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Published on: August 31, 2013
Tick-borne encephalitis virus infection of cultured mouse macrophages
Arunee Ahantarig1, Daniel Růzek, Marie Vancová
1Department of Biology, Faculty of Science, Mahidol University, Bangkok, Thailand. scaah@mahidol.ac.th
Abstract:
The interactions of tick-borne encephalitis virus (TBEV) with mouse macrophages were studied at the electron microscopic level. The cultured mouse macrophages were sensitive to infection with TBEV strain Hypr (a highly neuroinvasive and neurovirulent strain for laboratory mice) and produced relatively high virus titers. However, these macrophage cells remained morphologically inactivated. Viral particles were located mainly in the ER but were also present in other exocytic compartments. No virus production was observed in cells infected with the attenuated, non-neuroinvasive TBEV strain 263. In this case, the infection led to a clear morphological activation of the macrophages. In conclusion, the virus replication process in mouse macrophage cells might be different from that in other mammalian cell lines since the smooth membrane structures, which are thought to be the sites for flavivirus replication, were not observed. Moreover, different TBEV strains exhibited a different interaction with the host macrophages. The inability of strain 263 to replicate in mouse macrophages as the first site of significant viral replication in vivo could be associated with the inability of this strain to establish a serious infection in mice.
Insights
Tick-borne encephalitis virus (TBEV) interactions with mouse macrophages differ by strain. Neurovirulent TBEV replicates in macrophages, causing inactivation, while attenuated strains do not, leading to activation.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Tick-borne encephalitis virus (TBEV) is a significant human pathogen.
- Macrophages play a crucial role in the innate immune response to viral infections.
- Understanding TBEV-macrophage interactions is key to deciphering viral pathogenesis.
Purpose of the Study:
- To investigate the ultrastructural interactions between mouse macrophages and different TBEV strains.
- To compare the replication and cellular response to neurovirulent (Hypr) and attenuated (263) TBEV strains in macrophages.
- To explore potential mechanisms of TBEV neuroinvasion and neurovirulence related to macrophage tropism.
Main Methods:
- Primary mouse macrophage cultures were infected with TBEV strains Hypr and 263.
- Electron microscopy was employed to examine viral particle localization and cellular morphology.
- Virus titers were measured to assess replication efficiency.
Main Results:
- Mouse macrophages supported replication of the neurovirulent TBEV Hypr strain, with viral particles found mainly in the endoplasmic reticulum (ER).
- Infection with TBEV Hypr resulted in morphologically inactivated macrophages.
- The attenuated TBEV strain 263 did not replicate in macrophages and induced clear morphological activation.
- Absence of typical flavivirus replication sites (smooth membrane structures) suggests unique replication mechanisms in macrophages.
Conclusions:
- TBEV replication in mouse macrophages may differ from other cell types.
- Distinct TBEV strains exhibit strain-specific interactions with host macrophages.
- The inability of attenuated TBEV strain 263 to replicate in macrophages might correlate with its reduced neuroinvasiveness and virulence in vivo.
