“…1 & Additional file 1: Figure S1), indicating that the virus infects both neuronal and glial cells, but neither exclusively. Our results agree with Sorgeloos et al [16] who showed infection of both neuronal and glial cells, but not with Kotani et al [17] who showed infection of glial cells, but not neuronal cells, in both early adult (6 week-old) and neonatal brains of ddY and BALB/c mice. However it should be noted that Sorgeloos et al [16] showed a preference to glial cells over neuronal cells.…”
Section: Resultssupporting
confidence: 82%
“…Our results agree with Sorgeloos et al [16] who showed infection of both neuronal and glial cells, but not with Kotani et al [17] who showed infection of glial cells, but not neuronal cells, in both early adult (6 week-old) and neonatal brains of ddY and BALB/c mice. However it should be noted that Sorgeloos et al [16] showed a preference to glial cells over neuronal cells. We believe that our results are not contradictory, but rather compliments the data shown in Kotani et al [16] by highlighting the varied outcomes seen in different strains of virus, mice breed, and age.Fig.…”
Section: Resultssupporting
confidence: 82%
“…In order to do that, we used AG129 mice which we have previously shown to be a good model for SAFV infection in the CNS [15]. We used previously isolated genotype 3 SAFV [16] as a model of SAFV infection due to its high prevalence [7]. Infectious clone used in this study was obtained as previously described in Tan et al [15].…”
Section: Resultsmentioning
confidence: 99%
“…However it should be noted that Sorgeloos et al [16] showed a preference to glial cells over neuronal cells. We believe that our results are not contradictory, but rather compliments the data shown in Kotani et al [16] by highlighting the varied outcomes seen in different strains of virus, mice breed, and age.Fig. 1Immunohistochemical co-localisation of SAFV VP1 with NeuN or GFAP.…”
Section: Resultsmentioning
confidence: 99%
“…It should however be noted that we did not stain specifically for oligodendrocytes, but rather took a more general approach of staining for a general glial marker GFAP. Kotani et al [16], who similarly showed SAFV infection of GFAP positive cells, however showed no viral infection of oligodendroglial suggesting viral induced apoptosis of oligodendrocytes is unlikely to happen in the brain of SAFV infected animal. This could explain why we did not observe any demyelination.Fig.…”
BackgroundSaffold Virus (SAFV) is a human cardiovirus that is suspected of causing infection of the central nervous system (CNS) in children. While recent animal studies have started to elucidate the pathogenesis of SAFV, very little is known about the mechanisms behind it.MethodIn this study, we attempted to elucidate some of the mechanisms of the pathogenesis of SAFV in the brain of a juvenile mouse model by using immunohistochemical methods.ResultsWe first showed that SAFV is able to infect both neuronal and glial cells in the brain of 2 week-old AG129 mice. We then showed that SAFV is able to induce apoptosis in both neuronal and glial cells in the brain. Lastly, we showed that SAFV infection does not show any signs of gross demyelination in the brain.ConclusionOverall, our results provide important insights into the mechanisms of SAFV in the brain.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-016-0654-8) contains supplementary material, which is available to authorized users.
“…1 & Additional file 1: Figure S1), indicating that the virus infects both neuronal and glial cells, but neither exclusively. Our results agree with Sorgeloos et al [16] who showed infection of both neuronal and glial cells, but not with Kotani et al [17] who showed infection of glial cells, but not neuronal cells, in both early adult (6 week-old) and neonatal brains of ddY and BALB/c mice. However it should be noted that Sorgeloos et al [16] showed a preference to glial cells over neuronal cells.…”
Section: Resultssupporting
confidence: 82%
“…Our results agree with Sorgeloos et al [16] who showed infection of both neuronal and glial cells, but not with Kotani et al [17] who showed infection of glial cells, but not neuronal cells, in both early adult (6 week-old) and neonatal brains of ddY and BALB/c mice. However it should be noted that Sorgeloos et al [16] showed a preference to glial cells over neuronal cells. We believe that our results are not contradictory, but rather compliments the data shown in Kotani et al [16] by highlighting the varied outcomes seen in different strains of virus, mice breed, and age.Fig.…”
Section: Resultssupporting
confidence: 82%
“…In order to do that, we used AG129 mice which we have previously shown to be a good model for SAFV infection in the CNS [15]. We used previously isolated genotype 3 SAFV [16] as a model of SAFV infection due to its high prevalence [7]. Infectious clone used in this study was obtained as previously described in Tan et al [15].…”
Section: Resultsmentioning
confidence: 99%
“…However it should be noted that Sorgeloos et al [16] showed a preference to glial cells over neuronal cells. We believe that our results are not contradictory, but rather compliments the data shown in Kotani et al [16] by highlighting the varied outcomes seen in different strains of virus, mice breed, and age.Fig. 1Immunohistochemical co-localisation of SAFV VP1 with NeuN or GFAP.…”
Section: Resultsmentioning
confidence: 99%
“…It should however be noted that we did not stain specifically for oligodendrocytes, but rather took a more general approach of staining for a general glial marker GFAP. Kotani et al [16], who similarly showed SAFV infection of GFAP positive cells, however showed no viral infection of oligodendroglial suggesting viral induced apoptosis of oligodendrocytes is unlikely to happen in the brain of SAFV infected animal. This could explain why we did not observe any demyelination.Fig.…”
BackgroundSaffold Virus (SAFV) is a human cardiovirus that is suspected of causing infection of the central nervous system (CNS) in children. While recent animal studies have started to elucidate the pathogenesis of SAFV, very little is known about the mechanisms behind it.MethodIn this study, we attempted to elucidate some of the mechanisms of the pathogenesis of SAFV in the brain of a juvenile mouse model by using immunohistochemical methods.ResultsWe first showed that SAFV is able to infect both neuronal and glial cells in the brain of 2 week-old AG129 mice. We then showed that SAFV is able to induce apoptosis in both neuronal and glial cells in the brain. Lastly, we showed that SAFV infection does not show any signs of gross demyelination in the brain.ConclusionOverall, our results provide important insights into the mechanisms of SAFV in the brain.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-016-0654-8) contains supplementary material, which is available to authorized users.
Saffold virus (SAFV) is an emerging human cardiovirus that has been shown to be ubiquitous. Initial studies of SAFV focused on respiratory and gastrointestinal infection; however, it has also recently been associated with diverse clinical symptoms including the endocrine, cardiovascular, and neurological systems. Given the systemic nature of SAFV, and its high prevalence, understanding its pathogenicity and clinical impact is of utmost importance. This comprehensive review highlights and discusses recent developments in epidemiology, human pathogenicity, animal, and molecular studies related to SAFV. It also provides detailed insights into the neuropathogenicity of SAFV. We argue that human studies have been confounded by coinfections and therefore require support from robust molecular and animal research. Thereby, we aim to provide foresight into further research to better understand this emerging virus.
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