene Proteins
PubMed: 36377393
DOI: 10.1002/jmv.28310 -
Frontiers in Immunology 2020IFI16, hnRNPA2B1, and nuclear cGAS are nuclear-located DNA sensors that play important roles in initiating host antiviral immunity and modulating tumorigenesis. IFI16... (Review)
Review
IFI16, hnRNPA2B1, and nuclear cGAS are nuclear-located DNA sensors that play important roles in initiating host antiviral immunity and modulating tumorigenesis. IFI16 triggers innate antiviral immunity, inflammasome, and suppresses tumorigenesis by recognizing double-stranded DNA (dsDNA), single-stranded DNA (ssDNA), damaged nuclear DNA, or cooperatively interacting with multiple tumor suppressors such as p53 and BRCA1. hnRNPA2B1 initiates interferon (IFN)-α/β production and enhances STING-dependent cytosolic antiviral signaling by directly binding viral dsDNA from invaded viruses and facilitating -methyladenosine (mA) modification of cGAS, IFI16, and STING mRNAs. Nuclear cGAS is recruited to double-stranded breaks (DSBs), suppresses DNA repair, and promotes tumorigenesis. This review briefly describes the nuclear functions of IFI16, hnRNPA2B1, and cGAS, and summarizes the transcriptional, post-transcriptional, and post-translational regulation of these nuclear DNA sensors.
Topics: Cell Transformation, Viral; DNA Virus Infections; DNA Viruses; DNA, Viral; Heterogeneous-Nuclear Ribonucleoprotein Group A-B; Humans; Interferon-alpha; Interferon-beta; Nuclear Proteins; Nucleotidyltransferases; Phosphoproteins; Tumor Suppressor Protein p53; Ubiquitin-Protein Ligases
PubMed: 33505405
DOI: 10.3389/fimmu.2020.624556 -
Annual Review of Virology Sep 2019Persistent viral infections require a host cell reservoir that maintains functional copies of the viral genome. To this end, several DNA viruses maintain their genomes... (Review)
Review
Persistent viral infections require a host cell reservoir that maintains functional copies of the viral genome. To this end, several DNA viruses maintain their genomes as extrachromosomal DNA minichromosomes in actively dividing cells. These viruses typically encode a viral protein that binds specifically to viral DNA genomes and tethers them to host mitotic chromosomes, thus enabling the viral genomes to hitchhike or piggyback into daughter cells. Viruses that use this tethering mechanism include papillomaviruses and the gammaherpesviruses Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus. This review describes the advantages and consequences of persistent extrachromosomal viral genome replication.
Topics: Chromosomes; DNA Replication; DNA Viruses; DNA, Viral; Genome, Viral; Herpesvirus 4, Human; Herpesvirus 8, Human; Host Microbial Interactions; Humans; Papillomaviridae; Virus Replication
PubMed: 31283444
DOI: 10.1146/annurev-virology-092818-015716 -
Nature Reviews. Microbiology Oct 2020Eukaryotic gene expression is regulated not only by genomic enhancers and promoters, but also by covalent modifications added to both chromatin and RNAs. Whereas... (Review)
Review
Eukaryotic gene expression is regulated not only by genomic enhancers and promoters, but also by covalent modifications added to both chromatin and RNAs. Whereas cellular gene expression may be either enhanced or inhibited by specific epigenetic modifications deposited on histones (in particular, histone H3), these epigenetic modifications can also repress viral gene expression, potentially functioning as a potent antiviral innate immune response in DNA virus-infected cells. However, viruses have evolved countermeasures that prevent the epigenetic silencing of their genes during lytic replication, and they can also take advantage of epigenetic silencing to establish latent infections. By contrast, the various covalent modifications added to RNAs, termed epitranscriptomic modifications, can positively regulate mRNA translation and/or stability, and both DNA and RNA viruses have evolved to utilize epitranscriptomic modifications as a means to maximize viral gene expression. As a consequence, both chromatin and RNA modifications could serve as novel targets for the development of antivirals. In this Review, we discuss how host epigenetic and epitranscriptomic processes regulate viral gene expression at the levels of chromatin and RNA function, respectively, and explore how viruses modify, avoid or utilize these processes in order to regulate viral gene expression.
Topics: Animals; Antiviral Agents; Chromatin; DNA Viruses; Epigenesis, Genetic; Eukaryotic Cells; Gene Expression Regulation, Viral; Histones; Host-Pathogen Interactions; Humans; Promoter Regions, Genetic; Protein Biosynthesis; RNA Processing, Post-Transcriptional; RNA Viruses; Transcriptome; Virus Latency; Virus Replication
PubMed: 32533130
DOI: 10.1038/s41579-020-0382-3 -
Microbiology and Molecular Biology... Jun 2018When a virus infects a host cell, it hijacks the biosynthetic capacity of the cell to produce virus progeny, a process that may take less than an hour or more than a... (Review)
Review
When a virus infects a host cell, it hijacks the biosynthetic capacity of the cell to produce virus progeny, a process that may take less than an hour or more than a week. The overall time required for a virus to reproduce depends collectively on the rates of multiple steps in the infection process, including initial binding of the virus particle to the surface of the cell, virus internalization and release of the viral genome within the cell, decoding of the genome to make viral proteins, replication of the genome, assembly of progeny virus particles, and release of these particles into the extracellular environment. For a large number of virus types, much has been learned about the molecular mechanisms and rates of the various steps. However, in only relatively few cases during the last 50 years has an attempt been made-using mathematical modeling-to account for how the different steps contribute to the overall timing and productivity of the infection cycle in a cell. Here we review the initial case studies, which include studies of the one-step growth behavior of viruses that infect bacteria (Qβ, T7, and M13), human immunodeficiency virus, influenza A virus, poliovirus, vesicular stomatitis virus, baculovirus, hepatitis B and C viruses, and herpes simplex virus. Further, we consider how such models enable one to explore how cellular resources are utilized and how antiviral strategies might be designed to resist escape. Finally, we highlight challenges and opportunities at the frontiers of cell-level modeling of virus infections.
Topics: Animals; DNA Viruses; Genome, Viral; Host-Pathogen Interactions; Humans; Kinetics; Models, Theoretical; RNA Viruses; Viral Proteins; Virus Diseases; Virus Replication
PubMed: 29592895
DOI: 10.1128/MMBR.00066-17