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Feline Calicivirus: Alan D. R, Karen P. C, Susan D, Carol J. P, Rosalind M. G
Feline Calicivirus: Alan D. R, Karen P. C, Susan D, Carol J. P, Rosalind M. G
Feline calicivirus
University of Liverpool Veterinary Teaching Hospital, Leahurst, Chester High Road, Neston, S. Wirral,
CH64 7TE, United Kingdom
Abstract – Feline calicivirus (FCV) is an important and highly prevalent pathogen of cats. It be-
longs to the family Caliciviridae which includes other significant pathogens of man and animals. As
an RNA virus, high polymerase error rates convey upon FCV a high genome plasticity, and allow the
virus to respond rapidly to environmental selection pressures. This makes the virus very adaptable
and has important implications for clinical disease and its control. Being genetically diverse, FCV
is associated with a range of clinical syndromes from inapparent infections to relatively mild oral
and upper respiratory tract disease with or without acute lameness. More recently, highly virulent
forms of the virus have emerged associated with a systemic infection that is frequently fatal. A pro-
portion of FCV infected cats that recover from acute disease, remain persistently infected. In such
cats, virus evolution is believed to help the virus to evade the host immune response. Such long-
term carriers may only represent a minority of the feline population but are likely to be crucial to
the epidemiology of the virus. Vaccination against FCV has been available for many years and has
effectively reduced the incidence of clinical disease. However, the vaccines do not prevent infection
and vaccinated cats can still become persistently infected. In addition, FCV strain variability means
that not all strains are protected against equally. Much progress has been made in understanding the
biology and pathogenesis of this important feline virus. Challenges for the future will necessarily
focus on how to control the variability of this virus particularly in relation to emerging virulent
strains and vaccination.
Table of contents
1. Aetiology.......................................................................................................... 320
2. Clinical signs..................................................................................................... 321
3. Pathogenesis ..................................................................................................... 322
3.1. FCV-associated oral and upper respiratory tract disease ...................................... 322
3.2. FCV-associated lameness.............................................................................. 322
3.3. FCV-associated virulent systemic disease ......................................................... 322
3.4. Molecular pathogenesis ................................................................................ 324
4. The FCV carrier state .......................................................................................... 325
5. Epidemiology .................................................................................................... 325
6. Prevention, control and vaccination ........................................................................ 326
6.1. Vaccines ................................................................................................... 326
> 20% different based on nucleotide se- 95]. This is reminiscent of rabbit haemor-
quence of capsid region E [84, 87, 88]. rhagic disease virus (RHDV). Retrospec-
Observed genetic variability correlates tive studies have shown that RHDV existed
with earlier serological studies. Most FCV in rabbit populations for many years in a
isolates can be distinguished antigenically. seemingly non-pathogenic form [9,11,70].
However, there appears to be sufficient Then, in the 1980s, highly lethal forms
antigenic overlap between isolates to de- were first reported in China, and have since
fine the viruses as belonging to a single appeared worldwide [58, 72].
diverse serotype [81, 82]. As well as upper respiratory tract dis-
Antigenic and genetic variability is also ease, cats affected by FCV-associated
a feature of other caliciviruses, especially VSD show to varying degrees pyrexia,
the human noroviruses, where highly vari- cutaneous oedema, ulcerative dermatitis,
able genogroups containing multiple geno- anorexia and jaundice, with up to 50%
types are described [2, 34]. The origins of of cats dying or being euthanased in ex-
this diversity are poorly understood. As a tremis. Adult cats are frequently affected
result, studies of the evolution of FCV may more severely than kittens, and worryingly,
shed new light on the diversification of field vaccination does not appear to be pro-
other caliciviruses. tective. Outbreaks start quickly, generally
effect less than 100 animals and disap-
pear rapidly. FCV can be isolated from oral
2. CLINICAL SIGNS or conjunctival swabs of affected cats. So
far, FCV-associated VSD has mainly been
Due to the large number of different reported in the USA. In the UK, one out-
strains of FCV, a range of clinical signs break in 2003 has been described affecting
may be seen. The most characteristic le- a group of five cats in two households [15].
