| Summary: | Alphaviruses are globally distributed and predominately transmitted by mosquitoes. <i>Aedes</i> species are common vectors for the clinically important alphaviruses—Chikungunya, Sindbis, and Ross River (RRV) viruses—with <i>Aedes aegypti</i> also being a vector for the flaviviruses dengue, Yellow Fever, and Zika viruses. <i>Ae. aegypti</i> was putatively implicated in the large 1979–1980 South Pacific Islands outbreak of RRV—the leading cause of arboviral disease in Australia today. The RNA interference (RNAi) defense response in mosquitoes involves a number of small RNAs, with their kinetics induced by alphaviruses being poorly understood, particularly at the tissue level. We compared the small RNA profiles between RRV-infected and noninfected <i>Ae. aegypti</i> midgut and fat body tissues at 2, 6, and 12 days post-inoculation (dpi). RRV induced an incremental RNAi response, yielding short interfering and P-element-induced-wimpy-testis (PIWI)-interacting RNAs. Fourteen host microRNAs were differentially expressed due to RRV with the majority in the fat body at 2 dpi. The largely congruent pattern of microRNA regulation with previous reports for alphaviruses and divergence from those for flaviviruses suggests a degree of conservation, whereas patterns of microRNA expression unique to this study provide novel insights into the tissuespecific hostvirus attributes of <i>Ae. aegypti</i> responses to this previously unexplored oldworld alphavirus.
|
|---|
