Inhibition of Vesicular Stomatitis Virus Glycoprotein Expression by Chloroquine

Identification and characterisation of small molecule inhibitors of feline coronavirus replication

“…A number of different mechanisms of action have been suggested to account for the antiviral properties of the compounds identified in this study against other viruses. For chloroquine antiviral effects have been ascribed to inhibition of glycosylation of viral proteins (Savarino et al, 2004) or cellular receptors for viral attachment (Vincent et al, 2005), inhibition of glycoprotein expression (Dille and Johnson, 1982), or inhibition of endosome mediated viral entry (Savarino et al, 2003). The antiviral effect of mefloquine against JC virus has been postulated to be due to its action as an adenosine mimetic (Brickelmaier et al, 2009), while for hexamethylene amiloride it has been suggested antiviral properties against different viruses may arise through competitive inhibition of viral RNA polymerase (Gazina et al, 2011), an indirect mutagenic effect (Levi et al, 2010), or inhibition of viroporins (Wilson et al, 2006).…”

Weak bases affect late stages of Mayaro virus replication cycle in vertebrate cells

“…Dille and Johnson [9] found that when vesicular stomatitis virus (VSV)-infected neuroblastoma cells were treated with chloroquine, the virus glycoproteins reached the Golgi complex but were not transported to the plasma membrane. The observations of Mayaro virus particles inside vacuoles and rare budding processes at the plasma membrane suggest that the same mechanism of inhibition of glycoprotein transport could be operating in the present study.…”

Attenuation of vesicular stomatitis virus infection of brain using antiviral drugs and an adeno-associated virus-interferon vector

“…The 12 compounds tested were chosen based on their previously reported antiviral effects on peripheral or CNS infection of VSV or related viruses: IFN (Detje et al, 2009; Wollmann, Robek, and van den Pol, 2007), ribavirin (Toltzis and Huang, 1986; Willoughby et al, 2005), octyl gallate (Yamasaki et al, 2007), mycophenolic acid (MPA) (Ye et al, 2012), dansylcadaverine (Schlegel et al, 1982), rimantadine (Kolocouris et al, 1996), amantadine (Schlegel et al, 1982; Superti et al, 1985; Willoughby et al, 2005), adenine 9-β-D-arabinofuranoside (Ara-a) (Grant and Sabina, 1972), chloroquine (Dille and Johnson, 1982), acetylsalicylic acid (aspirin) (Chen, Warner, and Reiss, 2000), adenosine (Schnitzlein and Reichmann, 1980), and S-Nitroso-N-acetylpenicillamine (SNAP) (Bi and Reiss, 1995). These drugs act by a variety of mechanisms including interfering with RNA metabolism and replication via nucleoside analogues (ribavirin, Ara-A) or non-nucleoside inhibitors (mycophenolic acid), delaying of viral replication (octyl gallate), inhibition of virus internalization and uncoating (dansylcadaverine, amantadine, rimantadine), G-protein processing (chloroquine), and nitric oxide supply (SNAP).…”