sion is oral ulceration, which may often In addition, the authors are aware of two
go unreported. Ocular and nasal discharge outbreaks in France1 and it is possible that
also frequently occur [8]. Occasionally, in- considerably more outbreaks occur than
apparent infections or pneumonia may also have been reported. VSD has been repro-
be seen. Rarely, and usually in young kit- duced experimentally, strongly supporting
tens, the more severe respiratory infections a role for FCV in this disease [77].
can be fatal [49, 60]. Calicivirus strains Feline calicivirus has also been as-
can also cause an acute febrile lameness sociated with other clinical syndromes
syndrome which has been recreated exper- although these have not been recreated
imentally [20, 75]. It has been suggested experimentally. The most striking associ-
that lameness and oral/respiratory disease ation is with the severe chronic oral dis-
represent two extremes of a clinical con- ease, lymphoplasmacytic gingivitis stom-
tinuum, with some individual strains tend- atitis (LPGS) complex. In some studies,
ing to either extreme, and the majority of approximately 80% of cats with LPGS
strains being able to induce both of these have been shedding FCV compared to 20%
clinical signs [108]. of controls [52, 59, 109]. Although acute
More recently, and more worryingly, faucitis has been reproduced experimen-
highly virulent strains of FCV have tally [91], the chronic disease has not been
emerged that are associated with outbreaks induced in experimental cats [53, 79]. It is
of disease with high mortality and a new therefore likely that factors not associated
range of clinical features (FCV-associated with FCV, including other pathogens [52,
virulent systemic disease (VSD) – previ-
1
ously haemorrhagic-like fever) [42, 43, 77, Poulet H., personal communication.
322 A.D. Radford et al.
59, 116] and host factors [37], may also necrosis of the overlying epithelium and
play a role in this complex and serious syn- infiltration of neutrophils at the periph-
drome. There have been several attempts ery and base [30]. Healing generally takes
to identify consistent genetic and antigenic place over a period of two to three weeks.
differences between FCV isolates from Pulmonary lesions occur more rarely and
cats with LPGS and those from cats with appear to result from an initial focal alve-
other FCV-associated diseases, and these olitis, leading to areas of acute exudative
have met with variable results. Those based pneumonia and then to the development of
on sequencing and monoclonal antibodies a proliferative, interstitial pneumonia. Al-
have failed to identify consistent differ- though primary interstitial pneumonia may
ences [31,33,65]. However, those based on occur with FCV, it is possible that its im-
polyclonal antisera reactivity have shown portance in natural cases of disease has
some differences between those isolates been over emphasised in the past. This is
associated with chronic stomatitis and because many early experimental studies
those associated with other diseases, which used aerosol challenge to infect cats, rather
has been attributed to evolution of these than the more natural oronasal route of in-
FCV isolates in such chronically infected fection.
cats [19, 79].
There has also been some debate about
the role of FCV in feline urinary tract dis- 3.2. FCV-associated lameness
ease [27,92]. Although virus can be visual-
ized in, and isolated from, urine, there are Lesions seen in joints of cats with FCV-
currently no studies demonstrating a clear associated lameness consist of an acute
association between infection and disease. synovitis with thickening of the synovial
membrane and an increase in quantity of
synovial fluid within the joint [20]. Viral
3. PATHOGENESIS antigen has been identified in macrophage-
like cells in the synovial membrane of
Cats can be infected with FCV via the
joints from affected cats [20].
nasal, oral or conjunctival routes. The virus
replicates mainly in the oral and respira-
tory tissues, although some strains vary
in their tissue tropisms and pathogenic- 3.3. FCV-associated virulent systemic
disease
ity, such that virus has also been found
in visceral tissues, faeces and occasionally
in urine. The significance of this to trans- How the pathogenesis of virulent sys-
mission is unknown but is thought to be temic disease (VSD) differs from more
minimal. typical disease is unknown. However, it
is clear that in cases of VSD, virus
gains access to cellular compartments not
3.1. FCV-associated oral and upper normally associated with FCV. Lesions
respiratory tract disease are widespread and include subcutaneous
oedema, ulceration of the mouth, and vari-
Oral ulceration is the most consistent able levels of ulceration of the skin par-
pathological feature of FCV-induced oral ticularly on the pinnae and pawpads and
and upper respiratory tract disease. Ul- nares [77]. Other lesions are more variable
cers begin as vesicles, typically on the and include bronchointerstitial pneumonia
margin of the tongue but also in other lo- and necrosis in the liver, spleen and pan-
cations. These subsequently rupture, with creas. In the most detailed study, viral
Feline calicivirus 323
antigen has been detected in the skin, nasal quenced to date, or indeed a combination
mucosa, lung, pancreas and endothelial of the two. In addition, it may be possible
cells of the dermis associated with necro- to evolve virulence by different mutation
sis [78]. Virus particles were also identified pathways. This may explain slight differ-
by electron microscopy in the cytoplasm ences in the clinical signs and pathology
and nuclei of lytic epithelial cells undergo- observed in the individual outbreaks.
