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      Membranous Replication Factories Induced by Plus-Strand RNA Viruses

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          Abstract

          In this review, we summarize the current knowledge about the membranous replication factories of members of plus-strand (+) RNA viruses. We discuss primarily the architecture of these complex membrane rearrangements, because this topic emerged in the last few years as electron tomography has become more widely available. A general denominator is that two “morphotypes” of membrane alterations can be found that are exemplified by flaviviruses and hepaciviruses: membrane invaginations towards the lumen of the endoplasmatic reticulum (ER) and double membrane vesicles, representing extrusions also originating from the ER, respectively. We hypothesize that either morphotype might reflect common pathways and principles that are used by these viruses to form their membranous replication compartments.

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          Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures.

          Richard E. Randall, Stephen Goodbourn (2008)
          The interferon (IFN) system is an extremely powerful antiviral response that is capable of controlling most, if not all, virus infections in the absence of adaptive immunity. However, viruses can still replicate and cause disease in vivo, because they have some strategy for at least partially circumventing the IFN response. We reviewed this topic in 2000 [Goodbourn, S., Didcock, L. & Randall, R. E. (2000). J Gen Virol 81, 2341-2364] but, since then, a great deal has been discovered about the molecular mechanisms of the IFN response and how different viruses circumvent it. This information is of fundamental interest, but may also have practical application in the design and manufacture of attenuated virus vaccines and the development of novel antiviral drugs. In the first part of this review, we describe how viruses activate the IFN system, how IFNs induce transcription of their target genes and the mechanism of action of IFN-induced proteins with antiviral action. In the second part, we describe how viruses circumvent the IFN response. Here, we reflect upon possible consequences for both the virus and host of the different strategies that viruses have evolved and discuss whether certain viruses have exploited the IFN response to modulate their life cycle (e.g. to establish and maintain persistent/latent infections), whether perturbation of the IFN response by persistent infections can lead to chronic disease, and the importance of the IFN system as a species barrier to virus infections. Lastly, we briefly describe applied aspects that arise from an increase in our knowledge in this area, including vaccine design and manufacture, the development of novel antiviral drugs and the use of IFN-sensitive oncolytic viruses in the treatment of cancer.
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            Composition and Three-Dimensional Architecture of the Dengue Virus Replication and Assembly Sites

            Sonja Welsch, Sven Miller, Inés Romero-Brey … (2009)
            Summary Positive-strand RNA viruses are known to rearrange cellular membranes to facilitate viral genome replication. The biogenesis and three-dimensional organization of these membranes and the link between replication and virus assembly sites is not fully clear. Using electron microscopy, we find Dengue virus (DENV)-induced vesicles, convoluted membranes, and virus particles to be endoplasmic reticulum (ER)-derived, and we detect double-stranded RNA, a presumed marker of RNA replication, inside virus-induced vesicles. Electron tomography (ET) shows DENV-induced membrane structures to be part of one ER-derived network. Furthermore, ET reveals vesicle pores that could enable release of newly synthesized viral RNA and reveals budding of DENV particles on ER membranes directly apposed to vesicle pores. Thus, DENV modifies ER membrane structure to promote replication and efficient encapsidation of the genome into progeny virus. This architecture of DENV replication and assembly sites could explain the coordination of distinct steps of the flavivirus replication cycle.
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              Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome.

              Serena G L Choo, Celine Choo, Beverly Bradley … (1989)
              A random-primed complementary DNA library was constructed from plasma containing the uncharacterized non-A, non-B hepatitis (NANBH) agent and screened with serum from a patient diagnosed with NANBH. A complementary DNA clone was isolated that was shown to encode an antigen associated specifically with NANBH infections. This clone is not derived from host DNA but from an RNA molecule present in NANBH infections that consists of at least 10,000 nucleotides and that is positive-stranded with respect to the encoded NANBH antigen. These data indicate that this clone is derived from the genome of the NANBH agent and are consistent with the agent being similar to the togaviridae or flaviviridae. This molecular approach should be of great value in the isolation and characterization of other unidentified infectious agents.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Journal ID (iso-abbrev): Viruses
                Journal ID (publisher-id): viruses
                Title: Viruses
                Publisher: MDPI
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 22 July 2014
                Publication date Collection: July 2014
                Volume: 6
                Issue: 7
                Pages: 2826-2857
                Affiliations
                Department of Infectious Diseases, Molecular Virology, Heidelberg University, Im Neuenheimer Feld 345, 69120 Heidelberg, Germany
                Author notes
                [* ]Authors to whom correspondence should be addressed; E-Mails: ines_romero-brey@ 123456med.uni-heidelberg.de (I.R.-B.); ralf_bartenschlager@ 123456med.uni-heidelberg.de (R.B.); Tel.: +49-0-6221-566306 (I.R.-B.); +49-0-6221-564225 (R.B.); Fax: +49-0-6221-564570 (I.R.-B. & R.B.).
                Article
                Publisher ID: viruses-06-02826
                DOI: 10.3390/v6072826
                PMC ID: 4113795
                PubMed ID: 25054883
                SO-VID: b8d6b2d9-f078-465e-b14e-96ed27e48795
                Copyright © © 2014 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 29 April 2014
                Date revision received : 02 June 2014
                Date accepted : 24 June 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: membrane rearrangements,electron microscopy,electron tomography,ultrastructure,double-membrane vesicles,membranous replication factories,hepatitis c virus,flaviviruses,picornaviruses,coronaviruses
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: membrane rearrangements, electron microscopy, electron tomography, ultrastructure, double-membrane vesicles, membranous replication factories, hepatitis c virus, flaviviruses, picornaviruses, coronaviruses

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