Chloroquine can also impair another early stage of virus replication by interfering with the pH-dependent endosome-mediated viral entry of enveloped viruses such as Dengue virus or Chikungunya virus [60,61]. Due to the alkalisation of endosomes, chloroquine was an effective in vitro treatment against Chikungunya virus when added to Vero cells prior to virus exposure [30]. The mechanism of inhibition likely involved the prevention of endocytosis and/or rapid elevation of the endosomal pH and abrogation of virus–endosome fusion. A pH-dependant mechanism of entry of coronavirus into target cells was also reported for SARS-CoV-1 after binding of the DC-SIGN receptor [62]. The activation step that occurs in endosomes at acidic pH results in fusion of the viral and endosomal membranes leading to the release of the viral SARS-CoV-1 genome into the cytosol [63]. In the absence of antiviral drug, the virus is targeted to the lysosomal compartment where the low pH, along with the action of enzymes, disrupts the viral particle, thus liberating the infectious nucleic acid and, in several cases, enzymes necessary for its replication [64]. Chloroquine-mediated inhibition of hepatitis A virus was found to be associated with uncoating, thus blocking its entire replication cycle [22].