Feline Coronaviruses

Tekes, Gergely; Thiel, Heinz-Jürgen

doi:10.1016/bs.aivir.2016.08.002

Cited by 124 publications

(80 citation statements)

References 121 publications

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“…We next evaluated the capacity of the PDF-2180 chimera to infect cells of the digestive tract. While uncommon in humans, several animal CoVs have been shown to cause severe disease via the enteric pathway (23,24). In addition, most bat CoV sequences, including PDF-2180-CoV, were isolated from bat guano samples, suggesting an enteric etiology.…”

Section: Mers-uganda Spike Replicates In Human Cellsmentioning

confidence: 99%

Trypsin Treatment Unlocks Barrier for Zoonotic Bat Coronavirus Infection

Menachery

Dinnon

Yount

et al. 2020

J Virol

184

170

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Traditionally, the emergence of coronaviruses (CoVs) has been attributed to a gain in receptor binding in a new host. Our previous work with severe acute respiratory syndrome (SARS)-like viruses argued that bats already harbor CoVs with the ability to infect humans without adaptation. These results suggested that additional barriers limit the emergence of zoonotic CoV. In this work, we describe overcoming host restriction of two Middle East respiratory syndrome (MERS)-like bat CoVs using exogenous protease treatment. We found that the spike protein of PDF2180-CoV, a MERS-like virus found in a Ugandan bat, could mediate infection of Vero and human cells in the presence of exogenous trypsin. We subsequently show that the bat virus spike can mediate the infection of human gut cells but is unable to infect human lung cells. Using receptor-blocking antibodies, we show that infection with the PDF2180 spike does not require MERS-CoV receptor DPP4 and antibodies developed against the MERS spike receptor-binding domain and S2 portion are ineffective in neutralizing the PDF2180 chimera. Finally, we found that the addition of exogenous trypsin also rescues HKU5-CoV, a second bat group 2c CoV. Together, these results indicate that proteolytic cleavage of the spike, not receptor binding, is the primary infection barrier for these two group 2c CoVs. Coupled with receptor binding, proteolytic activation offers a new parameter to evaluate the emergence potential of bat CoVs and offers a means to recover previously unrecoverable zoonotic CoV strains. IMPORTANCE Overall, our studies demonstrate that proteolytic cleavage is the primary barrier to infection for a subset of zoonotic coronaviruses. Moving forward, the results argue that both receptor binding and proteolytic cleavage of the spike are critical factors that must be considered for evaluating the emergence potential and risk posed by zoonotic coronaviruses. In addition, the findings also offer a novel means to recover previously uncultivable zoonotic coronavirus strains and argue that other tissues, including the digestive tract, could be a site for future coronavirus emergence events in humans.

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Section: Mers-uganda Spike Replicates In Human Cellsmentioning

confidence: 99%

Trypsin Treatment Unlocks Barrier for Zoonotic Bat Coronavirus Infection

Menachery

Dinnon

Yount

et al. 2020

J Virol

184

170

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“…Feline coronaviruses (FCoVs) belong to the genus alphacoronavirus in the family Coronaviridae . As a ubiquitous viral pathogen among domestic and wild feline populations, FCoV can be horizontally transmitted via the fecal-oral route with persistent infection, and the prevalence and seropositivity in multi-cat households or shelters may achieve 90% 1 , 2 . With regard to pathogenicity, FCoV exists as two biotypes, namely feline enteric coronavirus (FECV) and feline infectious peritonitis virus (FIPV) 3 .…”

Section: Introductionmentioning

confidence: 99%

Nanoparticulate vacuolar ATPase blocker exhibits potent host-targeted antiviral activity against feline coronavirus

Chang

Fang

et al. 2017

Sci Rep

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Feline infectious peritonitis (FIP), caused by a mutated feline coronavirus, is one of the most serious and fatal viral diseases in cats. The disease remains incurable, and there is no effective vaccine available. In light of the pathogenic mechanism of feline coronavirus that relies on endosomal acidification for cytoplasmic entry, a novel vacuolar ATPase blocker, diphyllin, and its nanoformulation are herein investigated for their antiviral activity against the type II feline infectious peritonitis virus (FIPV). Experimental results show that diphyllin dose-dependently inhibits endosomal acidification in fcwf-4 cells, alters the cellular susceptibility to FIPV, and inhibits the downstream virus replication. In addition, diphyllin delivered by polymeric nanoparticles consisting of poly(ethylene glycol)-block-poly(lactide-co-glycolide) (PEG-PLGA) further demonstrates an improved safety profile and enhanced inhibitory activity against FIPV. In an in vitro model of antibody-dependent enhancement of FIPV infection, diphyllin nanoparticles showed a prominent antiviral effect against the feline coronavirus. In addition, the diphyllin nanoparticles were well tolerated in mice following high-dose intravenous administration. This study highlights the therapeutic potential of diphyllin and its nanoformulation for the treatment of FIP.

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“…In some cats, pleural effusion and ascitic fluid accumulated (Pedersen NC, 2009). The FCoV virion is mainly composed of nucleocapsid (N), envelope (E), membrane (M), and peplomer spike (S) proteins (Tekes and Thiel, 2016). FECV and FIPV are classified into 2 serotypes, type I and II FCoV, based on differences in the amino acid sequence of S protein (Motokawa et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Differential induction of type I interferon by type I and type II feline coronaviruses in vitro

Doki

Yabe

Takano

et al. 2018

Research in Veterinary Science

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A B S T R A C TFeline infectious peritonitis (FIP) is a feline coronavirus (FCoV)-induced fatal disease in wild and domestic cats. There are two FCoV serotypes. Both type I and II FCoV can replicate in Felis catus whole fetus (fcwf)-4 cells, but the replicability of type I FCoV in feline cell lines is lower than that of type II FCoV, the reason for which is unclear. Inhibition of IFNβ production by non-structural and structural proteins, excluding spike protein has been reported in many coronavirus infections. In this study, we investigated whether IFNβ is involved in the difference in replicability in feline cell lines between types I and II FCoV. When fcwf-4 cells were infected with FCoV, the virus titer of type II FCoV in the culture supernatant was higher than that of type I FIPV. When the IFNβ expression level in FCoV-infected fcwf-4 cells was semi-quantitatively analyzed, infection with type I FIPV, excluding type I FIPV UCD-1, highly induced IFNβ expression. In contrast, induction of IFNβ by type II FCoV infection was significantly lower than that by type I FIPV. In addition, when fcwf-4 cells were adsorbed by FIPV and then stimulated with Poly(I:C), type II FCoV infection inhibited Poly(I:C)-induced IFNβ gene expression. Also, the proliferation of type I FIPV was enhanced by a IFN inhibitor. These findings clarified that, unlike type I FIPV, type II FCoV strongly inhibits IFNβ expression in infected cells. It was also suggested that the IFNβ-inducing ability is different among type I FIPV strains.

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Feline Coronaviruses

Cited by 124 publications

References 121 publications

Trypsin Treatment Unlocks Barrier for Zoonotic Bat Coronavirus Infection

Trypsin Treatment Unlocks Barrier for Zoonotic Bat Coronavirus Infection

Nanoparticulate vacuolar ATPase blocker exhibits potent host-targeted antiviral activity against feline coronavirus

Differential induction of type I interferon by type I and type II feline coronaviruses in vitro

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