- •Clinical outcomes in FIV-infected cats are variable and poorly defined. The immunodeficiency that accompanies infection can, and often does, remain subclinical.
- •FIV infection is lifelong. Serology is the first-line diagnostic test to identify infected cats. PCR is available for confirmation if required.
- •Viral, host, and environmental factors that influence prognosis in individual FIV-infected cats are unclear. Reliable surrogate markers to predict clinical progression are not available.
- •Key to the management of FIV-infected cats is preventive health care and early detection and investigation of clinical problems.
- •A commercial FIV vaccine is available in only a few regions including Australia, New Zealand, and Japan. Interference with diagnostic testing by the commercial FIV vaccine is largely resolved, but vaccine efficacy in the field remains questionable. FIV vaccination is classified as noncore by WSAVA Vaccination Guidelines Group.
Discovery and Origins
- •FIV was discovered in Petaluma, California, USA in 1986 in group-housed cats displaying signs suggesting an underlying immunodeficiency [].
- •FIV originated among wild felids in Africa between 5 and 2.5 million years ago, disseminated through the Panthera lineage and ancestors of the African lion, then globally among New World cats as species-specific strains [].
- ○FIV-Fca (the FIV strain infecting domestic cats, Felis catus), as inferred by comparative genomic analyses, has a more recent evolutionary origin, having been in coexistence with its host for much shorter period than FIV strains infecting wild cats (eg, FIV-Pca, FIV-Ppa).
- •FIV is genetically more closely related to ungulate retroviruses (equine infectious anemia virus, bovine immunodeficiency virus, caprine arthritis and encephalitis virus), but resembles primate lentiviruses in its ability to cause a clinical immunodeficiency [].
Virion Structure and Genomic Organization
- •FIV belongs to the family Retroviridae, subfamily Orthoretrovirinae, genus Lentivirus.
- •The FIV virion is an enveloped, spherical particle that contains 2 copies of a positive-stranded RNA within the viral core (Fig. 1).
- •The genome contains approximately 9400 nucleotides comprising 3 major genes: gag, pol, and env [] (Fig. 2).
- ○Additional accessory and regulatory genes (vif, orf-A, and rev) have a role in viral replication, trafficking of viral RNA from the nucleus to cytosol, virus release, and defense against host restriction factors.
- •The envelope bears heavily glycosylated proteins (Env) that interact with cellular receptor for the virus. Mutations within the env gene facilitate immune evasion [].
Viral Diversity on the Population Level
- •FIV-Fca forms a phylogenetically diverse group of viruses distributed among domestic cats worldwide []. Based on sequence diversity of a highly variable V3-V5 region of env, FIV is classified into 5 subtypes (clades), A to E []. Diversity can reach 26% between isolates and likely reflects independent viral coevolution in different geographic areas (Fig. 3).ABCD. Feline Immunodeficiency Virus ABCD guidelines on prevention and management.
- •Clinical significance of specific subtypes has not been determined in natural infections. There is no convincing evidence that one subtype is more pathogenic than the other.
- •Genetic diversity is generated by point mutations, introduced by an error-prone reverse transcriptase (RT) and recombination between viral variants [,].
- ○Recombination can occur between viral variants of the same or different subtypes. Recombination is facilitated by the (1) presence of 2 RNA molecules within each virion and (2) the ability of RT to switch between the 2 RNA genomes during provirus formation.
- ○Concurrent infection of the host with different strains of the virus may lead to the emergence of novel variants with altered properties such as pathogenicity or infectivity.
Intrahost Viral Diversity and Intrahost Evolution
- •FIV exists within the host as closely related variants referred to as viral quasi-species that collectively contribute to the characteristics of the viral population [].
- •The intrahost diversity and rate of intrahost evolution of FIV env is relatively low when compared with that of HIV [].
- •When contrasted with pathogenic and rapidly evolving human HIV counterparts, and compared with less pathogenic bovine immunodeficiency virus (BIV), which exhibits little sequence variation [], the relative genetic stability of FIV likely reflects a long period of coexistence between the virus and the host; this may contribute to lower pathogenicity and explain why many FIV-infected cats do not progress to the terminal-stage disease [].
- •FIV is distributed globally with a seroprevalence ranging between less than 2.5 and greater than 14% [].
- •Risk factors for FIV seropositivity are presented in Table 1.Table 1Risk Factors for Feline Immunodeficiency Virus Infection
High-Risk Low-Risk Age Adult Young Sex Male Female Neuter status Entire Neutered Environment Outdoor Indoor Breed Mixed breed Pure breed Health status Sick Healthy
- •Average age at the time of diagnosis is 6 years, with male cats being almost 5 times more likely to be seropositive than females [].
