Abstract
To date, no safe vaccine or antivirals for Zika virus (ZIKV) infection have been found. The pathogenesis of severe Zika, where host and viral factors participate, remains unclear. For the control of Zika, it is important to understand how ZIKV interacts with different host cells. Knowledge of the targeted cellular pathways which allow ZIKV to productively replicate and/or establish prolonged viral persistence contributes to novel vaccines and therapies. Monocytes and endothelial vascular cells are the main ZIKV targets. During the infection process, cells are capable of releasing extracellular vesicles (EVs). EVs are mediators of intercellular communication. We found that mosquito EVs released from ZIKV-infected (C6/36) cells carry viral RNA and ZIKV-E protein and are able to infect and activate naïve mosquito and mammalian cells. ZIKV C6/36 EVs promote the differentiation of naïve monocytes and induce a pro-inflammatory state with tumor necrosis factor-alpha (TNF-α) mRNA expression. ZIKV C6/36 EVs participate in endothelial vascular cell damage by inducing coagulation (TF) and inflammation (PAR-1) receptors at the endothelial surface of the cell membranes and promote a pro-inflammatory state with increased endothelial permeability. These data suggest that ZIKV C6/36 EVs may contribute to the pathogenesis of ZIKV infection in human hosts.
Highlights
Zika virus (ZIKV) is an emerging arthropod-borne Flavivirus, transmitted mainly by mosquitoes of the genus Aedes, but the ZIKV infection could be produced by sexual contact or vertical transmission from mother to child [1,2]
We found that, when using a multiplicity of infection (MOI) of 1 at 48 h PI, the mosquito cells had high levels (38.60 ± 1.05%) of ZIKV E protein at the membrane surface level (Figure 1A)
The molecular and cellular events occurring in vector–pathogen–host interactions are critical in determining the outcome of the vector-borne diseases
Summary
Zika virus (ZIKV) is an emerging arthropod-borne Flavivirus, transmitted mainly by mosquitoes of the genus Aedes, but the ZIKV infection could be produced by sexual contact or vertical transmission from mother to child [1,2]. ZIKV was first isolated in 1947 from the blood of a sentinel Rhesus monkey. In 1948, ZIKV was isolated in the same forest from a pool of Aedes (Ae) africanus mosquitoes. In 2007, ZIKV caused an outbreak of relatively mild disease characterized by rash, arthralgia, and conjunctivitis on Yap Island in the Southwestern Pacific Ocean. This was the first time that the virus was detected outside of Africa [3]
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