Differential effect of cholesterol on type I and II feline coronavirus infection

Takano, Tomomi; Satomi, Yui; Oyama, Yuu; Doki, Tomoyoshi; Hohdatsu, Tsutomu

doi:10.1007/s00705-015-2655-0

Cited by 18 publications

(22 citation statements)

References 36 publications

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“…However, a few studies on type I FCoV have been performed because of its low replication ability in feline cell lines. We previously reported that type I FCoV is closely associated with cholesterol throughout the viral life cycle (Takano et al, 2016). We also confirmed that an increase in plasma membrane cholesterol enhances type I FCoV infection.…”

Section: Introductionsupporting

confidence: 85%

“…In contrast to type I FCoV, no inhibitory effects of U18666A on type II FCoV replication were noted. We previously reported that type I FCoV infection is dependent on plasma membrane cholesterol, but type II FCoV does not (Takano et al, 2016). Our findings of the present and previous studies suggest that type I FCoV requires cholesterol to infect cells, but type II FCoV does not require cholesterol for its infection.…”

Section: Discussionsupporting

confidence: 62%

“…In this study, U18666A did not inhibit type II FCoV and type II CCoV production. On the contrary, it was previously reported that MbCD, a cholesterol extracting agents, inhibited type II CCoV but not type II FCoV (Pratelli and Colao, 2015;Takano et al, 2016). MbCD disrupts cholesterol-and caveolin-rich membrane domain (caveolae) (D'Alessio et al, 2005).…”

Section: Discussionmentioning

confidence: 87%

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The cholesterol transport inhibitor U18666A inhibits type I feline coronavirus infection

et al. 2017

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Feline infectious peritonitis (FIP) is a feline coronavirus (FCoV)-induced fatal disease in wild and domestic cats. FCoV exists in two serotypes. Type I FCoV is the dominant serotype worldwide. Therefore, it is necessary to develop antiviral drugs against type I FCoV infection. We previously reported that type I FCoV is closely associated with cholesterol throughout the viral life cycle. In this study, we investigated whether U18666A, the cholesterol synthesis and transport inhibitor, shows antiviral effects against type I FCoV. U18666A induced cholesterol accumulation in cells and inhibited type I FCoV replication. Surprisingly, the antiviral activity of U18666A was suppressed by the histone deacetylase inhibitor (HDACi), Vorinostat. HDACi has been reported to revert U18666A-induced dysfunction of Niemann-Pick C1 (NPC1). In conclusion, these findings demonstrate that NPC1 plays an important role in type I FCoV infection. U18666A or other cholesterol transport inhibitor may be considered as the antiviral drug for the treatment of cats with FIP.

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Section: Introductionsupporting

confidence: 85%

Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 87%

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The cholesterol transport inhibitor U18666A inhibits type I feline coronavirus infection

et al. 2017

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“…Cholesterol is an essential component of lipid rafts, and it plays important roles in various aspects of the virus life cycle, especially viral entry [15]. In particular, the successful entry of enveloped viruses including many coronaviruses requires the presence of cholesterol in either the viral and cellular membranes or both [3,5,[10][11][12]16]. However, the potential relationship between cholesterol and PDCoV replication remains undetermined.…”

mentioning

confidence: 99%

Cholesterol is important for the entry process of porcine deltacoronavirus

Jeon

Lee

2018

Arch Virol

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The present study was conducted to examine whether cellular and/or viral cholesterol levels play a role in porcine deltacoronavirus (PDCoV) replication. Our results showed that depletion of cholesterol from cells or virions by treating them with methyl-β-cyclodextrin (MβCD) diminished PDCoV infection in a dose-dependent manner. The addition of exogenous cholesterol to MβCD-treated cells or virions moderately restored PDCoV infectivity. Furthermore, the pharmacological sequestration of cellular or viral cholesterol efficiently blocked both virus attachment and internalization. Taken together, the current data indicate that the cholesterol present in the cell membrane and viral envelope contributes to PDCoV replication by acting as a key component in viral entry.

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“…Unlike these drugs, voriconazole and fluconazole may be unable to bind SDD. On the other hand, it was suggested that itraconazole, posaconazole, U18666A, and 25-hydroxycholesterol interfere with the binding of type I FCoV to NPC1, in addition to inducing cholesterol accumulation, by binding SDD [48]. However, in cells treated with SDD-binding cholesterol, type I FCoV infection increased.…”

Section: Discussionmentioning

confidence: 99%

Endocytic Pathway of Feline Coronavirus for Cell Entry: Differences in Serotype-Dependent Viral Entry Pathway

2019

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Feline coronavirus (FCoV) is a pathogen causing a lethal infectious disease in cats, feline infectious peritonitis. It has two serotypes (type I FCoV and type II FCoV). According to our previous study, type I FCoV infection is inhibited by compounds inducing intracellular cholesterol accumulation, whereas type II FCoV infection is not inhibited. Intracellular cholesterol accumulation was reported to disrupt late endosome function. Based on these findings, types I and II FCoV are considered to enter the cytosol through late and early endosomes, respectively. We investigated whether the antiviral activities of a late endosome trafficking inhibitor and cholesterol-accumulating agents are different between the FCoV serotypes. The late endosome trafficking inhibitor did not inhibit type II FCoV infection, but it inhibited type I FCoV infection. Type I FCoV infection was inhibited by cholesterol-accumulating triazoles, but not by non-cholesterol-accumulating triazoles. These phenomena were observed in both feline cell lines and feline primary macrophages. This study provides additional information on the differences in intracellular reproductive cycle between type I and type II FCoV.

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Differential effect of cholesterol on type I and II feline coronavirus infection

Cited by 18 publications

References 36 publications

The cholesterol transport inhibitor U18666A inhibits type I feline coronavirus infection

The cholesterol transport inhibitor U18666A inhibits type I feline coronavirus infection

Cholesterol is important for the entry process of porcine deltacoronavirus

Endocytic Pathway of Feline Coronavirus for Cell Entry: Differences in Serotype-Dependent Viral Entry Pathway

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