Zika viruses of African and Asian lineages cause fetal harm in a mouse model of vertical transmission

by Anna S. Jaeger, Reyes A. Murrieta, Lea R. Goren, Chelsea M. Crooks, Ryan V. Moriarty, Andrea M. Weiler, Sierra Rybarczyk, Matthew R. Semler, Christopher Huffman, Andres Mejia, Heather A. Simmons, Michael Fritsch, Jorge E. Osorio, Jens C. Eickhoff, Shelby L. O’Connor, Gregory D. Ebel, Thomas C. Friedrich, Matthew T. Aliota

Congenital Zika virus (ZIKV) infection was first linked to birth defects during the American outbreak in 2015/2016. It has been proposed that mutations unique to the Asian/American-genotype explain, at least in part, the ability of Asian/American ZIKV to cause congenital Zika syndrome (CZS). Recent studies identified mutations in ZIKV infecting humans that arose coincident with the outbreak in French Polynesia and were stably maintained during subsequent spread to the Americas. Here we show that African ZIKV can infect and harm fetuses and that the S139N substitution that has been associated with the American outbreak is not essential for fetal harm. Our findings, in a vertical transmission mouse model, suggest that ZIKV will remain a threat to pregnant women for the foreseeable future, including in Africa, Southeast Asia, and the Americas. Additional research is needed to better understand the risks associated with ZIKV infection during pregnancy, both in areas where the virus is newly endemic and where it has been circulating for decades.

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