Apoptosis in the lymphatic organs of piglets inoculated with classical swine fever virus

Sato, Mariko; Mikami, Osamu; Kobayashi, Mitsuo; Nakajima, Yasuyuki

doi:10.1016/s0378-1135(00)00198-x

Cited by 35 publications

(29 citation statements)

References 21 publications

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“…Taking into account other viral infections (16,21,23,28), it appears that when apoptosis is implicated in the pathogenesis of lymphocyte depletion lesions, its incidence is usually increased and can be demonstrated by in situ detection in lymphoid tissues. Moreover, it appears that higher rates of apoptosis are found during the acute phase of infection, when active virus replication occurs.…”

Section: Discussionmentioning

confidence: 99%

Selective Lymphocyte Depletion during the Early Stage of the Immune Response to Foot-and-Mouth Disease Virus Infection in Swine

Segundo

Salguero

Ávila

et al. 2006

J Virol

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Foot-and-mouth disease virus (FMDV) is the causative agent of a highly contagious vesicular disease of cloven-hoofed animals. In the present study we use FMDV serotype C infection of swine to determine, by analytical techniques, the direct ex vivo visualization of virus-infected immune cells during the first 17 days of infection. We report, for the first time, that FMDV C-S8c1 can infect T and B cells at short periods of time postinoculation, corresponding with the peak of the viremia. There is a significant lymphopenia that involves cells in lymph nodes and spleen is observed. This selective depletion of T cells is not due mainly to in situ death via apoptosis as visualized by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique. Thus, early infection of T cells by FMDV may be the main cause of the observed T-cell depletion.Importantly, this lack of T cells is reflected in a reduced response to mitogen activation, which in many cases is totally eliminated. These data suggest a mechanism by which the virus causes a transient immunosuppression, subvert the immune systems, and spreads. These results have important implications for our understanding of early events in the development of a robust immune response against FMDV.

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Section: Discussionmentioning

confidence: 99%

Selective Lymphocyte Depletion during the Early Stage of the Immune Response to Foot-and-Mouth Disease Virus Infection in Swine

Segundo

Salguero

Ávila

et al. 2006

J Virol

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“…Histopathology studies of ASFVinfected pig tissue revealed that the disease is characterized by DIC (47), fibrinolysis (46), and lymphopenia, due to extensive apoptosis in lymph nodes (12,31). An important feature of the pathology for ASFV involves bystander apoptosis of uninfected lymphocytes, which interestingly has been seen for other VHFs, such as Ebola virus and classical swine fever virus (16,38).…”

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confidence: 94%

African Swine Fever Virus Infection of Porcine Aortic Endothelial Cells Leads to Inhibition of Inflammatory Responses, Activation of the Thrombotic State, and Apoptosis

Vallée

Tait

Powell

2001

J Virol

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“…In vivo, elevated levels of cell death by apoptosis are thought to account for the characteristic depletion of circulating leukocytes (Sanchez-Cordon et al, 2002;Summerfield et al, 2000Summerfield et al, , 2001. However, it has been found that apoptotic cells rarely contain detectable viral antigen, indicating that apoptotic cells are generally not CSFV-infected (Choi et al, 2004;Sato et al, 2000;Summerfield et al, 2001). This finding, together with the observation that acutely infected animals develop high viral loads, suggest a possible role for cell populations that are resistant to virus-induced apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Classical swine fever virus infection protects aortic endothelial cells from pIpC-mediated apoptosis

Johns

Bensaude

Rocca

et al. 2009

Journal of General Virology

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Classical swine fever virus (CSFV) causes severe disease in pigs associated with leukopenia, haemorrhage and fever. We show that CSFV infection protects endothelial cells from apoptosis induced by the dsRNA mimic, pIpC, but not from other apoptotic stimuli, FasL or staurosporine. CSFV infection inhibits pIpC-induced caspase activation, mitochondrial membrane potential loss and cytochrome c release as well as the pro-apoptotic effects of truncated Bid (tBid) overexpression. The CSFV proteins N pro and E rns both contribute to CSFV inhibition of apoptosis. We conclude that CSFV infection can inhibit apoptotic signalling at multiple levels, including at the caspase-8 and the mitochondrial checkpoints. By supporting viral replication, endothelial cells may promote CSFV pathogenesis. INTRODUCTIONClassical swine fever virus (CSFV), a pestivirus within the family Flaviviridae, is related in terms of its sequence and genome organization to other members of the flavivirus group that give rise to human diseases such as hepatitis C and dengue fever. CSFV is a positive-sense RNA virus, and is the causative agent of classical swine fever (CSF), a notifiable disease of pigs (Le Potier et al., 2006). Disease outbreaks are associated with considerable economic loss and adverse effects on animal welfare (Paton & GreiserWilke, 2003). In its most virulent form, CSFV infection causes severe immunopathological signs, including leukopenia, haemorrhage and fever, accompanied by high morbidity and mortality. However, within an infected population, some animals are found to recover or develop chronic disease (Le Potier et al., 2006). These observations suggest a complex interplay between the virus and the host immune system. CSFV infection is accompanied by depression of cellular immune defences (Ganges et al., 2008) and particularly innate responses mediated by interferon (Bensaude et al., 2004; La Rocca et al., 2005; Ruggli et al., 2005;Seago et al., 2007). In vivo, elevated levels of cell death by apoptosis are thought to account for the characteristic depletion of circulating leukocytes (Sanchez-Cordon et al., 2002;Summerfield et al., 2000Summerfield et al., , 2001. However, it has been found that apoptotic cells rarely contain detectable viral antigen, indicating that apoptotic cells are generally not CSFV-infected (Choi et al., 2004;Sato et al., 2000;Summerfield et al., 2001). This finding, together with the observation that acutely infected animals develop high viral loads, suggest a possible role for cell populations that are resistant to virus-induced apoptosis. These may include endothelial cells.Apoptosis is a controlled cell death programme employed by multicellular organisms to eliminate damaged, aberrant or infected cells (Benedict et al., 2002). A characteristic of apoptotic cell death is the activation of the caspase family of proteases. Caspases that function near the apex of cell death cascades are designated initiators and include caspases-8 and -9, whereas those involved in the terminal stages of cell death, such as ...

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Apoptosis in the lymphatic organs of piglets inoculated with classical swine fever virus

Cited by 35 publications

References 21 publications

Selective Lymphocyte Depletion during the Early Stage of the Immune Response to Foot-and-Mouth Disease Virus Infection in Swine

Selective Lymphocyte Depletion during the Early Stage of the Immune Response to Foot-and-Mouth Disease Virus Infection in Swine

African Swine Fever Virus Infection of Porcine Aortic Endothelial Cells Leads to Inhibition of Inflammatory Responses, Activation of the Thrombotic State, and Apoptosis

Classical swine fever virus infection protects aortic endothelial cells from pIpC-mediated apoptosis

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