Mosquito‐infecting virus Espirito Santo virus inhibits replication and spread of dengue virus

• Published in: Journal of medical virology 2021-06, Vol.93 (6), p.3362-3373
• Main Authors: White, Avian V., Fan, Ming, Mazzara, Jordan M., Roper, Rachel L., Richards, Stephanie L.
• Format: Article
• Language: English
• Subjects: Aedes aegypti; Cell culture; dengue; Dengue fever; Gene expression; Genomes; Insect cells; Insects; insect‐specific virus (ISV); Kinetics; Mammalian cells; Mammals; Mosquitoes; mosquito‐infecting virus; mosquito‐specific virus; Protein biosynthesis; Protein synthesis; Proteins; Public health; Replication; superinfection; Tissue culture; vector competence; Vector-borne diseases; Virology; Viruses
• ISSN: 0146-6615; 1096-9071
• DOI: 10.1002/jmv.26686

The primary vector of dengue virus (DENV) is Aedes aegypti. The mosquito‐infecting virus, Espirito Santo virus (ESV), does not infect Vero (mammalian) cells and grows in mosquito (C6/36) cells without cytopathic effects. Effects of ESV infection on replication of DENV were explored in vitro and in vivo, analyzing protein, RNA genome expression, and plaque formation. ESV and DENV simultaneous coinfection did not block protein synthesis from either virus but did result in inhibition of DENV replication in mosquito cells. Furthermore, ESV superinfected with DENV resulted in inhibition of DENV replication and spread in A. aegypti, thus reducing vector competence. Tissue culture experiments on viral kinetics of ESV and DENV coinfection showed that neither virus significantly affects the replication of the other in Vero, HeLa, or HEK cells. Hence, ESV blocks DENV replication in insect cells, but not the mammalian cells evaluated here. Our study provides new insights into ESV‐induced suppression of DENV, a globally important pathogen impacting public health. Highlights ESV and DENV simultaneous coinfection did not block protein synthesis from either virus, but inhibited DENV replication in mosquito cells. ESV superinfected with DENV results in inhibition of DENV replication and spread in Aedes aegypti, thus reducing vector competence. In vitro experiments on viral kinetics of ESV and DENV coinfection showed that neither virus significantly affects the replication of the other in Vero, HeLa, or HEK cells. Hence, ESV blocks DENV replication in insect cells, but not mammalian cells under the conditions evaluated here.