Science Immunology

Supplementary Materials

Supplementary Material for:

Type I interferons instigate fetal demise after Zika virus infection

Laura J. Yockey, Kellie A. Jurado, Nitin Arora, Alon Millet, Tasfia Rakib, Kristin M. Milano, Andrew K. Hastings, Erol Fikrig, Yong Kong, Tamas L. Horvath, Scott Weatherbee, Harvey J. Kliman, Carolyn B. Coyne, Akiko Iwasaki*

*Corresponding author. Email: akiko.iwasaki{at}yale.edu

Published 5 January 2018, Sci. Immunol. 2, eaao1680 (2017)
DOI: 10.1126/sciimmunol.aao1680

This PDF file includes:

  • Methods
  • Fig. S1. ISG expression is elevated in Ifnar1+/− placentas and fetuses but not in Irf3−/−Irf7−/− after ZIKV infection.
  • Fig. S2. Ifnar1−/− placentas harbor more infectious ZIKV compared with Ifnar1+/− littermates.
  • Fig. S3. Global gene expression analysis reveals elevated ISG levels in infected Ifnar1+/− placentas.
  • Fig. S4. ZIKV infection of the maternal-fetal interface is restricted to the decidua.
  • Fig. S5. Placental architecture of Ifnar1+/− fetuses is normal at E9.5 but disrupted at E11.5 and E12.5.
  • Fig. S6. Labyrinth of Ifnar1+/− placenta exhibits decreased fetal endothelial cells.
  • Fig. S7. Ifnar1+/− but not Ifnar1−/− fetuses are resorbed after subcutaneous infection with Brazilian ZIKV.
  • Table S1. Primers for mouse qPCR.
  • Table S2. Top differentially regulated genes and pathways in ZIKV-infected Ifnar1+/− versus Ifnar1−/− placentas.
  • Legend for table S3
  • References (56—61)

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Other Supplementary Material for this manuscript includes the following:

  • Table S3 (Microsoft Excel format). Individual values included in all graphs.

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