- •Horizontal transmission via inoculation of virus in saliva or blood during aggressive territorial fights is predominant [].
- •Vertical, perinatal, and postnatal queen to kitten transmission is rarely documented, unless the queen becomes infected during pregnancy [].
- ○Perinatal infection of 1 kitten does not imply infection of the whole litter.
- •Virus can be isolated from semen, but natural sexual transmission of FIV has not been documented [].
- •Transmission of FIV among naturally infected cats cohabiting in stable households is infrequent [].
- •Cats used as blood donors must be free from FIV infection because iatrogenic transmission by this route is inevitable [].
- •Infection commences with binding of the viral Env to the viral receptor on susceptible cells.
- ○FIV preferentially targets CD4+ T cells, CD4+CD25 regulatory T cells, macrophages, monocytes, neuroglia, CD8+ T cells, and B cells.
- ○The virus uses feline CD134 as its primary receptor [] and CXCR4 as a coreceptor [].
- ○CD134 is expressed on feline CD4+ T lymphocytes consistent with progressive depletion of CD4+ lymphocytes during disease progression [].
- ○Structurally, the extracellular domain of CD134 is composed of 3 cysteine-rich domains (CRD-1, CRD-2, and CRD-3) (Fig. 4).
- ○Understanding the structure of CD134 is important in deciphering the nature of virus-host interaction, because different strains of FIV have different affinity for the primary entry receptor [] (see Fig. 4).
- ○Some strains of the virus (often referred as “early” variants), require stringent interaction with determinants on both cysteine-rich domains (CRD-1 and CRD-2) of CD134 to achieve productive infection []. In contrast, “late” variants can infect susceptible cells via interaction with a first cysteine-rich domain (CRD-1) alone [].
- ○Data from experimental [] and natural infections [] reveal that the virus changes the way it interacts with its primary receptor during the course of disease, similar to the receptor switch observed during progression of HIV infection [].
- ○In naturally infected cats, CRD-2-dependent viral variants dominate in early infection, and evolve toward CRD-2 independence during disease progression (late infection) [].
- ○Emergence of “late,” CRD-2 independent viral variants segregates with declining clinical status and onset of immunodeficiency [,].
Correlates of Immune Protection
- •Cell-mediated immunity is governed by cytotoxic CD8+ T lymphocytes (CTLs). This immunity develops within weeks postexposure and is responsible for the subsequent decline in plasma viral load seen during the “asymptomatic” stage of infection [,].
- ○The antiviral activity of CD8+ T cells is mediated through (a) noncytotoxic, non-antigen-specific CD8+ T cells [] and (b) major histocompatibility complex (MHC) class I-restricted CTLs [].
- ▪Nonspecific CD8+ T cells appear approximately 1 week postexposure and target the virus via contact-dependent or contact-independent noncytotoxic mechanisms.
- ▪Typical MHC class I-restricted CD8+ T cells are primed against specific viral proteins (Gag, Pol, and Env) and are detectable as early as 2 weeks postexposure.
- ○CD8+ T-cell numbers increase throughout infection and decline only at the terminal stage [].
- •Humoral, B-cell-mediated immunity elicited against Gag and Env viral proteins, and manifested by increased IgG immunoglobulin plasma levels, is detectable within 2 to 4 weeks postinfection [,].
- ○Additional immunity is provided by virus neutralizing antibodies (VNAbs), which, although detectable within 30 days postinfection, take several months to fully develop [].
- ▪VNAbs’ interaction with epitopes on the Env interferes with, or blocks, cellular entry of the virus, thus preventing the infection (antibody-mediated viral neutralization).
- ▪Autoantibodies against the primary receptor for FIV, CD134, provide additional protection against the virus in some infected cats [].
- ▪Although presence of VNAbs can be beneficial, or at least neutral, antibody-dependent enhancement has also been documented [].
- •Intrinsic immunity represented by cellular-based antiviral restriction factors provides additional protection that controls almost every stage of retroviral life cycle. Intrinsic retroviral restriction factors encoded by the feline genome include APOBEC3G [] and Tetherin/BST-2 proteins [].
- ○APOBEC3G (apolipoprotein B messenger RNA [mRNA]-editing enzyme catalytic polypeptide-like 3 G) operates during reverse transcription causing accumulation of guanosine to adenosine substitutions in a positive-strand viral DNA, subsequent accumulation of premature stop codons and inhibition of viral replication by hypermutation, and degradation of viral genomic material.
