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A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Heat shock effect upon dengue virus replication into U937 cells
Salvador Chavez-Salinas1, Ivonne Ceballos-Olvera, Jorge Reyes-Del Valle
1Departamento de Patología Experimental, Centro de Investigación y de Estudios Avanzados del IPN, Av. I.P.N. 2508, Col. San Pedro Zacatenco, México D.F. C.P. 07360, Mexico.
Virus Research
|September 24, 2008
Summary
Heat shock increases dengue virus infectivity in human monocytic cells by enhancing viral entry and replication. This is linked to increased surface heat shock proteins (Hsps), Hsp90 and Hsp70, crucial for dengue virus infection.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- The molecular mechanisms of dengue virus entry into human cells remain largely unknown.
- Previous research identified heat shock proteins (Hsps), specifically Hsp90 and Hsp70, as components of a receptor complex in monocytic cells involved in viral entry.
- Understanding these interactions is critical for developing antiviral strategies.
Purpose of the Study:
- To investigate the effect of heat shock (HS) on dengue virus infectivity in human monocytic cells.
- To determine if HS influences viral entry, replication, or both.
- To elucidate the role of surface heat shock proteins in heat shock-induced changes in dengue virus infection.
Main Methods:
- Treatment of U937 monocytic cells with heat shock.
- Infection of treated cells with dengue virus.
- Quantification of viral infectivity and viral entry.
- Analysis of heat shock protein expression and localization on the cell surface, particularly in membrane microdomains.
Main Results:
- Heat shock treatment resulted in a greater than twofold increase in dengue virus infectivity in U937 cells.
- This enhanced infectivity was primarily attributed to increased viral entry, correlated with a higher presence of Hsp90 and Hsp70 on the monocytic cell surface.
- Heat shock applied post-infection also led to increased viral yields, suggesting a positive modulation of dengue virus replication.
Conclusions:
- Heat shock significantly enhances dengue virus infectivity in monocytic cells.
- The increased infectivity is mediated by elevated surface expression of heat shock proteins (Hsp90 and Hsp70), which facilitate viral entry.
- Heat shock may also positively influence dengue virus replication, indicating a multifaceted role in the viral life cycle.
