Punta Toro virus (Bunyaviridae, Phlebovirus) infection in mice: Strain differences in pathogenesis and host interferon response

Mendenhall, Michelle; Wong, Min-Hui; Skirpstunas, Ramona T.; Morrey, John D.; Gowen, Brian B.

doi:10.1016/j.virol.2009.09.003

Cited by 17 publications

(21 citation statements)

References 32 publications

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“…In contrast to previous reports examining PTV-A infections (Mendenhall et al, 2009; Pifat and Smith, 1987), we found that C57BL/6 mice were resistant to the virus. However, we tested C57BL/6NCr (from the NCI), whereas the other investigators used C57BL/6J mice (from Jackson Laboratory).…”

Section: Discussioncontrasting

confidence: 99%

“…When susceptible 129S1 mice and resistant FVB mice were inoculated with 10 2 PFU PTV, the 129S1 mice had mild piecemeal hepatocellular necrosis and centrolobular hepatocyte degeneration, whereas no pathological changes were observed in FVB mice (data not shown). The severe liver damage in the 129S1 strain after PTV infection is consistent with previous reports of PTV-induced hepatic damage in mice and hamsters (Fisher et al, 2003; Mendenhall et al, 2009; Pifat and Smith, 1987). …”

Section: Resultssupporting

confidence: 92%

“…PTV is genetically similar to RVFV and has been studied in small rodents as a model for RVFV (Anderson et al, 1990; Fisher et al, 2003; Gowen et al, 2006; Mendenhall et al, 2009; Perrone et al, 2007; Pifat and Smith, 1987). Two strains of PTV, Adames (PTV-A) and Balliet (PTV-B), differ in their virulence in hamsters and mice (Anderson et al, 1990; Mendenhall et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

“…Two strains of PTV, Adames (PTV-A) and Balliet (PTV-B), differ in their virulence in hamsters and mice (Anderson et al, 1990; Mendenhall et al, 2009). PTV-A is highly virulent, while isolates of PTV-B are of lower virulence.…”

Section: Introductionmentioning

confidence: 99%

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Host genetic variation in susceptibility to Punta Toro virus

Ashley¹,

Ameres²,

Gerrard³

et al. 2011

Virus Research

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SUMMARY Infection of small laboratory animals by Punta Toro virus (PTV), family Bunyaviridae, genus Phlebovirus, is a model for the study of the human pathogen Rift Valley fever virus (RVFV). We have identified inbred mouse strains with significant differences in host response to the Adames strain of PTV. Nine inbred strains of mice representing major branches in the Mus musculus phylogeny were inoculated subcutaneously with a high dose of PTV in survival experiments. Two inbred strains of mice, NZW/LacJ and 129S1/SvImJ, died ~4 days after PTV infection, whereas 7 other strains survived the challenge and showed no clinical signs of disease. Histologically, 129S1/SvImJ mice showed massive hepatocellular necrosis and had additional lesions in lung, brain, and spleen, whereas NZW/LacJ mice had mild piecemeal hepatocellular necrosis. PTV viral loads in the livers of infected mice were determined by reverse transcriptase quantitative PCR. Inbred mice from strains that showed clinical signs and succumbed to PTV infection had higher liver viral loads than did mice of resistant strains. Hybrid F1 mice were generated by crossing susceptible 129S1 and resistant FVB/N mice and tested for susceptibility. The hybrid F1 mice showed significantly higher viral loads in the liver than the resistant parental FVB/N mice, suggesting that susceptibility is dominant. These findings will enable an unbiased genetic approach to identify host genes mediating susceptibility to PTV.

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Section: Discussioncontrasting

confidence: 99%

Section: Resultssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Host genetic variation in susceptibility to Punta Toro virus

Ashley¹,

Ameres²,

Gerrard³

et al. 2011

Virus Research

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“…Previous results have shown that TOSV activates transcription of IFN-␤ during infection, in contrast to that observed for other members of the Bunyaviridae family (9). In fact, many of these viruses possess the nonstructural protein NSs, which counteracts IFN-␤ production, resulting in viral escape from the host immune response (15,17,20,(24)(25)(26)(27)(28)(29). To better address the mechanisms which regulate IFN-␤ production in TOSV infection, the role of RIG-I was investigated.…”

Section: Resultsmentioning

confidence: 99%

Toscana Virus NSs Protein Inhibits the Induction of Type I Interferon by Interacting with RIG-I

Savellini

Valentini

Cusi

2013

J Virol

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Toscana virus (TOSV) is a phlebovirus, of the. In this study, we investigated whether an upstream sensor, which has a role in the signaling cascade leading to the production of type I IFN, was involved. We found a significant decrease in RIG-I protein levels in cells overexpressing TOSV NSs, suggesting that the nonstructural protein interacts with RIG-I and targets it for proteasomal degradation. In fact, the MG-132 proteasome inhibitor was able to restore IFN-␤ promoter activation in cells expressing NSs, demonstrating the existence of an evasion mechanism based on inhibition of the RIG-I sensor. Furthermore, a C-terminal truncated NSs protein (⌬NSs), although able to interact with RIG-I, did not affect the RIG-I-mediated IFN-␤ promoter activation, suggesting that the NSs domains responsible for RIG-I-mediated signaling and interaction with RIG-I are mapped on different regions. These results contribute to identify a novel mechanism for bunyaviruses by which TOSV NSs counteracts the early IFN response.

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Structural and functional similarities in bunyaviruses: Perspectives for pan‐bunya antivirals

Horst

Conceição-Neto

Neyts

et al. 2019

Reviews in Medical Virology

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The order of Bunyavirales includes numerous (re)emerging viruses that collectively have a major impact on human and animal health worldwide. There are no vaccines for human use or antiviral drugs available to prevent or treat infections with any of these viruses. The development of efficacious and safe drugs and vaccines is a pressing matter. Ideally, such antivirals possess pan-bunyavirus antiviral activity, allowing the containment of every bunya-related threat. The fact that many bunyaviruses need to be handled in laboratories with biosafety level 3 or 4, the great variety of species and the frequent emergence of novel species complicate such efforts. We here examined the potential druggable targets of bunyaviruses, together with the level of conservation of their biological functions, structure, and genetic similarity by means of heatmap analysis. In the light of this, we revised the available models and tools currently available, pointing out directions for antiviral drug discovery.

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Punta Toro virus (Bunyaviridae, Phlebovirus) infection in mice: Strain differences in pathogenesis and host interferon response

Cited by 17 publications

References 32 publications

Host genetic variation in susceptibility to Punta Toro virus

Host genetic variation in susceptibility to Punta Toro virus

Toscana Virus NSs Protein Inhibits the Induction of Type I Interferon by Interacting with RIG-I

Structural and functional similarities in bunyaviruses: Perspectives for pan‐bunya antivirals

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