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      Cytopathic effects: virus-modulated manifestations of innate immunity?

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      Author(s): 1 , 2
      Publication date (Electronic):
      Journal: Trends in Microbiology
      Publisher: Elsevier Ltd.
      Keywords: virus-induced apoptosis, virus-induced necrosis, picornaviruses

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          Abstract

          The capacity to injure infected cells is a widespread property of viruses. Usually, this cytopathic effect (CPE) is ascribed to viral hijacking of cellular resources to fulfill viral needs. However, evidence is accumulating that CPE is not necessarily directly coupled to viral reproduction but may largely be due to host defensive and viral antidefensive activities. A major part in this virus–cell interaction appears to be played by a putative host-encoded program with multiple competing branches, leading to necrotic, apoptotic, and, possibly, other types of cell suicide. Manifestations of this program are controlled and modulated by host, viral, and environmental factors.

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          CASPASE 8 inhibits programmed necrosis by processing CYLD

          Marie O'Donnell, Eva Pérez-Jiménez, Andrew Oberst … (2011)
          CASPASE 8 initiates apoptosis downstream of TNF death receptors by undergoing autocleavage and processing the executioner CASPASE 3 1 . However, the dominant function of CASPASE 8 is to transmit a pro-survival signal that suppresses programmed necrosis (or necroptosis) mediated by RIPK1 and RIPK3 2–6 during embryogenesis and hematopoiesis 7–9 . Suppression of necrotic cell death by CASPASE 8 requires its catalytic activity but not the autocleavage essential for apoptosis 10 , however, the key substrate processed by CASPASE 8 to block necrosis has been elusive. A key substrate must meet three criteria: (1) it must be essential for programmed necrosis; (2) it must be cleaved by CASPASE 8 in situations where CASPASE 8 is blocking necrosis; and (3) mutation of the CASPASE 8 processing site on the substrate should convert a pro-survival response to necrotic death without the need for CASPASE 8 inhibition. We now identify CYLD as a novel substrate for CASPASE 8 that satisfies these criteria. Upon TNF stimulation, CASPASE 8 cleaves CYLD to generate a survival signal. In contrast, loss of CASPASE 8 prevented CYLD degradation resulting in necrotic death. A CYLD substitution mutation at D215 that cannot be cleaved by CASPASE 8 switches cell survival to necrotic cell death in response to TNF.
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            Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways.

            Gary W. Kaiser, Jason Upton, Edward Mocarski (2012)
            Pathogens specifically target both the caspase 8-dependent apoptotic cell death pathway and the necrotic cell death pathway that is dependent on receptor-interacting protein 1 (RIP1; also known as RIPK1) and RIP3 (also known as RIPK3). The fundamental co-regulation of these two cell death pathways emerged when the midgestational death of mice deficient in FAS-associated death domain protein (FADD) or caspase 8 was reversed by elimination of RIP1 or RIP3, indicating a far more entwined relationship than previously appreciated. Thus, mammals require caspase 8 activity during embryogenesis to suppress the kinases RIP1 and RIP3 as part of the dialogue between two distinct cell death processes that together fulfil reinforcing roles in the host defence against intracellular pathogens such as herpesviruses.
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              Myxomatosis in Australia and Europe: a model for emerging infectious diseases.

              Peter J Kerr (2012)
              Myxoma virus is a poxvirus naturally found in two American leporid (rabbit) species (Sylvilagus brasiliensis and Sylvilagus bachmani) in which it causes an innocuous localised cutaneous fibroma. However, in European rabbits (Oryctolagus cuniculus) the same virus causes the lethal disseminated disease myxomatosis. The introduction of myxoma virus into the European rabbit population in Australia in 1950 initiated the best known example of what happens when a novel pathogen jumps into a completely naïve new mammalian host species. The short generation time of the rabbit and their vast numbers in Australia meant evolution could be studied in real time. The carefully documented emergence of attenuated strains of virus that were more effectively transmitted by the mosquito vector and the subsequent selection of rabbits with genetic resistance to myxomatosis is the paradigm for pathogen virulence and host-pathogen coevolution. This natural experiment was repeated with the release of a separate strain of myxoma virus in France in 1952. The subsequent spread of the virus throughout Europe and its coevolution with the rabbit essentially paralleled what occurred in Australia. Detailed molecular studies on myxoma virus have dissected the role of virulence genes in the pathogenesis of myxomatosis and when combined with genomic data and reverse genetics should in future enable the understanding of the molecular evolution of the virus as it adapted to its new host. This review describes the natural history and evolution of myxoma virus together with the molecular biology and experimental pathogenesis studies that are informing our understanding of evolution of emerging diseases. Crown Copyright © 2012. Published by Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                Vadim I. Agol
                Journal
                Journal ID (nlm-ta): Trends Microbiol
                Journal ID (iso-abbrev): Trends Microbiol
                Title: Trends in Microbiology
                Publisher: Elsevier Ltd.
                ISSN (Print): 0966-842X
                ISSN (Electronic): 1878-4380
                Publication date PMC-release: 13 October 2012
                Publication date (Print): December 2012
                Publication date (Electronic): 13 October 2012
                Volume: 20
                Issue: 12
                Pages: 570-576
                Affiliations
                [1 ]M.P. Chumakov Institute of Poliomyelitis and Viral Encephalitides, Russian Academy of Medical Sciences, Moscow 142782, Russia
                [2 ]A.N. Belozersky Institute of Physico-Chemical Biology, M.V. Lomonosov Moscow State University, Moscow 119991, Russia
                Article
                Publisher ID: S0966-842X(12)00173-4
                DOI: 10.1016/j.tim.2012.09.003
                PMC ID: 7126625
                PubMed ID: 23072900
                SO-VID: 9902e3ff-688d-4de7-8c83-15d21f9c47a4
                Copyright statement: Copyright © 2012 Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: virus-induced apoptosis,virus-induced necrosis,picornaviruses
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: virus-induced apoptosis, virus-induced necrosis, picornaviruses

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