Several flaviviruses such as Hepatitis C virus, West Nile virus, Dengue virus and Japanese Encephalitis virus exploit the raft platform to enter host cells whereas the involvement of
lipid rafts in Zika virus-host cell interaction has not yet been demonstrated.
Zika virus disease is caused by a flavivirus transmitted by Aedes spp. Mosquitoes, although other mechanisms such as
blood transfusion, sexual and maternal-fetal transmission have been demonstrated. Symptoms are generally mild, such as
fever,
rash,
joint pain and
conjunctivitis, but neurological complications, including
Guillain-Barré syndrome, have been associated to this
viral infection. During pregnancy, it can cause
microcephaly and other
congenital abnormalities in the fetus, as well as
pregnancy complications, representing a serious health threat. In this study, we show for the first time that Zika virus employs
cell membrane lipid rafts as a portal of entry into Vero cells. We previously demonstrated that the antifungal drug
Amphotericin B (
AmphB) hampers a microbe-host cell interaction through the disruption of
lipid raft architecture. Here, we found that
Amphotericin B by the same mechanism of action inhibits both Zika virus cell entry and replication. These data encourage further studies on the
off-label use of
Amphotericin B in Zika virus
infections as a new and alternate
antiviral therapy.