Apoptosis in Vero cells infected with Akabane, Aino and Chuzan virus

Lim, Seong In; Kweon, Chang-Hee; Yang, Dong Kun; Tark, Dong Seob; Kweon, Jun Hun

doi:10.4142/jvs.2005.6.3.251

Cited by 18 publications

(14 citation statements)

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“…Induction of apoptosis was observed in infection with La Crosse virus, a bunyavirus, in BHK and neuroblastoma cells as well as in the brain of newborn mice 31 32 . Similar results have been observed in Hantaan 33 , Bunyamwera 34 , Akabane, and Aino viruses in Vero cells 35 , and Punta Toro virus in hamster hepatocytes 32 . Liver damage in SFTSV-infected humans and mice may be attributed to apoptosis induced in liver epithelial cells upon infection as shown in our study, in contrast to the previous observation that SFTSV caused no cell death in many cell types including monocytes, Vero cells, HeLa, and HEK 293 cells 1 14 .…”

Section: Discussionsupporting

confidence: 86%

Host Responses and Regulation by NFκB Signaling in the Liver and Liver Epithelial Cells Infected with A Novel Tick-borne Bunyavirus

Sun

Jin

Zhu

et al. 2015

Sci Rep

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Infection in humans by severe fever with thrombocytopenia syndrome virus (SFTSV), a novel bunyavirus transmitted by ticks, is often associated with pronounced liver damage, especially in fatal cases. Little has been known, however, about how liver cells respond to SFTSV and how the response is regulated. In this study we report that proinflammatory cytokines were induced in liver tissues of C57/BL6 mice infected with SFTSV, which may cause tissue necrosis in mice. Human liver epithelial cells were susceptible to SFTSV and antiviral interferon (IFN) and IFN-inducible proteins were induced upon infection. We observed that infection of liver epithelial cells led to significant increases in proinflammatory cytokines and chemokines, including IL-6, RANTES, IP-10, and MIP-3a, which were regulated by NFκB signaling, and the activation of NFκB signaling during infection promoted viral replication in liver epithelial cells. Viral nonstructural protein NSs was inhibitory to the induction of IFN-β, but interestingly, NFκB activation was enhanced in the presence of NSs. Therefore, NSs plays dual roles in the suppression of antiviral IFN-β induction as well as the promotion of proinflammatory responses. Our findings provide the first evidence for elucidating host responses and regulation in liver epithelial cells infected by an emerging bunyavirus.

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Section: Discussionsupporting

confidence: 86%

Host Responses and Regulation by NFκB Signaling in the Liver and Liver Epithelial Cells Infected with A Novel Tick-borne Bunyavirus

Sun

Jin

Zhu

et al. 2015

Sci Rep

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“…In case of severe acute respiratory syndrome-coronavirus, p38 MAPK induces cell death in Vero E6 cells and JNK is related to persistent infection (Mizutani et al, 2004(Mizutani et al, , 2005. Viruses in the Simbu serogroup replicate and induce apoptosis in cultured cells (Lim et al, 2005;Barry et al, 2014;Varela et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…AKAV infects cultured neuronal cells and astroglia cells and causes degenerative death (Kitani et al, 2000). AKAV induces cytopathic effects (CPE) and apoptosis via the activation of caspase-3 in Vero E6 cells (Lim et al, 2005). However, there have been no detailed studies of the signaling pathways involved in AKAV-induced apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Activation of c-Jun N-terminal kinase by Akabane virus is required for apoptosis

Mitomo

Omatsu

Tsuchiaka

et al. 2016

Research in Veterinary Science

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Akabane virus (AKAV) belongs to the Simbu serogroup of the genus Orthobunyavirus in the family Bunyaviridae. It has been shown that AKAV induces apoptosis in mammalian cells. It is necessary to understand the signaling pathways involved in AKAV-induced apoptosis to further elucidate the molecular virology of AKAV. c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) are mediators of apoptosis; therefore, we investigated the roles of JNK and p38 MAPK cascades in AKAV-infected cells. We found that JNK and p38 MAPK as well as their downstream substrates, c-Jun and heat shock protein 27 (HSP27), were phosphorylated in response to AKAV infection. A JNK inhibitor (SP600125) inhibited AKAV-mediated apoptosis whereas a p38 MAPK inhibitor (SB203580) did not. We conclude that AKAV infection activates the JNK and p38 MAPK signaling pathways, and the JNK cascade plays a crucial role in AKAV-induced apoptosis in vitro.

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“…SNT against AINOV, AKAV, BEFV, CHUV and IBAV were performed in flat-bottomed 96-well plates. Briefly, two-fold serial dilutions of sera were mixed with equal volumes of virus containing 200 TCID 50 /0.1 m l and inoculated with Vero cells [ 8 , 11 ]. The plates were microscopically examined after 3 and 5 days for evidence of virus-specific cytopathic effects (CPE).…”

mentioning

confidence: 99%

Seroprevalence of five arboviruses in sentinel cattle as part of nationwide surveillance in South Korea, 2009−2012

Kim

Oem

Eunyong

et al. 2015

The Journal of Veterinary Medical Science

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To investigate the possible circulation of arboviruses in South Korea, nationwide surveillance of five arbovirues was conducted in sentinel calves during 2009−2012. We used serum neutralization tests to investigate the presence of antibodies for the Aino virus, Akabane virus, bovine ephemeral fever virus, Chuzan virus and Ibaraki virus. In 2009, 2011 and 2012, the seropositive rates for these five arboviruses were all less than 14.1%. In 2010, however, the seropositive rates for Aino virus and Akabane virus were 33.2% and 40.2%, respectively. High seropositive rates were also associated with a large-scale outbreak of Akabane viral encephalomyelitis in cattle in southern Korea in 2010. Continued seroprevalence surveillance will be useful for monitoring natural arboviral diseases.

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Apoptosis in Vero cells infected with Akabane, Aino and Chuzan virus

Cited by 18 publications

References 0 publications

Host Responses and Regulation by NFκB Signaling in the Liver and Liver Epithelial Cells Infected with A Novel Tick-borne Bunyavirus

Host Responses and Regulation by NFκB Signaling in the Liver and Liver Epithelial Cells Infected with A Novel Tick-borne Bunyavirus

Activation of c-Jun N-terminal kinase by Akabane virus is required for apoptosis

Seroprevalence of five arboviruses in sentinel cattle as part of nationwide surveillance in South Korea, 2009−2012

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