Abstract
Felis catus gammaherpesvirus-1 (FcaGHV1), a novel candidate oncogenic virus, infects cats worldwide. Whether the oropharynx is a site of virus shedding and persistence, and whether oronasal carcinomas harbor FcaGHV1 nucleic acid were investigated. In a prospective molecular epidemiological study, FcaGHV1 DNA was detected by cPCR in oropharyngeal swabs from 26/155 (16.8%) of cats. Oropharyngeal shedding was less frequently detected in kittens ≤3 months of age (5/94, 5.3%) than in older animals; >3 months to ≤1 year: 8/26, 30.8%, (p = 0.001, OR 7.91, 95% CI (2.320, 26.979)); >1 year to ≤6 years: 10/20, 50%, (p < 0.001, OR 17.8 95% CI (5.065, 62.557)); >6 years: 3/15, 33% (p = 0.078). Provenance (shelter-owned/privately owned) was not associated with shedding. In situ hybridization (ISH) identified FcaGHV1-infected cells in salivary glandular epithelium but not in other oronasal tissues from two of three cats shedding viral DNA in the oropharynx. In a retrospective dataset of 11 oronasopharyngeal carcinomas, a single tumor tested positive for FcaGHV1 DNA by ISH, a papillary carcinoma, where scattered neoplastic cells showed discrete nuclear hybridization. These data support the oronasopharynx as a site of FcaGHV1 shedding, particularly after maternal antibodies are expected to decline. The salivary epithelium is identified as a potential site of FcaGHV1 persistence. No evidence supporting a role for FcaGHV1 in feline oronasal carcinomas was found in the examined tumours.
Highlights
Gammaherpesviruses are a subfamily of Herpesviridae that have co-evolved over millennia with a diverse range of mammals
Felis catus gammaherpesvirus 1 (FcaGHV1) is one of several novel gammaherpesviruses recently identified in animals [4–7]
We have investigated whether FcaGHV1 DNA can be detected in secretions and cells shed in the oropharyngeal cavity
Summary
Gammaherpesviruses are a subfamily of Herpesviridae that have co-evolved over millennia with a diverse range of mammals. Factors that precipitate gammaherpesvirus-associated diseases are incompletely understood, but include compromised host immunity in a natural host or “jumping” of a virus from a well-adapted host to a closely related but non-adapted host. Examples of the former include some human. Understanding whether or when such viruses are pathogenic is complicated by the likely sporadic and diverse nature of any associated disease, coupled with high rates of infection among clinically normal animals. Given the frequent detection of FcaGHV1 in healthy cats, it is reasonable to assume that asymptomatic infection is common, with host immunity expected to eliminate the virus from all but a small reservoir of persistently infected cells
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