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Animal Models of Human Respiratory Viral Infections
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Kayla A. Weiss, Cory J. Knudson, Allison F. Christiaansen, Steven M. Varga
Two biotypes comprise feline coronaviruses—feline enteric coronavirus (FeCoV) and feline infectious peritonitis virus (FIPV). FeCoV induces asymptomatic disease, whereas FIPV infection causes severe disease with significant mortality. FIPV is able to replicate in macrophages leading to systemic spread of the virus.108
Human Coronaviruses Respiratory Pathogens Revisited as Infectious Neuroinvasive, Neurotropic, and Neurovirulent Agents
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Marc Desforges, Dominique J. Favreau, Élodie Brison, Jessica Desjardins, Mathieu Meessen-Pinard, Hélène Jacomy, Pierre J. Talbot
Feline infectious peritonitis (FIP) is a common cause of death in cats, caused by a highly virulent variant of the feline coronavirus (FCoV), called FIPV, which either represents a naturally distinct circulating virulent form of FCoV (Brown et al. 2009) or which emerges from the less virulent virus feline enteric coronavirus (FECV) after acquiring mutations (Rottier et al. 2005; Vennema et al. 1998). The intestine was identified as the major site of persistence (Meli et al. 2004; Foley et al. 1997), but the virus also persists in macrophages of healthy cats (Kipar et al. 2010). These infected macrophages disseminate systemically and trigger immunological responses, which result in microgranuloma formation, vasculitis, organ failure, and death (Vennema et al. 1998; Poland et al. 1996; Pedersen and Boyle 1980). Neurological FTP may occur in about one cat out of three with FIP disease (Foley et al. 1998; Kline et al. 1994).
Order Nidovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The early coronavirus studies were performed with murine hepatitis virus (MHV), a member of the Murine coronavirus species. Thus, Krijnse Locker et al. (1995) performed the vaccinia virus-driven expression of the MHV gene encoding the membrane glycoprotein M and found that the independently synthesized protein M accumulated in the Golgi apparatus in homomultimeric, detergent-insoluble structures, presumably as part of its retention mechanism. When Opstelten et al. (1995) used the vaccinia virus-driven coexpression of the MHV proteins M and S, the formation of the heteromultimeric M-S complexes was detected in the absence of other coronaviral proteins. Vennema et al. (1996) described the assembly of the MHV envelope independent of a nucleocapsid. The membrane particles containing coronaviral envelope proteins were assembled in and released from animal cells coexpressing the corresponding genes from transfected plasmids. Of the three viral membrane proteins, only two were required for particle formation, namely the membrane glycoprotein M and the small envelope protein E, while the spike protein S was dispensable but was incorporated when present. Therefore, the nucleocapsid protein N was neither required nor taken into the particles when present. The envelope vesicles formed a homogeneous population of spherical particles indistinguishable from authentic coronavirions in size (~100 nm in diameter) and shape but less dense than the virions (Vennema et al. 1996). Remarkably, Maeda et al. (1999) have found that the expression of the MHV protein E alone was sufficient for the VLP production. Godeke et al. (2000) constructed the two chimeric proteins S of MHV and an alphacoronavirus, namely feline infectious peritonitis virus (FIPV), or feline coronavirus (FCoV), a member of the Tegacovirus subgenus, which is described earlier. The chimeric MHV-FIPV proteins S consisted of the ectodomain of the one virus and the transmembrane and endodomain of the other. They were found to assemble only into viral particles of the species from which their C-terminal domain originated. Thus, the 64-terminal-residue sequence sufficed to draw the 1,308 (MHV)- or 1,433 (FIPV)-aa-long mature S protein into the VLPs (Godeke et al. 2000).
Advances in the pharmacological management of bacterial peritonitis
Published in Expert Opinion on Pharmacotherapy, 2021
Daniel Pörner, Sibylle Von Vietinghoff, Jacob Nattermann, Christian P Strassburg, Philipp Lutz
While bacteria are the most common cause of peritonitis, one should be aware that other infectious and noninfectious forms of peritonitis may occur. Viral peritonitis in humans is very uncommon. The few published case reports include peritonitis induced by Cytomegalovirus [6] and Coxsackievirus B virus [7]. Interestingly, in cats, coronavirus can cause a well-known veterinary disease, called feline infectious peritonitis [8]. However, similar conditions have not been described in humans. This applies also to the pandemic SARS coronavirus 2 (SARS-CoV-2). In contrast to viral peritonitis, fungal peritonitis is encountered rarely, but regularly. It occurs almost exclusively in patients with severe immunodeficiency such as AIDS, in patients with liver cirrhosis or on PD. In particular, infection with Cryptococcus neoformans may manifest as peritonitis [9]. In patients with cirrhosis, fungal peritonitis [10] is usually caused by Candida species and associated with a very poor prognosis. Similarly, in patients on PD, fungal peritonitis is most frequently caused by Candida species and usually necessitates at least temporary removal of the peritoneal catheter [11]. However, mortality of fungal peritonitis in patients on PD is lower than in patients with cirrhosis. Noninfectious peritonitis may occur in autoimmune diseases (e.g., systemic lupus erythematodes), after intraperitoneal application of antineoplastic agents or in the case of intraperitoneal bile leakage after injury to the biliary tract.
Can the Coronavirus Disease 2019 (COVID-19) Affect the Eyes? A Review of Coronaviruses and Ocular Implications in Humans and Animals
Published in Ocular Immunology and Inflammation, 2020
Interestingly, 5% of cats affected by FECV will develop feline infectious peritonitis (FIP).35 Apart from the tropism toward epithelial cells in the gut, a small proportion of FECV can affect monocytes as well. It has been suggested that within the monocytes, the FECV acquires mutations in the genome which result in the transformation to FIPV.36 The FIPV then display an altered cell tropism, infecting monocytes and macrophages more efficiently as compared to FECV. These cells play a pivotal role in the drastically different clinical manifestation of the disease. The FIP disease is characterized by fibrinous and granulomatous serositis, protein-rich serous effusion in body cavities and granulomatous lesions. It has been suggested that the underlying pathogenic mechanism is a vasculitis triggered by the infected monocytes and macrophages leading to endothelial barrier dysfunction and extravasation of these immune cells into the tissue.37 These lesions are multi-systemic and lead to an extremely poor prognosis of the infected felines. Those affected had fever, loss of appetite, and weight loss. The majority of felines who have been experimentally infected with FIPV died within 4–5 weeks.38
The ocular surface, coronaviruses and COVID‐19
Published in Clinical and Experimental Optometry, 2020
Mark Dp Willcox, Karen Walsh, Jason J Nichols, Philip B Morgan, Lyndon W Jones
For the less pathogenic human coronaviruses, hCoV‐229E uses CD13 to infect cells,25 OC43 and HKU1 bind to 9‐O‐acetylated sialic acid (Neu5,9Ac2),26 and NL63 uses ACE2 to bind to host cells.27 NL63 and SARS‐CoV first anchor to cells via heparan sulfate proteoglycans before interacting with the ACE2 entry receptor,201119,27,28 but this binding alone is not sufficient for infection.19 In fact many viruses, not just coronaviruses, utilise heparan sulfate on cell surfaces for initial binding.29 Feline infectious peritonitis virus uses CD13 (aminopeptidase N) or CD209 to bind to its host cells.15 Bovine coronavirus binds to 9‐O‐acetylated sialic acid on its host cells.30