{Reference Type}: Journal Article
{Title}: Zika Virus Exploits Lipid Rafts to Infect Host Cells.
{Author}: Peruzzu D;Amendola A;Venturi G;de Turris V;Marsili G;Fortuna C;Fecchi K;Gagliardi MC;Peruzzu D;Amendola A;Venturi G;de Turris V;Marsili G;Fortuna C;Fecchi K;Gagliardi MC;
{Journal}: Viruses
{Volume}: 14
{Issue}: 9
{Year}: 09 2022 16
{Factor}: 5.818
{DOI}: 10.3390/v14092059
{Abstract}: 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.