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      Coronavirus MHV-3-Induced Apoptosis in Macrophages

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          Abstract

          Infection with mouse hepatitis virus strain 3 (MHV-3) results in lethal fulminant hepatic necrosis in fully susceptible BALB/c mice compared to the minimal disease observed in resistant strain A/J mice. Macrophages play a central role in the pathogenesis of MHV-3-induced hepatitis. In the present study we have shown that MHV-3 infection of macrophages induces these cells to undergo apoptosis. Three methods to detect apoptosis were applied: flow cytometry analysis of nuclear DNA content, fluorescence microscopic visualization of apoptotic cells labeled by the TUNEL assay, and gel electrophoresis to detect DNA laddering. Apoptosis in A/J and BALB/c macrophages was first detected at 8 h postinfection (p.i.) and reached a maximum by 12 h p.i. The degree of MHV-3-induced apoptosis was much greater in A/J-derived macrophages than in BALB/c-derived cells. Apoptosis was inversely correlated with the development of typical MHV cytopathology, namely syncytia formation. Infected macrophages from A/J mice did not form synctia in contrast to the extensive synctia formation observed in BALB/c-derived macrophages. In MHV-3-infected BALB/c macrophage cultures, apoptotic cells were not incorporated into syncytia. Apoptosis was also inversely correlated with the expression of MHV-3-induced fgl2 prothrombinase in macrophages. These results add the murine coronavirus MHV-3 to the list of RNA-containing viruses capable of inducing apoptosis.

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          Most cited references55

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          Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation

          Programmed cell death (PCD) plays a key role in developmental biology and in maintenance of the steady state in continuously renewing tissues. Currently, its existence is inferred mainly from gel electrophoresis of a pooled DNA extract as PCD was shown to be associated with DNA fragmentation. Based on this observation, we describe here the development of a method for the in situ visualization of PCD at the single-cell level, while preserving tissue architecture. Conventional histological sections, pretreated with protease, were nick end labeled with biotinylated poly dU, introduced by terminal deoxy- transferase, and then stained using avidin-conjugated peroxidase. The reaction is specific, only nuclei located at positions where PCD is expected are stained. The initial screening includes: small and large intestine, epidermis, lymphoid tissues, ovary, and other organs. A detailed analysis revealed that the process is initiated at the nuclear periphery, it is relatively short (1-3 h from initiation to cell elimination) and that PCD appears in tissues in clusters. The extent of tissue-PCD revealed by this method is considerably greater than apoptosis detected by nuclear morphology, and thus opens the way for a variety of studies.
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            Cell death: the significance of apoptosis.

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              When two strands are better than one: the mediators and modulators of the cellular responses to double-stranded RNA.

              Double-stranded RNA is a potent inducer of interferon, a modulator of the expression of a number of other genes involved in the response of cells to virus infection, an activator of the interferon-induced antiviral state, and may be involved in differentiation, induction of apoptosis, and control of oncogenic transformation. This review will attempt to summarize what is known about the cellular proteins that act to mediate the response of cells to double-stranded RNA and the viral and cellular macromolecules that may be able to modulate these responses.
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                Author and article information

                Journal
                Virology
                Virology
                Virology
                Academic Press.
                0042-6822
                1096-0341
                25 May 2002
                10 October 1998
                25 May 2002
                : 250
                : 1
                : 41-49
                Affiliations
                [a ]Department of Pathology and Laboratory Medicine, Texas A&M University College of Medicine, 208 Reynolds Building, College Station, Texas, 77843–1114
                [b ]Multi Organ Transplant Program, The Toronto Hospital, University of Toronto, 621 University Ave. NU-10–151, Toronto, Ontario, Canada, M5G 2C4
                Author notes
                [1]

                Present address: Department of Entomology, Texas A&M University, College Station, TX 77843-2475.

                [2]

                To whom correspondence and reprint requests should be addressed at Department of Pathology and Laboratory Medicine, Texas A&M University College of Medicine, 208 Reynolds Medical Building, College Station, TX 77843-1114. Fax: (409) 862-1299. E-mail:jleibowitz@tamu.edu.

                Article
                S0042-6822(98)99356-4
                10.1006/viro.1998.9356
                7131070
                9770418
                632b8db8-c4d2-4de6-8ae4-315e8b553be8
                Copyright © 1998 Academic Press. All rights reserved.

                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.

                History
                : 20 February 1998
                : 13 March 1998
                : 5 August 1998
                Categories
                Article

                Microbiology & Virology
                Microbiology & Virology

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