- ○Feline Tetherin/BST-2 retains the FIV virion on the cell surface preventing its release, but not the cell-to-cell spread of the virus.
The Course of Feline Immunodeficiency Virus Infection and Clinical Signs
- •Acute, primary stage, which is defined by a rapid viral replication and subsequent viremia. The virus replicates in CD4+ T cells, macrophages, and dendritic cells. Plasma viral load peaks at 8 to 12 weeks postinfection.
- ○Transient nonspecific clinical signs such as lethargy, inappetence, and pyrexia may be detected. Generalized lymphadenopathy and neutropenia may occur and persist for several months [].
- ○Rapid depletion of CD4+ T cells and subsequent excessive production of CD8+ T cells results in an inversion of the CD4:CD8 ratio, which is often lifelong.
- ○The immune response curtails viral replication but fails to clear virus.
- •Silent, subclinical stage with mild or inapparent clinical signs.
- ○Plasma viral loads are suppressed.
- ○CD4+ T lymphocyte numbers, after an initial rebound, continue to decline progressively.
- ○Combination of immunosuppression and immune hyperactivation contributes to FIV-induced immune dysregulation, which variably affects individual cats. Transient nonspecific clinical signs include hyporexia, lethargy, intermittent pyrexia, and lymphadenopathy.
- ○Feline chronic gingivostomatitis, which has a complex and multifactorial cause, is frequently seen in infected cats [,] (Fig. 6).
- ○Declining numbers of CD4+ T cells, and subsequent decreased production of cytokines such as interferon (IFN)-γ, interleukin (IL)-2, IL-10, and IL-12 contribute to impaired immunity and opportunistic infections []; more pronounced clinical signs associated with pathogens as documented for Toxoplasma gondi [], and Listeria monocytogenes []; and indirect predisposition for neoplasia [].
- ○Owing to incompletely understood reasons, some infected cats remain in this phase for life, whereas others progress to the terminal stage of disease [].
- •Terminal stage is characterized by progressive immune depletion, subsequent escape of the virus from the immune surveillance, and onset of clinical signs compatible with a profound immunodeficiency. Persistent neutropenia is frequently documented [,], and increases the risk of atypical and refractory bacterial, viral, fungal, and parasitic infections. Some cats develop neoplasia and neurologic disease.
- ○Weight loss, resembling HIV-associated “wasting syndrome,” is frequently observed []. The underlying cause is multifactorial with altered hypermetabolism, cytokine effects, and hyporexia being quoted as the main contributors.
- ○Concurrent infections include bacterial pyodermas, demodicosis, disseminated cowpox, cryptococcosis, mycobacteriosis, and lungworm [,45,46,47]. These infections tend to be more severe and more difficult to treat than in immunocompetent cats.
- ○Neuropathogenesis is attributed to actions of monocytes and macrophages, which carry the virus across the blood-brain barrier resulting in progressive encephalitis. Stereotypic behavioral and circadian rhythm changes, aggression, tremors, and delayed pupillary light reflexes have all been attributed to FIV-induced neuropathogenesis [].
- ○Nephropathy and presence of proteinuria, but not renal azotemia, have been reported []. Potential underlying mechanisms include glomerular deposition of viral-antibody immune complexes, direct viral infection of renal epithelial cells, and thrombotic microangiopathy.
- ○FIV-associated impairment of the antineoplastic immune control capacity and its consequences are the most likely reason why infected cats are 5 to 6 times more likely to develop lymphoma when compared with their FIV-negative counterparts [].
- ▪Chronic hyperstimulation of the B-cell compartment is another mechanism rendering cells more prone to neoplastic transformation [].
- ▪Furthermore, FIV-induced immune dysregulation may reveal oncogenic potential of other viruses. Any role for recently discovered Felis catus gammaherpesvirus 1 in lymphomagenesis in FIV-infected cats remains to be established [51,52,53].
- •In a study examining the long-term outcome of natural retroviral infections, the survival rate for FIV-infected cats at 6 years postdiagnosis was 65%, compared with 90% for uninfected control cats []. The decision on euthanasia around the time of diagnosis of FIV infection is one of the main reasons for reported decreased survival of infected cats. In the same study, after exclusions of cats that were euthanized or died within 100 days postdiagnosis, the survival rate for FIV-infected cats at 3 and 6 years was 94% and 80%, respectively, when compared with controls [].