ing vacuolar degeneration in these lesions. Most outbreaks of FCV-associated VSD
In this study, viral antigen was not detected have been associated with the introduction
in the liver of cats despite the presence of of cats from large rescue colonies into an-
pathological lesions. This is in contrast to other population [43]. It is possible that
one study in the UK, in which viral anti- the high levels of replication of normal
gen was found in the liver of jaundiced FCV strains in large groups of cats such
cats [15]. This significance of this discrep- as rescue shelters may provide the required
ancy remains unclear. conditions necessary for the independent
It is interesting to speculate on the emergence of these hypervirulent strains.
mechanism of FCV-associated VSD in This is consistent with theories for the evo-
cats. It is clear that the virus alone is suf- lution of increased virulence in host popu-
ficient to cause the disease as the disease lations with high levels of non-neutralising
has now been re-created experimentally at immunity [29, 61]. Under these conditions,
least twice to the authors’ knowledge. This viral variants that are capable of replicat-
suggests that mutations within the viral ing faster and to higher titres will be more
genome may be responsible for the highly likely to be transmitted and therefore posi-
virulent phenotype. So far, the FCV strains tively selected for. Within the originating
from each reported outbreak of VSD have colony the matched immune response to
been genetically distinct from each other. the virus may damp down these high lev-
Therefore, if viral mutations are required els of virus replication in individual cats
to cause the hyper-virulent phenotype, then and therefore the more virulent forms of
they must evolve independently in each disease are not seen. However, when these
outbreak. Attempts are now being made to virus strains gain access to naïve popula-
identify mutations that are markers of the tions that have not been exposed to that
virulent phenotype. To date, no consistent particular strain before, extreme levels of
genetic motif has been reported within the virus replication lead to the clinical man-
available capsid sequences to differentiate ifestation that is VSD. We have recently
FCV isolates associated with VSD from shown that virus replication in endemi-
those associated with more typical FCV- cally infected colonies of cats is associated
associated disease. However, interestingly, with markedly higher levels of biodiversity
for the two VSD isolates so far sequenced, than those normally seen within a single
there is some suggestion that sequence dif- strain of FCV [14, 90]. This diversity ap-
ferences lead to the acquisition of an extra pears to be driven by immune-mediated
glycosylation site in both cases [1, 28]. positive selection both within individual
This difficulty of identifying clear genomic cats (see carriers below) and associated
markers for VSD is not without precedent with transmission between cats. In addi-
for FCV, in that attempts to identify mark- tion, the high prevalence of FCV in such
ers associated with lameness have also met colonies provides an ideal environment for
with failure [31, 33]. It therefore seems mixed infections. As a result recombina-
likely that any viral mutations associated tion events between strains, similar to those
with VSD are either subtle, or located in a reported for other caliciviruses [7, 46, 50,
different region of the genome to that se- 73], have been identified in such colonies,
324 A.D. Radford et al.
and provide a further mechanism for the di- 3.4. Molecular pathogenesis
versification of viruses [16]. Whether these
evolutionary events are associated with the The study of the molecular mechanism
selection of more virulent, faster replicat- by which FCV induces disease has bene-
ing viral variants remains to be determined. fited considerably from the fact that FCV
As stated previously, each outbreak for grows well in cell culture, and because an
which sequence data is available has been infectious clone is available [101]. This
caused by a distinct strain of FCV. Suc- is in contrast to other members of the
cessive outbreaks are not started by a sin- Caliciviridae such as human noro- and
gle virulent strain of FCV that is being sapoviruses which do not grow in cell cul-
widely transmitted. The reasons why each ture, and where infectious clones are not
outbreak seems to “burn out” as quickly available. This has led to the use of FCV
as it started are unknown but may in- infection as a model of calicivirus molecu-
clude, behavioural mechanisms (dying cats lar biology.
