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

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      https://www.riss.kr/link?id=O106506530

      • 저자
      • 발행기관
      • 학술지명
      • 권호사항
      • 발행연도

        2021년

      • 작성언어

        -

      • Print ISSN

        0146-6615

      • Online ISSN

        1096-9071

      • 등재정보

        SCI;SCIE;SCOPUS

      • 자료형태

        학술저널

      • 수록면

        3362-3373   [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]

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      • ⓒ COPYRIGHT THE BRITISH LIBRARY BOARD: ALL RIGHT RESERVED
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      부가정보

      다국어 초록 (Multilingual Abstract)

      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.


      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.
      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.
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      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 ...

      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.


      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.
      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.

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