Key result
Experimental mouse infection with Saffold virus strains 2 and 3 exhibited typical Cardiovirus tropism, with SAFV-3 causing severe encephalitis in IFN-receptor 1 deficient mice.
Saffold virus exhibits typical Cardiovirus tropism in mice and can cause severe encephalitis in interferon-deficient models, highlighting its potential neuropathogenesis.
Saffold virus (SAFV) is a highly seroprevalent human Cardiovirus discovered recently. No clear association between SAFV infection and human disease has been established. Rare infection cases, however, correlated with neurological symptoms. To gain insight into the pathogenesis potential of the virus, we performed experimental mouse infection with SAFV strains of genotypes 2 and 3 (SAFV-2 and SAFV-3). After intraperitoneal infection, both strains exhibited a typical Cardiovirus tropism. Viral load was most prominent in the pancreas. Heart, spleen, brain and spinal cord were also infected. In IFN-receptor 1 deficient (IFNAR-KO) mice, SAFV-3 caused a severe encephalitis. The virus was detected by immunohistochemistry in many parts of the brain and spinal cord, both in neurons and astrocytes, but astrocyte infection was more extensive. In vitro, SAFV-3 also infected astrocytes better than neurons in mixed primary cultures. Astrocytes were, however, very efficiently protected by IFN-α/β treatment.
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Sorgeloos et al. (2016) studied Saffold virus infection. Saffold virus strains (SAFV-2 and SAFV-3) was evaluated on Viral tropism and pathogenesis. Experimental mouse infection with Saffold virus strains 2 and 3 exhibited typical Cardiovirus tropism, with SAFV-3 causing severe encephalitis in IFN-receptor 1 deficient mice.
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