Summary of Section 2: Agent Properties:  Feline coronavirus (FCoV) is the causative agent of the serious disease of feline infectious peritonitis (FIP). FCoV is a large, pleomorphic spherical, enveloped virus particle with a single-stranded RNA genome. It is readily inactivated by most disinfectants.  Being an RNA virus, FCoV has a high level of genetic variation due to frequent errors (mutations) during RNA replication. The hypothesis is that genetic variation and subsequent selection facilitate the switching of cell tropism from a mostly mild enteric (less-virulent) FCoV pathotype to an FIP-associated FCoV pathotype. This switch occurs in an infected cat and FIP-associated FCoV systemically replicates efficiently within monocytes/macrophages and can lead to the serious disease of FIP. However, systemic (non-enteric) FCoV infection can also occur in cats without FIP.  The FCoV genome comprises many genes, including those encoding the spike [S], matrix, nucleocapsid, envelope proteins and non-structural accessory proteins 3a, 3b, 3c, 7a and 7b. Mutations in different genes, including the S gene, have been postulated to be associated with the switch to a more virulent FCoV pathotype. The S protein is a particular focus of attention as it mediates entry into feline host cells and has both receptor-binding and fusion functions. Specific mutations in the S gene have been postulated to be associated with FIP-associated FCoV but the definitive genes and mutations involved in the FCoV virulence genetic shift are still unknown.  Type I and type II FCoV are recognised to differ based on antigenic and genomic properties, with type I FCoV being more prevalent. However, type I FCoVs, unlike type II FCoVs, are difficult to grow in cell cultures and thus many in vitro studies are based on the less-common type II FCoV. Type I and II FCoV can both exist as less-virulent FCoV and FIP-associated FCoV.