Introduction: In Brazil, in 2016, around 91,000 cases of Zika were reported. In addition to neurological complications, ZIKV infection can also cause major short- or long-term cardiovascular disorders. Therefore, our aim is to evaluate the vascular responses in mice submitted to Zika virus infection and the molecular mechanisms that mediated them. Methods: Male SV129 mice deficient for the type I interferon receptor (IFN?/?R-/-) (8-12 weeks of age) were intravenously (tail vein) infected with 4x103 plaque-forming units (PFU) of ZIKV HS- 2015-BA-01. The control group received only vehicle (saline) by the same route. These animals were divided into three experimental groups: MOCK (control), IFN?/?R-/- 3 and 5 days after ZIKV infection. The interference of ZIKV on vascular reactivity was evaluated in thoracic aortas from the aforementioned groups. Results: Our preliminary data demonstrated that ZIKV infection leads to a significant loss of body weight (20%) when compared to the control group. In the infected group, a lower intake of standard diet and water was also detected. However, no change in the adiposity index was observed. In addition, the animals infected were hypotensive on the third day after the infection, which re-established itself on the fifth day. Interestingly, in vascular reactivity, the ZIKV 5D group is hyperreactive when compared to the control group, in the face of contractile stimulation by Potassium Chloride (KCl). In the phenylephrine-induced vasoconstriction, the ZIKV 3D group, in the presence of endothelium, showed no difference compared to the control. Surprisingly, in the absence of endothelium, ZIKV contraction did not modify. This difference was not seen on the fifth day of infection. Conclusion: Together, our preliminary data suggest that both the release of vasoconstrictor substances and vasodilators may be impaired in the group ZIKV. This alteration of vascular response depends on the time of infection and the signaling pathway studied.
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