Apoptosis: a mechanism of cell killing by influenza A and B viruses

Hinshaw, Virginia S.; Olsen, Christopher W.; Dybdahl‐Sissoko, Naomi; Evans, David T.

doi:10.1128/jvi.68.6.3667-3673.1994

Cited by 398 publications

(181 citation statements)

References 32 publications

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“…Other possible explanations for the different outcomes of MHV-3 infection of BALB/c and A/J macrophages might be variations in the levels of bcl-2, TNF-␣ or other cytokines important in decreasing programmed cell death in infected cells. In this regard, it was recently shown that overexpression of bcl-2 can block or delay apoptosis induced by Sindbis virus (Levine et al, 1996), La Crosse virus (Pekosz et al, 1996), adenovirus (Chiou et al, 1994), and influenza virus (Hinshaw et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Coronavirus MHV-3-Induced Apoptosis in Macrophages

et al. 1998

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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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Section: Discussionmentioning

confidence: 99%

Coronavirus MHV-3-Induced Apoptosis in Macrophages

et al. 1998

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“…Apoptosis is closely related to a number of aspects of influenza A virus (IAV) infection. For instance, apoptosis plays a pivotal role in IAV elimination through the removal of the virus infected cells, and tissue damage during the course of IAV infection including multiple organ dysfunction is caused by apoptosis [1,2]. Further, abnormal induction of lymphocyte apoptosis is related in the disease symptoms of influenza, and apoptosis is also important to terminate inflammation through the induction of activation-induced cell death (AICD).…”

Section: Introductionmentioning

confidence: 99%

Relevance of signaling molecules for apoptosis induction on influenza A virus replication

Iwai

Shiozaki

Miyazaki

2013

Biochemical and Biophysical Research Communications

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Apoptosis is an important mechanism to maintain homeostasis in mammals, and disruption of the apoptosis regulation mechanism triggers a range of diseases, such as cancer, autoimmune diseases, and developmental disorders. The severity of influenza A virus (IAV) infection is also closely related to dysfunction of apoptosis regulation. In the virus infected cells, the functions of various host cellular molecules involved in regulation of induction of apoptosis are modulated by IAV proteins to enable effective virus replication. The modulation of the intracellular signaling pathway inducing apoptosis by the IAV infection also affects extracellular mechanisms controling apoptosis, and triggers abnormal host responses related to the disease severity of IAV infections. This review focuses on apoptosis related molecules involved in IAV replication and pathogenicity, the strategy of the virus propagation through the regulation of apoptosis is also discussed.

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“…Infection by influenza A subtypes can occur through direct contact with an infected animal, exposure to contaminated environment, or ingestion of inadequately prepared food stuffs (7). Upon failure of host immunologic defenses (immunoglobulin A secretory antibody and mechanical respiratory mucociliary clearance), influenza viruses invade columnar respiratory epithelium, triggering a molecular cascade responsible for the inactivation of host-cell protein synthesis (9,13,14). Local destruction of respiratory epithelium, resulting in the release of pro-inflammatory cytokines, in addition to viral invasion of polymorphonuclear leukocytes, lymphocytes, and monocytes, are responsible for systemic symptoms (9,15).…”

Section: Discussionmentioning

confidence: 99%