High viral loads despite absence of clinical and pathological findings in cats experimentally infected with feline coronavirus (FCoV) type I and in naturally FCoV-infected cats

Abstract

Specified pathogen-free cats were naturally infected with FCoV or experimentally infected with FCoV type I. Seroconversion was determined and the course of infection was monitored by measuring the FCoV loads in faeces, whole blood, plasma and/or monocytes. Tissue samples collected at necropsy were examined for viral load and histopathological changes. Experimentally infected animals started shedding virus as soon as 2 days after infection. They generally displayed the highest viral loads in colon, ileum and mesenteric lymph nodes. Seroconversion occurred 3-4 weeks post infection. Naturally infected cats were positive for FCoV antibodies and monocyte-associated FCoV viraemia prior to death. At necropsy, most animals tested positive for viral shedding and FCoV RNA was found in spleen, mesenteric lymph nodes and bone marrow. Both experimentally and naturally infected cats remained clinically healthy. Pathological findings were restricted to generalized lymphatic hyperplasia. These findings demonstrate the presence of systemic FCoV infection with high viral loads in the absence of clinical and pathological signs.

Sites of feline coronavirus persistence in healthy cats

“…It differs from serotype II FCoV in that it hardly grows in tissue culture (Jacobse-Geels & Horzinek, 1983); however, oral administration of faeces or gut homogenates from shedding cats leads to intestinal infection and monocyte-associated viraemia (Meli et al, 2004).…”

“…In the literature, two FCoV biotypes have been distinguished: feline enteric coronaviruses (FECVs), which are endemic in cat populations and generally not associated with clinical disease, and FIP viruses (FIPVs), which might arise from endemic FECVs either as an in vivo mutation or as virulent strains and are responsible for the development of FIP (Vennema, 1999;Brown et al, 2009;Pedersen et al, 2009;Chang et al, 2010). Regardless of the development of FIP, FCoV spreads from its initial site of infection within the intestine via monocyte-associated viraemia (Gunn-Moore et al, 1998;Kipar et al, 1999Kipar et al, , 2005Meli et al, 2004) and can replicate within monocytes in healthy cats (Can-Sahna et al, 2007). The pathogenesis of FIP is not fully understood, but it has been shown that a monocyte-triggered vasculitis, in association with systemic monocyte and endothelial cell activation, represents the crucial event (Kipar et al, 2005), probably in combination with some antibody-mediated enhancement and complement activation (Dewerchin et al, 2006).…”

“…The pathogenesis of FIP is not fully understood, but it has been shown that a monocyte-triggered vasculitis, in association with systemic monocyte and endothelial cell activation, represents the crucial event (Kipar et al, 2005), probably in combination with some antibody-mediated enhancement and complement activation (Dewerchin et al, 2006). Cats can be FCoV carriers and generally remain healthy, despite systemic infection (Herrewegh et al, 1995;Addie et al, 1996;Gunn-Moore et al, 1998;Kipar et al, 1999;Meli et al, 2004). Previous studies indicate that FCoV persists within the intestine and is shed persistently or intermittently with the faeces (Foley et al, 1997;Herrewegh et al, 1997;Harpold et al, 1999;Meli et al, 2004).…”

“…Cats can be FCoV carriers and generally remain healthy, despite systemic infection (Herrewegh et al, 1995;Addie et al, 1996;Gunn-Moore et al, 1998;Kipar et al, 1999;Meli et al, 2004). Previous studies indicate that FCoV persists within the intestine and is shed persistently or intermittently with the faeces (Foley et al, 1997;Herrewegh et al, 1997;Harpold et al, 1999;Meli et al, 2004). Therefore, persistently infected, healthy carriers are believed to play a key role in the epidemiology of FIP (Foley et al, 1997;Meli et al, 2004).…”

“…Previous studies indicate that FCoV persists within the intestine and is shed persistently or intermittently with the faeces (Foley et al, 1997;Herrewegh et al, 1997;Harpold et al, 1999;Meli et al, 2004). Therefore, persistently infected, healthy carriers are believed to play a key role in the epidemiology of FIP (Foley et al, 1997;Meli et al, 2004).…”