are less likely to transmit virus), disease In cell culture, infected cells show a
control measures instigated during each characteristic cytopathic effect associated
outbreak, and evolved attenuation. These with cell rounding and membrane bleb-
virulent FCV outbreaks represent a clear bing [51]. Under these conditions, infec-
opportunity to explore the mechanisms that tion with FCV leads to an inhibition of cel-
underlie both the evolution of virulence lular protein synthesis (shut-off) associated
and mechanisms of attenuation. One ob- with cleavage of the host translation initia-
vious concern is that the virus will evolve tion factors [117]. Such a mechanism may
to be efficiently transmitted among the cat allow the virus to divert the cellular trans-
population. How likely this is to occur is lation machinery from cap dependant to
unknown, but if it does, the consequences cap-independent translation thereby stop-
would be severe, particularly as current ping translation of cellular mRNAs and
vaccines seem to offer little protection. allowing translation to focus on the viral
VpG-bound RNA. A similar system is also
As well as viral mutations, it is also used by the closely related picornaviruses.
possible that host and immune factors Molecular studies have now shown that
play a role in this disease. It is certainly virus infection in cell culture triggers the
true that not all cats die in each out- mitochondrial pathway, leading to caspase
break. Some have suggested an immune- activation and apoptosis [71,104]. Whether
mediated contribution to the pathogenesis this is what happens in the entire animal
for FCV-associated VSD [15, 28], partly remains unknown.
based on the fact that adult cats seem to A big break through for FCV research
develop more severe disease than young was recently reported when the junctional
animals [43]. A possible immune-mediated adhesion molecule-1 (JAM-1) was iden-
pathogenesis has been shown for other tified as a cellular receptor for FCV in
FCV infections such as lameness [4], and cell culture [62]. Transfection of non-
in some cases, vaccination appears to po- permissive cells with a JAM-1 expression
tentiate FCV infection [17]. system rendered the cell line permissive
Although outbreaks of VSD have only for FCV and anti-feline JAM-1 antibodies
recently been described it is interesting to reduced replication of FCV in permissive
note that several case reports in the past cells. Whether strains of FCV associated
have described similar clinical findings in with different types of disease use different
FCV infected cats including jaundice [26] receptors remains to be determined. In hu-
and sudden death [60]. man noroviruses, different host expression
Feline calicivirus 325
Within the cat population, FCV is cination. In pet cats living in small pop-
present in acutely infected cats and in ulations, this is likely to be sufficient. In
clinically-recovered carrier cats. The virus larger groups of cats, where the prevalence
can also persist in the environment for and amount of virus shed is likely to be
several days to several weeks on dried higher, vaccination needs to be accompa-
surfaces at room temperature, and longer nied by careful management procedures.
in colder wetter conditions [12, 23, 24]. Treatment is non-specific. The control of
Indirect transmission can therefore occur, outbreaks of FCV-associated VSD will be
especially within the close confines of a considered separately.
cattery where secretions may contaminate
cages, feeding and cleaning utensils or per- 6.1. Vaccines
sonnel. It is generally accepted that there
are no known reservoirs or alternative hosts Several types of vaccines are now avail-
for FCV, and in utero transmission does able for FCV. They are generally consid-
not seem to occur. However interestingly, ered to be safe and effective at reduc-
as well as having there own specific ca- ing or preventing classical oral/respiratory
nine calicivirus, FCV-like viruses have also disease, but do not protect against infec-
been isolated from dogs [39, 64, 93]. The tion or the development of the carrier
role of these viruses in the epidemiology state. Evidence from the field suggests that
of FCV in the cat (and dog) is uncertain. the current vaccines do not prevent FCV-
In one study, an association was shown associated VSD with outbreaks occurring
between the presence of dogs and FCV in- in vaccinated cats [15,42,77,95]. However,
fection in cats [5], whilst a second study there is some experimental data to support
has suggested cat households with dogs their use [6, 77]. The impact of vaccina-
have a lower prevalence of FCV infec- tion on LPGS is unclear. Vaccinated cats
tion [40]. certainly develop LPGS and no vaccine
The immune response has a somewhat carries a data sheet claim for preventing
limited impact on FCV infection. It is clear this disease. This is consistent with the un-
that pre-existing immunity, acquired either certain role of FCV in this syndrome.
