Modeling neuro-immune interactions during Zika virus infection
Author(s) -
Pinar Mesci,
Ángela Macia,
Christopher N. LaRock,
Leon Tejwani,
Isabella Rodrigues Fernandes,
Nicole A. Suarez,
Paolo Marinho de Andrade Zanotto,
Patrícia Cristina Baleeiro Beltrão-Braga,
Victor Nizet,
Alysson R. Muotri
Publication year - 2017
Publication title -
human molecular genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.811
H-Index - 276
eISSN - 1460-2083
pISSN - 0964-6906
DOI - 10.1093/hmg/ddx382
Subject(s) - zika virus , microglia , immune system , biology , virology , immunology , virus , neuroinflammation , viral replication , inflammation
Although Zika virus (ZIKV) infection is often asymptomatic, in some cases, it can lead to birth defects in newborns or serious neurologic complications in adults. However, little is known about the interplay between immune and neural cells that could contribute to the ZIKV pathology. To understand the mechanisms at play during infection and the antiviral immune response, we focused on neural precursor cells (NPCs)-microglia interactions. Our data indicate that human microglia infected with the current circulating Brazilian ZIKV induces a similar pro-inflammatory response found in ZIKV-infected human tissues. Importantly, using our model, we show that microglia interact with ZIKV-infected NPCs and further spread the virus. Finally, we show that Sofosbuvir, an FDA-approved drug for Hepatitis C, blocked viral infection in NPCs and therefore the transmission of the virus from microglia to NPCs. Thus, our model provides a new tool for studying neuro-immune interactions and a platform to test new therapeutic drugs.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom