A mosquito salivary protein promotes flavivirus transmission by activation of autophagy

Peng Sun, Kaixiao Nie, Yibin Zhu, Yang Liu, Pa Wu, Ziwen Liu, Senyan Du, Huahao Fan, Chun-Hong Chen, Renli Zhang, Penghua Wang and Gong Cheng ()
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Peng Sun: Tsinghua University
Kaixiao Nie: Tsinghua University
Yibin Zhu: Tsinghua University
Yang Liu: Tsinghua University
Pa Wu: Tsinghua University
Ziwen Liu: Tsinghua University
Senyan Du: Tsinghua University
Huahao Fan: Tsinghua University
Chun-Hong Chen: National Health Research Institutes, Zhunan
Renli Zhang: Shenzhen Center for Disease Control and Prevention
Penghua Wang: The University of Connecticut Health Center
Gong Cheng: Tsinghua University

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Transmission from an infected mosquito to a host is an essential process in the life cycle of mosquito-borne flaviviruses. Numerous studies have demonstrated that mosquito saliva facilitates viral transmission. Here we find that a saliva-specific protein, named Aedes aegypti venom allergen-1 (AaVA-1), promotes dengue and Zika virus transmission by activating autophagy in host immune cells of the monocyte lineage. The AG6 mice (ifnar1–/–ifngr1–/–) bitten by the virus-infected AaVA-1-deficient mosquitoes present a lower viremia and prolonged survival. AaVA-1 intracellularly interacts with a dominant negative binder of Beclin-1, known as leucine-rich pentatricopeptide repeat-containing protein (LRPPRC), and releases Beclin-1 from LRPPRC-mediated sequestration, thereby enabling the initialization of downstream autophagic signaling. A deficiency in Beclin-1 reduces viral infection in mice and abolishes AaVA-1-mediated enhancement of ZIKV transmission by mosquitoes. Our study provides a mechanistic insight into saliva-aided viral transmission and could offer a potential prophylactic target for reducing flavivirus transmission.

Date: 2020
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DOI: 10.1038/s41467-019-14115-z

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