- •There is no justification for euthanasia of healthy cats based on their FIV status.
- •CD4:CD8 ratio, a well-established surrogate marker to monitor progression of HIV infection, is not of diagnostic value because no correlation between inversion of CD4:CD8 and disease progression in FIV-infected cats has been found [,].
- •The plasma viral load is suggested to be a promising prognostic marker [], but its potential clinical utility remains to be established.
Detection and diagnosis
- •Serologic, point-of-care (POC) screening tests using lateral flow immunochromatography or bidirectional-flow enzyme-linked immunosorbent assay (ELISA) technologies, and laboratory-based ELISA assays that detect antibodies against nucleocapsid, p24 capsid, or Env viral proteins can be reliably used for diagnosis in most cases and are the diagnostic tests of choice [].
- ○Although antibodies to the virus can be detected approximately 2 to 4 weeks postexperimental infection [], in most cases seroconversion occurs within 60 days postexposure [].
- ○Maternal-derived antibodies (MDAs) from FIV-infected or vaccinated queens can persist for up to 5 months and could be responsible for false-positive serology results in young kittens []. In such cases, cats should be retested after 6 months of age.
- ○Fel-O-Vax FIV (Boehringer Ingelheim Pty Limited, NSW, Australia) vaccine-induced antibodies can confound the serologic diagnosis and differentiation between infected, vaccinated, and vaccinated and infected cats [].
- ▪In cats with prior FIV vaccination history, it is important to select the serologic test that can distinguish between natural infection and vaccine-induced antibodies.
- ▪The SNAP Combo FeLV Ag/FIV Ab Test (IDEXX Laboratories, Inc, Westbrook, ME, USA) is highly sensitive and specific but does not differentiate between the antibodies induced by natural infection and those induced by the vaccination.
- ▪Anigen Rapid FIV Ab/FeLV Ag Test Kit (Bionote, Inc, Hwaseong-si, South Korea) and WITNESS FeLV-FIV Test Kit (Zoetis, Inc, Florham Park, NJ, USA) seem to differentiate FIV-infected cats from annually vaccinated cats with 100% specificity []. However, caution is still needed in interpretation of those 2 POC test results in cats with a recent history of primary vaccination (3 doses, 2–4 weeks apart). Some immunized cats can potentially return false-positive results up to 22 weeks after receiving the final dose of primary vaccination [].
- •Additional serologic assays include Western blot and immunofluorescent antibody assay. These assays are technically demanding, potentially less sensitive, and more challenging to interpret than ELISA assays [].
- •Molecular PCR tests detect integrated DNA provirus or plasma viral RNA.
- ○PCR is not recommended as a screening test, but as an adjunct to serology in doubtful situations. PCR can be useful in determination of true FIV status in
- ▪seropositive cats that have been vaccinated against FIV,
- ▪seropositive kittens, where presence of anti-FIV MDAs is suspected, and
- ▪seronegative cats that may have been recently infected but where not enough time has lapsed for seroconversion to occur.
- ○Variable performance of FIV PCR tests has been reported []. The overall sensitivity has been estimated 5% to 15% lower than that of serologic assays [].
- ▪Lower sensitivity can be attributed to inability of the primers to detect all field isolates, poor sample quality, and low viral and provirus load [].
Management of infected cats
Environment and Housing Conditions
- •There are several studies that demonstrated that FIV infection does not adversely affect the longevity of infected cats [,,].
- •Housing conditions, appropriate nutrition, and husbandry are crucial to maintain FIV-infected cats in good health [].
- ○Stable, indoor households, are most suitable. Low-density housing not only seems to reduce the risk of disease progression but also lowers the risk of transmission to other cats.
- ○Overcrowded shelter conditions, environmental stress, and exposure to infectious agents can have a significant negative impact on FIV-infected cats leading to onset of the terminal-stage disease.
- ○Cats should be fed complete, balanced diets matched for the age and nutritional needs imposed by concurrent medical conditions. Raw diets are discouraged to avoid exposure to food-borne infectious diseases.
- ○Neutering is crucial in reducing roaming and aggressive behaviors.
Preventive Health Care
- •Hematology, biochemistry, and full urine analysis should be performed annually [] and any problems investigated.
- •Routine, ectoparasite and endoparasite prophylaxis, including heartworm control, is crucial.
- •Recommendation for vaccination of immunocompromised cats has been clarified by the most recent ABCD guidelines [].ABCD. ABCD guidelines on Vaccination of Immunocompromised Cats.
