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Published on: September 5, 2016
[Inclusion Bodies are Formed in SFTSV-infected Human Macrophages]
Abstract:
The severe fever with thrombocytopenia syndrome virus (SFTSV) is a new member in the genus Phlebovirus of the family Bunyaviridae identified in China. The SFTSV is also the causative pathogen of an emerging infectious disease: severe fever with thrombocytopenia syndrome. Using immunofluorescent staining and confocal microscopy, the intracellular distribution of nucleocapsid protein (NP) in SFTSV-infected THP-1 cells was investigated with serial doses of SFTSV at different times after infection. Transmission electron microscopy was used to observe the ultrafine intracellular structure of SFTSV-infected THP-1 cells at different times after infection. SFTSV NP could form intracellular inclusion bodies in infected THP-1 cells. The association between NP-formed inclusion bodies and virus production was analyzed: the size of the inclusion body formed 3 days after infection was correlated with the viral load in supernatants collected 7 days after infection. These findings suggest that the inclusion bodies formed in SFTSV-infected THP-1 cells could be where the SFTSV uses host-cell proteins and intracellular organelles to produce new viral particles.
Insights
Severe fever with thrombocytopenia syndrome virus (SFTSV) inclusion bodies in THP-1 cells may be replication sites. Larger inclusion bodies correlate with higher SFTSV viral loads, suggesting a role in virus production.
Area of Science:
- Virology
- Cell Biology
Context:
- Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging pathogen from China.
- SFTSV belongs to the Phlebovirus genus within the Bunyaviridae family.
Purpose:
- To investigate the intracellular distribution and role of SFTSV nucleocapsid protein (NP).
- To examine the formation and function of intracellular inclusion bodies in SFTSV-infected cells.
Summary:
- Immunofluorescent staining and electron microscopy revealed SFTSV NP forms intracellular inclusion bodies in THP-1 cells.
- The size of these inclusion bodies at 3 days post-infection correlated with viral load at 7 days post-infection.
- Findings suggest these inclusion bodies are sites for SFTSV replication, utilizing host factors.
Impact:
- Provides insights into the replication mechanisms of SFTSV.
- Highlights the potential role of inclusion bodies in the pathogenesis of SFTSV.
- Informs future strategies for controlling this emerging infectious disease.
