@article{fdi:010079547,
  title = {{JNK} pathway restricts {DENV}2, {ZIKV} and {CHIKV} infection by activating complement and apoptosis in mosquito salivary glands},
  author = {{C}howdhury, {A}. and {M}odahl, {C}. {M}. and {T}an, {S}. {T}. and {X}iang, {B}. {W}. {W}. and {M}iss{\'e}, {D}oroth{\'e}e and {V}ial, {T}homas and {K}ini, {R}. {M}. and {P}ompon, {J}ulien},
  editor = {},
  language = {{ENG}},
  abstract = {{A}uthor summary {A}rboviral diseases caused by dengue ({DENV}), {Z}ika ({ZIKV}) and chikungunya ({CHIKV}) viruses are responsible for large number of death and debilitation around the world. {T}hese viruses are transmitted to humans by the mosquito vector,{A}edes aegypti. {D}uring the bites, infected salivary glands ({SG}s) release saliva containing viruses, which initiate human infection. {A}s the tissue where transmitted viruses are produced, {SG} infection is a key determinant of transmission. {T}o bridge the knowledge gap in vector-virus molecular interactions in {SG}s, we describe the transcriptome after {DENV}, {ZIKV} and {CHIKV} infection using {RNA}-sequencing and characterized the immune response in this tissue. {O}ur study reveals the broad antiviral function of c-{J}un {N}-terminal kinase ({JNK}) pathway against {DENV}, {ZIKV} and {CHIKV} in {SG}s. {W}e further show that it is mediated by the complement system and apoptosis, identifying the mechanism. {O}ur study adds the {JNK} pathway to the immune arsenal that can be harnessed to engineer refractory vectors. {A}rbovirus infection of{A}edes aegyptisalivary glands ({SG}s) determines transmission. {H}owever, there is a dearth of knowledge on {SG} immunity. {H}ere, we characterized {SG} immune response to dengue, {Z}ika and chikungunya viruses using high-throughput transcriptomics. {W}e also describe a transcriptomic response associated to apoptosis, blood-feeding and lipid metabolism. {T}he three viruses differentially regulate components of {T}oll, {I}mmune deficiency ({IMD}) and c-{J}un {N}- terminal {K}inase ({JNK}) pathways. {H}owever, silencing of the {T}oll and {IMD} pathway components showed variable effects on {SG} infection by each virus. {I}n contrast, regulation of the {JNK} pathway produced consistent responses in both {SG}s and midgut. {I}nfection by the three viruses increased with depletion of the activator {K}ayak and decreased with depletion of the negative regulator {P}uckered. {V}irus-induced {JNK} pathway regulates the complement factor, {T}hioester containing protein-20 ({TEP}20), and the apoptosis activator, {D}ronc, in {SG}s. {I}ndividual and co-silencing of these genes demonstrate their antiviral effects and that both may function together. {C}o-silencing either{TEP}20or{D}roncwith{P}uckeredannihilates {JNK} pathway antiviral effect. {U}pon infection in {SG}s, {TEP}20 induces antimicrobial peptides ({AMP}s), while {D}ronc is required for apoptosis independently of {TEP}20. {I}n conclusion, we revealed the broad antiviral function of {JNK} pathway in {SG}s and showed that it is mediated by a {TEP}20 complement and {D}ronc-induced apoptosis response. {T}hese results expand our understanding of the immune arsenal that blocks arbovirus transmission.},
  keywords = {},
  booktitle = {},
  journal = {{PL}o{S} {P}athogens},
  volume = {16},
  numero = {8},
  pages = {e1008754 [24 ]},
  ISSN = {1553-7366},
  year = {2020},
  DOI = {10.1371/journal.ppat.1008754},
  URL = {https://www.documentation.ird.fr/hor/fdi:010079547},
}