- ○Booster vaccinations for previously vaccinated FIV-infected cats that live indoors are not recommended.
- ○Outdoor cats that are at risk of exposure to infectious diseases should be considered for vaccination, ideally with inactivated formulations classified as “core” vaccines.
- •Where surgery is indicated in FIV-infected cats, perioperative antibiotics should be reserved for cats with persistent neutropenia, or those at moderate to high risk of bacterial contamination of the surgical site [].
- •Infected cats should not be hospitalized in isolation wards to minimize their risk of exposure to communicable infectious diseases.
- •Given very low environmental persistence, there is a minimal risk of hospital-acquired virus transmission as long as standard biosecurity protocols are followed.
- •The response of FIV-infected cats to medical therapy is often similar to that of negative cats, but more aggressive or a longer course of treatment is sometimes needed. Antibiotic choice, when indicated, needs to be guided by culture and susceptibility results [].
- •Treatment with griseofulvin has been associated with myelosuppression and severe neutropenia [] in FIV-infected cats.
- •Use of glucocorticoids seems counterintuitive, because they have the potential to exacerbate the lentiviral infection. However, their judicious use in some circumstances for treatment of immune-mediated conditions can be beneficial [].
- •Cats diagnosed with lymphoma seem to respond to multiagent chemotherapy in a similar way as retrovirus-negative cats []. Cytotoxic treatments should therefore not be discouraged, but patients need to be more closely monitored for chemotherapy-induced myelosuppression.
- •Treatment of FIV-associated neutropenia has been attempted with a recombinant human G-CSF (granulocyte colony-stimulation factor) []. Although associated with a short-term positive response, G-CSF tends to promote viral replication and enhancement of infection []. The safe use of G-CSF is further impeded by development of antibodies to human G-CSF, which could cross-react with endogenous feline G-CSF to cause refractory agranulocytosis [].
- •Although studies in FIV-infected cats are lacking, anemia can be treated with darbepoetin [], which is less antigenic than previously recommended erythropoietin [].
- •Insulinlike growth factor I (rHuIGF-1) has been shown to stimulate thymic function, and increase the number of circulating T lymphocytes in juvenile experimentally infected cats [], but there are no studies assessing its efficacy in naturally acquired infections.
Immunomodulatory and Specific Antiviral Therapies
- •Interferon therapy has both immunomodulatory and antiviral effects [77,78,79]. Although in vivo data documenting treatment benefit are limited, IFNs can be considered for some infected cats.
- ○Recombinant human interferon-α (rHuIFN-α) has been shown to have antiviral activity against FIV in vitro. [] rHuIFN-α can be administered as subcutaneous (SC) injection at 104 to 106 U/kg every 24 hours. However, within 3 to 7 weeks, treated cats develop anti-human IFN antibodies, rendering rHuIFN-α ineffective [].
- ○Recombinant feline interferon-ω (rFeIFN-ω, Virbagen Omega, Virbac) is not antigenic, and prolonged therapy is not associated with any major side effects []. rFeIFN-ω can be given at 106 U/kg SC every 24 hours on 5 consecutive days for 3 series starting on days 0, 14, and 60. An alternative protocol also exists where rFeIFN-ω is administered orally at 105U/cat every 24 hours for 90 consecutive days []. Although IFN-ω suppresses FIV replication in vitro, [] its efficacy in vivo is much more variable; some studies reported an improvement of clinical scores and laboratory parameters, whereas others failed to demonstrate a clear benefit [,,].
- •Antiviral therapies consist of an impressive arsenal of drugs specifically designed for treatment of HIV infection. Although most are either noneffective or toxic for cats, 2 groups: 1) nucleoside analogue reverse transcriptase inhibitors (NARTIs) and 2) receptor antagonists, can be considered for off-license treatment of some infected cats.
Chimeric antigen receptor-modified T cells (CAR-T) therapies have been studied extensively, particularly over the last decade, as treatment options for various hemato-oncological diseases [] and as a cure for HIV-infected humans []. The potential of CAR-T to target the virus within latently infected cells, otherwise inaccessible to antiretroviral drugs, offers a promising therapeutic option not only for HIV-infected humans but also for FIV-infected cats and merits further investigation in this species. In summary, when compared with HIV infection where specific, widely available, and relatively safe antiviral therapies can almost completely inhibit viral replication, conclusions on the efficacy and safety of antiretroviral drugs and specific treatment recommendations for FIV infection are more difficult to make. Well-designed, long-term treatment trials, including assessment of novel CAR-T therapies, in naturally infected cats are needed to address this knowledge gap.
