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Published on: June 1, 2022
pH-dependent entry of chikungunya virus into Aedes albopictus cells
Bernard Gay1, Eric Bernard, Maxime Solignat
1Centre d'études d'agents Pathogènes et Biotechnologies pour Santé - CPBS, CNRS-UMR 5236-UM1-UM2, Montpellier, France.
Background:
The chikungunya virus (CHIKV) recently caused explosive outbreaks in Indian Ocean islands and India. During these episodes, the virus was mainly spread to humans through the bite of the mosquito Aedes albopictus. Concomitantly to the description of symptoms of an unexpected severity in infants and elderly patients, a viral genome microevolution has been highlighted, in particular consisting in the acquisition of an A226V mutation in the gene encoding envelope glycoprotein E1, which was later found to confer an increased fitness for A. albopictus. We previously decrypted the entry pathway used by CHIKV to infect human epithelial cells and showed that these mechanisms are modulated by the E1-A226V mutation. In this report we investigated the conditions for CHIKV entry into mosquito cells and we assessed the consequence of E1 gene mutation on these parameters.
Principal Findings:
Our main findings indicate that CHIKV infection of A. albopictus cell lines is sensitive to Bafilomycin A1 and chloroquine and to membrane cholesterol depletion. The E1-226V mutated LR-OPY1 isolate collected during the 2005 outbreak in La Réunion replicated more efficiently than the 37997 African reference strain in C6/36 cells. Moreover, the LR-OPY1 strain displayed greater membrane cholesterol dependence and was more sensitive to inhibition of endosomal pH acidification. Finally, using electron microscopy, we imaged CHIKV entry into C6/36 cells.
Conclusions:
Our data support that CHIKV is endocyted into A. albopictus cells and requires membrane cholesterol as well as a low-pH environment for entry. These features are modulated in some extent by the A226V mutation in the E1 gene of the LR-OPY1 isolate. Altogether, our data provide information regarding the pathways used by CHIKV to infect A. albopictus cells.
Insights
Chikungunya virus (CHIKV) enters mosquito cells via endocytosis, requiring cholesterol and low pH. The A226V mutation in the E1 gene enhances CHIKV replication and entry into Aedes albopictus cells.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Chikungunya virus (CHIKV) outbreaks have been linked to the mosquito Aedes albopictus.
- A specific mutation (A226V) in the CHIKV E1 gene enhances viral fitness in A. albopictus.
- Previous studies detailed CHIKV entry into human cells, but mosquito cell entry remained unclear.
Purpose of the Study:
- To investigate the entry mechanisms of CHIKV into Aedes albopictus mosquito cells.
- To assess the impact of the E1-A226V mutation on CHIKV entry into mosquito cells.
Main Methods:
- Infection of A. albopictus cell lines (C6/36) with CHIKV.
- Treatment with Bafilomycin A1, chloroquine, and cholesterol depletion agents.
- Comparative analysis of CHIKV isolates (LR-OPY1 with E1-226V mutation vs. African reference strain).
- Electron microscopy to visualize viral entry.
Main Results:
- CHIKV entry into A. albopictus cells is sensitive to Bafilomycin A1, chloroquine, and cholesterol depletion.
- The E1-226V mutated LR-OPY1 strain replicated more efficiently in C6/36 cells than the reference strain.
- The LR-OPY1 strain showed increased dependence on membrane cholesterol and sensitivity to endosomal acidification inhibition.
- Electron microscopy confirmed CHIKV entry into C6/36 cells.
Conclusions:
- CHIKV enters A. albopictus cells through endocytosis, dependent on membrane cholesterol and low pH.
- The E1-A226V mutation modulates these entry parameters to some extent.
- These findings elucidate the pathways of CHIKV infection in A. albopictus cells.
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