Abstract
Background:The outbreak of Zika virus (ZIKV) infection in Brazil has raised concerns that infection during pregnancy could cause microcephaly and other severe neurodevelopmental malformations in the fetus. The mechanisms by which ZIKV causes fetal abnormalities are largely unknown. The importance of pre-infection with dengue virus (DENV), or other flaviviruses endemic to Brazil, remains to be investigated. It has been reported that antibodies directed against DENV can increase ZIKV infectivity by antibody dependent enhancement (ADE), suggesting that a history of prior DENV infection might worsen the outcome of ZIKV infection.Methods:We used bioinformatics tools to design 18 peptides from the ZIKV envelope containing predicted HLA-I T-cell epitopes and investigated T-cell cross-reactivity between ZIKV-infected individuals and DENV-vaccinated subjects by IFNγ ELISPOT.Results:Three peptides induced IFNγ production in both ZIKV-infected subjects and in DENV-vaccinated individuals. Flow cytometry indicated that 1 ZIKV peptide induced a CD4+ T-cell response in DENV-vaccinated subjects.Conclusions:We demonstrated that vaccination against DENV induced a T-cell response against ZIKV and identified one such CD4+ T-cell epitope. The ZIKV-reactive CD4+ T cells induced by DENV vaccination and identified in this study could contribute to the appearance of cross-reactive antibodies mediating ADE.
Highlights
Zika virus (ZIKV) infection was first identified in the Ziika forest of Uganda in 1947 [1]
This virus is a member of the Flaviviridae, a family of viruses that includes Yellow Fever (YF), West Nile, and Dengue viruses (DENV), and ZIKV can be transmitted via mosquito bites, through sexual contact or blood transfusions, or from an infected pregnant woman to her developing fetus
Three different studies performed in French Polynesia, Rio de Janeiro, and Bahia have estimated the risk of microcephaly to be between 0.95% and 29% for pregnant women infected with ZIKV [10,11,12,13]
Summary
Zika virus (ZIKV) infection was first identified in the Ziika forest of Uganda in 1947 [1] This virus is a member of the Flaviviridae, a family of viruses that includes Yellow Fever (YF), West Nile, and Dengue viruses (DENV), and ZIKV can be transmitted via mosquito bites, through sexual contact or blood transfusions, or from an infected pregnant woman to her developing fetus. The recent epidemic of ZIKV in Brazil has raised concerns that ZIKV infection during pregnancy www.PaiJournal.com could cause severe neurodevelopmental malformations in the fetus, including microcephaly [2, 3]. The outbreak of Zika virus (ZIKV) infection in Brazil has raised concerns that infection during pregnancy could cause microcephaly and other severe neurodevelopmental malformations in the fetus. It has been reported that antibodies directed against DENV can increase ZIKV infectivity by antibody dependent enhancement (ADE), suggesting that a history of prior DENV infection might worsen the outcome of ZIKV infection
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