scholarly journals Host-directed combinatorial RNAi improves inhibition of diverse strains of influenza A virus in human respiratory epithelial cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (5) ◽  
pp. e0197246 ◽  
Author(s):  
Michael A. Estrin ◽  
Islam T. M. Hussein ◽  
Wendy B. Puryear ◽  
Anne C. Kuan ◽  
Stephen C. Artim ◽  
...  
2010 ◽  
Vol 185 (8) ◽  
pp. 4812-4823 ◽  
Author(s):  
Ronan Le Goffic ◽  
Edwige Bouguyon ◽  
Christophe Chevalier ◽  
Jasmina Vidic ◽  
Bruno Da Costa ◽  
...  

2015 ◽  
Vol 65 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Aaron Gingerich ◽  
Lan Pang ◽  
Jarod Hanson ◽  
Daniel Dlugolenski ◽  
Rebecca Streich ◽  
...  

2010 ◽  
Vol 285 (44) ◽  
pp. 34016-34026 ◽  
Author(s):  
Allen C. Bateman ◽  
Rositsa Karamanska ◽  
Marc G. Busch ◽  
Anne Dell ◽  
Christopher W. Olsen ◽  
...  

2011 ◽  
Vol 72 (8) ◽  
pp. 1071-1078 ◽  
Author(s):  
Ayshea M. Quintana ◽  
Stephen B. Hussey ◽  
Ema C. Burr ◽  
Heidi L. Pecoraro ◽  
Kristina M. Annis ◽  
...  

2016 ◽  
Vol 310 (5) ◽  
pp. L415-L425 ◽  
Author(s):  
Jackye Peretz ◽  
Andrew Pekosz ◽  
Andrew P. Lane ◽  
Sabra L. Klein

Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17β-estradiol (E2) or select estrogen receptor modulators (SERMs) and then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects were sex dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor-2 (ESR2) as neither genomic ESR1 nor nongenomic GPR30 was expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans.


2013 ◽  
Vol 13 (1) ◽  
pp. 104 ◽  
Author(s):  
Wai-Yip Lam ◽  
Apple Chung-Man Yeung ◽  
Karry Lei-Ka Ngai ◽  
Man-Shan Li ◽  
Ka-Fai To ◽  
...  

2008 ◽  
Vol 38 (6) ◽  
pp. 1559-1573 ◽  
Author(s):  
Kohsaku Uetani ◽  
Miki Hiroi ◽  
Tadamichi Meguro ◽  
Hiroshi Ogawa ◽  
Toshinori Kamisako ◽  
...  

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