naturally as maternal-derived antibodies All licensed FCV vaccines are based
(MDA) or artificially following vaccina- on whole viral antigens grown in cell
tion, can reduce or eliminate the clinical culture. Most are monovalent (based on
signs of subsequent FCV challenge. How- a single strain), although recently a bi-
ever, such pre-existing immunity does not valent vaccine has been licensed [80].
prevent infection and these animals may Live-attenuated and inactivated (both ad-
become carriers following sub-clinical in- juvanted and non-adjuvanted) vaccines are
fection with field virus. As with other sig- available in most countries, and are given
nificant pathogens, these “silent-carriers” parenterally. However, in some parts of
are likely to play a crucial role in the the world, live-attenuated vaccines are li-
epidemiology of this disease. There is no censed for intranasal use.
evidence that vaccination will ‘cure’ an ex- Live intranasal vaccines induce local
isting carrier state. mucosal immunity, and this is probably
more effective than immunity induced by
6. PREVENTION, CONTROL parenteral vaccines. However, because the
AND VACCINATION virus replicates at the site of inoculation,
clinical signs such as mild sneezing may
The main-stay of FCV-associated dis- be seen after several days in some individ-
ease control in the cat population is vac- uals [55, 74]. Where available, intranasal
Feline calicivirus 327
vaccines are particularly useful when a which is the USDA-approved FCV chal-
rapid onset of protection is required e.g. for lenge in the USA. It is therefore likely that
a cat going into a boarding cattery or in the shorter durations of immunity/protection
face of an outbreak of disease. In contrast would have been seen with a heterologous
to parenteral vaccines, only a single dose challenge, although how much shorter is
of intranasal vaccine is generally required unknown.
to induce immunity following primary vac- As with most vaccines, there are well
cination. Most published studies have used documented adverse reactions in a minor-
a feline herpesvirus challenge where high ity of cases. Along with other injections,
levels of protection have been shown four adjuvanted vaccines have been associated
days after intranasal vaccination and par- with injection-site reactions and sarco-
tial protection after two [55, 74]. These mas [69]. Parenteral modified-live FCV
vaccines may also overcome MDA better vaccines have been associated with clin-
than parenteral vaccines, although in gen- ical signs in the immediate period post-
eral their use is only licensed in kittens vaccination. Most of these appear to be due
from 12 weeks of age. Live intranasal vac- to coincidental infection with field virus
cines have shown an increase in popularity although in some cases, sequence analy-
amongst some veterinarians, in part due to sis has shown that vaccine virus may be
public concerns about the role of inacti- involved [84, 87]. Vaccine virus has also
vated vaccines in injection site reactions occasionally been detected circulating in
and sarcomas. the cat population, though the significance
Recommended vaccination schedules of this is not yet known [77,88,89]. A third
tend to be of the “traditional” type with potential problem for current vaccines is
a primary course at 8–9 and 12 weeks the antigenic variability of FCV strains,
followed by annual boosters. Some are li- which means that no vaccine is likely to
censed for earlier use [21]. There is now be able to neutralise all field isolates of
evidence to suggest that not all kittens are virus such that occasional vaccine break-
able to respond to vaccination at 12 weeks downs can occur [18]. In order to try and
of age, such that under some circum- circumvent some of these problems, a bi-
stances, later kitten vaccinations may be valent inactivated, non-adjuvanted vaccine
needed to overcome persistent MDA [21, has recently been marketed in Europe [80].