- ○Zidovudine (3′-azido-2′,3′-dideoxythymidine, AZT) has been studied as a potential therapeutic for FIV infection [85,86,87].
- ▪Zidovudine, a NARTI, inhibits viral replication in vitro and in vivo, with resultant decrease in plasma viral load and improvement of clinical status. The recommended dosage is at 5 to 10 mg/kg every 12 hours orally or SC.
- ▪Zidovudine can lead to myelosuppression. Nonregenerative anemia is one of the most common side effects. Complete blood cell count should be therefore monitored initially every week, and if no concerns are identified during the first month of treatment, once monthly thereafter. In cats that have developed drug-induced anemia, discontinuation of treatment results in a prompt improvement of hematocrit values.
- ▪Other limiting side effects include gastrointestinal disturbances and anorexia.
- ▪Although some cats can tolerate treatment beyond 2 years, resistance to zidovudine can develop as early as 6 months after initiation of treatment [].
- ○Receptor antagonists bind to either the cell surface receptor or the virus itself, thus inhibiting the virus receptor interaction and virus entry. Of receptor antagonists identified for HIV, only bicyclams have been investigated as a potential treatment of cats.
- ▪Plerixafor (1,1′-(1,4-phenylenbismethylene)-bis(1,4,8,11-tetraazacyclotetradecane)-octachlo-ride dehydrate, AMD3100) is a selective CXCR4 antagonist, which is licensed as a stem cell activator for human patients undergoing bone marrow transplant. Plerixafor has been studied in vitro and in vivo in FIV-infected cats. Based on a study of 40 cats, treatment at 0.5 mg/kg every 12 hours SC for 6 weeks was associated with decreased viral loads and improvement in clinical parameters with no apparent side effects [].
- •Development of lentiviral vaccine is associated with several major obstacles:
- ○Remarkable genetic diversity of the viral env gives virus a tremendous populational antigenic plasticity, making it difficult to design one vaccine that would protect against all strains worldwide.
- ○Potential superinfection events, error-prone nature of RT, and its propensity for recombination are additional mechanisms indirectly responsible for the enormous plasticity of the virus and resultant immune evasion.
- ○The ability of lentiviruses to establish latent infection in nondividing cells, where integrated provirus is inaccessible to the immune system until the cell becomes activated, provides an additional escape mechanism.
- ○Vaccine-induced enhancement of infection has been described in multiple studies where prototypic vaccines instead of protecting, render immunized subjects more susceptible to infection [].
- •Multiple studies informed development of a commercial dual subtype inactivated vaccine (Fel-O-Vax FIV).
- ○The vaccine consists of inactivated FIV Petaluma (clade A) and FIV Shizuoka (clade D)-infected whole cells [].
- ○Fel-O-Vax FIV was licensed based on encouraging efficacy data. However, it has been shown that the protection achieved in initial reported studies [94,95,96] did not extend to experimental challenge with a primary, virulent UK strain of the virus []. The vaccine was never licensed in Europe.
- ○Cats vaccinated against FIV and subsequently diagnosed with infection are reported [98,99,100]. The efficacy of the vaccine in Australia is estimated at 56% [].
- ○The FIV vaccine, which is regarded as “noncore” by the WSAVA, is still available in Australia, New Zealand, and Japan but has been discontinued in North America since 2015.
Clinics care points
- •Interpreting the results of FIV serology requires careful consideration of risk factors identified in patient signalment, history, and physical examination. Repeat serology and/or PCR testing may be indicated for confirmation of FIV infection status.
- •FIV subtype, often reported with PCR testing results, has no established clinical relevance at this time.
- •FIV-infected cats are likely to have a degree of immune dysfunction, even though this is often not clinically apparent. Regular health checks, preventive medicine, and owner education are important for maintaining optimal health.
- •Considering contribution, if any, of FIV infection to current clinical signs in infected cats is key to managing the case.
- •Reliable clinical prognostic markers for FIV infection are not available.
- •Cats used as blood donors should be established to be free from FIV infection by repeated testing.
- •FIV-infected cats should not be hospitalized in isolation wards on the basis of their FIV status alone because at these places potentially immunosuppressed cats are at unnecessary risk.
- •There is no justification for euthanasia of healthy cats solely based on their FIV infection status.
- •FIV poses no known zoonotic risk.
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The authors have no conflicts of interest to declare that are relevant to the content of this article.
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