Abstract
Tick-borne encephalitis (TBE) is a severe neurologic disease in Europe and Asia. Disease expression ranges from asymptomatic to severe neurological clinical pictures, involving meningitis, encephalitis, meningoencephalitis and potentially fatal outcome. Humans mostly become infected with TBE virus (TBEV) by the bite of an infected tick. Gastrointestinal (GI) symptoms in humans are mainly attributed to the first viremic phase of TBEV infection with unspecific symptoms and/or resulting from severe neurological impairment of the central nervous system (CNS). We used the subcutaneous TBEV-infection of C57BL/6 mice as a model to analyze GI complications of TBE. We observed the acute distension and segmental dilation of the intestinal tract in 10 of 22 subcutaneously infected mice. Histological analysis revealed an intramural enteric ganglioneuritis in the myenteric and submucosal plexus of the small and large intestine. The numbers of infiltrating macrophages and CD3+ T lymphocytes correlated with the severity of ganglioneuritis, indicating an immune-mediated pathogenesis due to TBEV-infection of the enteric plexus. Our study demonstrates that the inflammation of enteric intramural ganglia presents to be a common feature in TBEV-infected mice. Accordingly, the results of this mouse model emphasize that GI disease manifestation and consequences for long-term sequelae should not be neglected for TBEV-infections in humans and require further investigation.
Highlights
IntroductionTick-borne encephalitis (TBE) is a serious neurological disease in Eurasia, representing an increasing public health concern
Tick-borne encephalitis (TBE) ranges from asymptomatic or mild forms to severe neurological disease manifesting as meningitis, encephalitis, meningoencephalitis and meningoencephalomyelitis, resulting in long-term sequelae and potentially fatal outcome [1,2,3]
TBE virus (TBEV) mouse model, 22 mice were infected with 1000 viral particles of the TBEV strain
Summary
Tick-borne encephalitis (TBE) is a serious neurological disease in Eurasia, representing an increasing public health concern. TBE ranges from asymptomatic or mild forms to severe neurological disease manifesting as meningitis, encephalitis, meningoencephalitis and meningoencephalomyelitis, resulting in long-term sequelae and potentially fatal outcome [1,2,3]. The causative agent, TBE virus (TBEV) belongs to the genus Flavivirus (family: Flaviviridae), which further comprises several neurotropic viruses such as West. Nile virus (WNV), Japanese encephalitis virus (JEV), Zika virus (ZIKV) or Powassan virus (POWV). It is believed that the case fatality rates differ between the three main TBEV
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