Feline herpesvirus (FHV) is the agent of feline viral rhinotracheitis and is distributed
worldwide. The virus belongs to the family Herpesviridae, subfamily Alphaherpesvirinae,
genus Varicellovirus. Although only one serotype is described, the virulence can differ
between viral strains (Gaskell et al. 2007). Some differences can also be observed by
restriction endonuclease analysis of viral DNA (Hamano et al. 2005; Thiry 2006).
FHV is a typical herpesvirus: the genomic double-stranded DNA is packaged into an
icosahedral capsid surrounded by a proteinaceous tegument and a phospholipid envelope. At
least ten different glycoproteins are present on the envelope. FHV grows in both epithelial
cells of the conjunctiva and the upper respiratory tract, and in neurones. The neuronal
infection enables the virus to establish lifelong latency after primary infection. FHV is related
antigenically to canine herpesvirus and phocid herpesviruses 1 and 2, although there is no
known cross species transfer (Gaskell et al., 2006).
The virus is inactivated within 3 hours at 37°C and is susceptible to most commercially
available disinfectants, antiseptics and detergents. At low temperatures, the virus has shown
to remain infective for five months (154 days at 4°C), although its survival is shorter at higher
temperatures (33 days at 25°C, 4-5 minutes at 56°C) (Pedersen, 1987).
The domestic cat is the main host of FHV but the virus has been isolated also from other
felids, including cheetahs and lions, and antibodies have been detected in pumas. There is no
evidence of human infection.
Latent chronic infection is the typical outcome for FHV acute infection and intermittent
reactivation gives rise to viral shedding in oronasal and conjunctival secretions. Apart from in
catteries, contamination of the environment is not a primary source for transmission. Virus
shedding from acutely infected cats and from latently infected cats experiencing reactivation
are the two main sources of infection (Gaskell and Povey, 1982).
Transplacental infection has not been demonstrated in the field. Latently infected queens may
transmit FHV to their offspring because parturition and lactation are typical stress-inducing
factors leading to viral reactivation and shedding. Kittens may therefore acquire FHV
infection at a very early age before vaccination. The outcome depends on the level of
maternally derived antibodies (MDA). When high levels are present, kittens are protected
against disease and develop subclinical infection leading to latency whereas in the absence of
sufficient MDA, clinical disease may follow (Gaskell and Povey, 1992).
In healthy small populations, the prevalence of viral shedding may be less than 1% whereas in
large populations, especially with clinical disease present, prevalence may be up to 10 20%
(Coutts et al., 1994; Binns et al., 2000; Helps et al., 2005). In shelters, risk of contagion is
higher: with only 4% of shedding cats entering the shelter, 50% of cats present may excrete
the virus one week later (Pedersen et al., 2004). This low prevalence is likely to reflect the
intermittent nature of viral shedding during latency.