47]. The success of this in controlling disease
As with other small animal vaccines, and in the market place remains to be de-
the requirement for annual booster vacci- termined.
nations is currently being debated. It will The areas where vaccines could be im-
be important to consider the antigenic di- proved seem clear, and pose a considerable
versity of FCV as this debate is developed. challenge. Firstly, it will be important to
Moderate levels of virus neutralizing anti- increase the cross-reactivity of vaccines to
body have been shown to persist in a group maximise the chances of cross-protection,
of vaccinated cats for at least four years, minimise the number of vaccine break-
although after 7.5 years, titers had de- downs, and minimise the possibilities of
clined to low or non-detectable levels [97, evolving vaccine resistant strains [56].
98]. Protection against FCV challenge de- This approach will hopefully help with the
creased from 85% three weeks after vac- control of both typical and more virulent
cination to 63% after 7.5 years. However, forms of disease. The success of specifi-
this study represented a homologous chal- cally including antigens from outbreaks of
lenge, with both the vaccine and the chal- VSD in vaccines to protect against these
lenge virus being based on strain 255, more severe forms of disease is uncertain
328 A.D. Radford et al.
of some help. In some cases, the use of colonies that are known to be free of
appetite stimulants such as diazepam or virus (e.g. research colonies), inactivated
cyproheptadine may also be of some ben- vaccines may be used and animals com-
efit. Some severely affected cases may re- ing into the colony (stud cats, replace-
quire fluid therapy, and where anorexia is ments) should ideally be sourced from
prolonged, an oesophagostomy or gastro- similar FCV-negative colonies, and should
tomy tube may be indicated. be quarantined and tested on several oc-
For some viral diseases of humans, both casions to determine if they are free of
specific and more broad-spectrum thera- the virus. In endemically infected breed-
pies have made it to clinical practice. Spe- ing colonies control is generally aimed
cific antivirals for veterinary pathogens are at reducing clinical disease. Specific mea-
unlikely to be developed in the near fu- sures include reducing stocking density,
ture due to the prohibitive costs. Although early weaning kittens into isolation, and
some broad-spectrum antivirals are effec- early vaccination of kittens. Vaccinating
tive against FCV in cell culture, they are pregnant queens may reduce disease in
too toxic for use in the cat [83]. Interferon young kittens by boosting their MDA [45].
is used by some, although to the authors’ However, the safety of vaccines in preg-
knowledge, published evidence for its ef- nant queens is largely unknown and clin-
fectiveness remains limited to in vitro stud- icians should consult data sheets. Live vac-
ies [106], and it is not licensed for control cines should be avoided, particularly those
of FCV-disease in Europe. Experimental containing live feline parvovirus. It may
trials of chimeric mouse-cat monoclonal be possible to eradicate virus from such
antibodies have shown some promise in colonies by a test and remove strategy.
treatment [111, 112]. However, in practice, this is likely to be ex-
tremely difficult.
6.3. Management of FCV-associated
respiratory disease 6.4. Control of outbreaks
of FCV-associated VSD
In practice, controlling FCV is usually
associated with a similar need to control Diagnosing FCV-associated VSD in the
feline herpesvirus. A more detailed de- cat remains somewhat of a conundrum
scription of the control measures for these since there are no unique clinical or lab-
two pathogens is given elsewhere [30]. oratory markers for the disease. Although
Briefly, the control measures for FCV- the clinical features can be quite striking
associated respiratory disease depend en- with relatively few differential diagnoses,
tirely on the population of cats. For indi- FCV strain variability means that each
vidual household cats where prevalence is outbreak can be associated with slightly
low, vaccination is likely to be sufficient. different clinical signs. The authors are fre-
In boarding and rescue catteries, vacci- quently asked about individual cats with
nation, quarantine facilities, batching of suspicious signs, some of which are also
arrivals, good husbandry/hygiene, well de- FCV positive. Such individual cats must
signed pens which prevent direct contact be treated carefully, but whether these rep-
between cats, and avoiding overcrowding resent actual sporadic cases of VSD is
are critical to minimising viral loads and unknown. The index of suspicion for VSD
the spread of virus through the popula- increases dramatically when two or more
tion. Molecular studies on FCV suggest cats present with the same clinical signs.
that if this is done well, FCV transmis- However, ultimately as we seek to un-
sion can be minimal [88]. In breeding derstand the mechanism of this disease,
330 A.D. Radford et al.
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