ABSTRACT
In 2002, a severe-to-fatal respiratory disease began in China and was named severe acute respiratory syndrome (SARS). The causative agent was soon found to be a coronavirus and was named SARS-coronavirus (SARS-CoV). Infection was traced to contact with live palm civet cats or raccoon dogs in live animal food markets (“wet markets”) and later, person-to-person. Visiting these markets or restaurants housing these animals before preparing them for customer consumption were among the risk factors for infection in addition to frequent use of taxis and comorbidities. After its initial appearance, SARS spread rapidly through parts of Asia and then to countries around the world before almost completely disappearing in 2003. It caused 8096 cases and 774 deaths. SARS-CoV is a betacoronavirus linage B. The single-stranded RNA genome of coronaviruses is the largest among RNA viruses. The size of the genome, the inaccuracy of replication in most coronaviruses, and homogenous and heterogenous genetic recombination contribute to the high frequency of mutation. The viral spike (S) protein binds to angiotensin-converting enzyme 2 on the host cell before entry. Mutations in the S protein make a substantial contribution to viral transmission to additional host species and cell types in addition to viral virulence as the virus adapted to its new hosts. Interestingly, SARS-CoV isolates from the initial stages of the 2002–2003 epidemic were more virulent than those isolated later and are associated with a 29-nucleotide deletion in the S protein gene. Several insectivorous Chinese bats appear to serve as reservoir hosts for the ancestorial coronavirus. New forms of protection against infection were implemented in China and some other countries and include wearing face masks, thermal screening, and avoiding travel in taxis and public transportation. Their effectiveness in decreasing transmission and the rapid end of the epidemic is unknown.
ABSTRACT
We conducted an exploratory serological survey to evaluate the exposure of Bornean wild carnivores to several viruses common to domestic felids, at interface areas between protected forest and industrial agriculture in the Kinabatangan floodplain (Sabah, Malaysia). Blood samples, collected from wild carnivores (n = 21) and domestic cats (n = 27), were tested for antibodies against feline coronavirus (FCoV), feline panleukopenia virus (FPLV), feline herpesvirus (FHV) and feline calicivirus (FCV), using commercial enzyme-linked immunosorbent assay (ELISA) test kits. Anti-FCoV antibodies were detected in most species, including one flat-headed cat (Prionailurus planiceps, [1/2]), leopard cats (Prionailurus bengalensis, [2/5]), Malay civets (Viverra tangalunga, [2/11]) and domestic cats (Felis catus, [2/27]). Anti-FCV antibodies were present in all domestic cats and one flat-headed cat, while anti-FPLV antibodies were identified in Sunda clouded leopards (Neofelis diardi, [2/2]), domestic cats [12/27] and Malay civets [2/11]. Anti-FHV antibodies were only detected in domestic cats [2/27]. Our findings indicate pathogen transmission risk between domestic and wild carnivore populations at the domestic animal-wildlife interface, emphasizing the concern for wildlife conservation for several endangered wild carnivores living in the area. Special consideration should be given to species that benefit from their association with humans and have the potential to carry pathogens between forest and plantations (e.g., Malay civets and leopard cats). Risk reduction strategies should be incorporated and supported as part of conservation actions in human-dominated landscapes.