Neurological disease and encephalitis  in cats experimentally infected with Borna disease virus

Lundgren, A.; Johannisson, Anders; Zimmermann, Wolfgang; Bode, Liv; Rozell, Barbro Lundh; Muluneh, Aemero; Lindberg, R.; Ludwig, Hanns

doi:10.1007/s004010050630

Cited by 38 publications

(43 citation statements)

References 30 publications

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“…Moreover, a feline BDV has been isolated from the central nervous system of cats with SD [24]. Cats also developed neurological signs and encephalitis when experimentally infected with this feline BDV isolate [21]. These findings support the hypothesis that BDV may correlate with SD in cats.…”

supporting

confidence: 64%

“…Experimental infection of cats with BDV gave neurologic disease and encephalitis comparable to SD [21]. Cats with naturally occurring neurologic symptoms also have a higher seroprevalence of antibodies to BDV antigens than controls without neurologic disease [23,29,34].…”

Section: Discussionmentioning

confidence: 99%

“…suppurative meningoencephalomyelitis of unknown aetiology [18] or SD [31] may have an association with BDV infection [2,3,21,23,24,29,30,34]. Experimental infection of cats with BDV gave neurologic disease and encephalitis comparable to SD [21].…”

Section: Discussionmentioning

confidence: 99%

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Prevalence of Circulating Antibodies to p10, a Non-structural Protein of the Borna Disease Virus in Cats with Ataxia.

Ouchi

Kusumoto

Kobayashi

et al. 2001

The Journal of Veterinary Medical Science

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ABSTRACT. Japanese domestic cats were surveyed for circulating antibodies to the p10 and p24 proteins of the Borna disease virus (BDV) by Western blotting. Twenty-four of 52 cats (46.2%) with ataxia and other neurologic symptoms of unknown cause were positive for antibodies to BDV p10 and/or p24. In contrast, cats without neurological symptoms gave a significantly lower prevalence of anti-BDV antibodies to p10 and/or p24 (36 of 152 cats, 23.7%). Thirty specific pathogen-free (SPF) cats tested as controls were uniformly negative to BDV p10 and p24 antigens. These results suggest that BDV may play a role in ataxia in cats. Additionally, our results suggest that it is necessary to use both p10 and p24 as antigens to detect circulating antibodies to BDV in cats. KEY WORDS: anti-BDV antibody, ataxia, Borna disease virus, feline.J. Vet. Med. Sci. 63(12): 1279-1285, 2001 Borna disease (BD) is a progressive encephalomyelitis of horses and sheep caused by infection with the neurotropic Borna disease virus (BDV) that is an enveloped, non-segmented, negative-stranded (NNS) RNA virus [6,8,19,39]. BDV is the prototype genus of the new family of Bornaviridae. Epidemiological studies have documented that diverse species of warm-blooded animals including cats possess circulating antibodies to BDV. In cats, a spontaneous non-suppurative meningoencephalomyelitis with clinical signs of ataxia and behavioral abnormalities, referred to as staggering disease (SD), is thought to be a counterpart of Borna-encephalitis, because the prevalence of BDV-specific antibodies seen in these cats is higher than that seen in randomly selected domestic cats, not having neurological disorders [18,20,22,23,28,30,31,34]. Moreover, a feline BDV has been isolated from the central nervous system of cats with SD [24]. Cats also developed neurological signs and encephalitis when experimentally infected with this feline BDV isolate [21]. These findings support the hypothesis that BDV may correlate with SD in cats.Molecular biological studies on BDV have shown that the BDV antigenome consists of at least 6 open reading frames (ORFs), ORF I to ORF V and ORFx1 [5,9,10]. ORF I encodes the viral nucleoprotein N (p38/40) of 38/40 kDa [25,33,40]. ORF II encodes the phosphoprotein P (p24) of approximately 24 kDa [40,41], and ORF V encodes for a 190-kDa protein that may be the putative viral polymerase L [43]. Studies on the replication of other NNS-RNA viruses have shown that the minimal replicative and infectious unit for these viruses is the ribonucleoprotein containing the genomic RNA that is tightly associated with the N, P and L proteins, whereas the precise nature of the minimal replicative unit of BDV is unclear. Unlike other NNS-RNA viruses, BDV replicates in the nucleus [6,8]. We and others have studied the BDV protein p10 of approximately 10 kDa that is encoded by ORFx1, and translated from mRNA representing the second transcription unit of the BDV genome [27,44]. The p10 are found in brain cells of naturally and experimentally infected animals as well a...

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supporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

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Prevalence of Circulating Antibodies to p10, a Non-structural Protein of the Borna Disease Virus in Cats with Ataxia.

Ouchi

Kusumoto

Kobayashi

et al. 2001

The Journal of Veterinary Medical Science

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“…Both viral antigen and RNA have been detected in brain tissue of diseased cats (51,53). Moreover, SPF cats inoculated with BDV isolated from a cat with SD developed disease (50). These findings, together with the failure to detect other infectious agents in the CNS of SD cats, suggest a possible causative role of BDV in SD.…”

Section: Discussionmentioning

confidence: 68%

Borna Disease Virus Persistence Causes Inhibition of Glutamate Uptake by Feline Primary Cortical Astrocytes

Billaud

Phillips

et al. 2000

J Virol

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Borna disease virus (BDV), a nonsegmented, negative-stranded (NNS) RNA virus, causes central nervous system (CNS) disease in a broad range of vertebrate species, including felines. Both viral and host factors contribute to very diverse clinical and pathological manifestations associated with BDV infection. BDV persistence in the CNS can cause neurobehavioral and neurodevelopmental abnormalities in the absence of encephalitis. These BDV-induced CNS disturbances are associated with altered cytokine and neurotrophin expression, as well as cell damage that is very restricted to specific brain regions and neuronal subpopulations. BDV also targets astrocytes, resulting in the development of prominent astrocytosis. Astrocytes play essential roles in maintaining CNS homeostasis, and disruption of their normal activities can contribute to altered brain function. Therefore, we have examined the effect of BDV infection on the astrocyte's physiology. We present here evidence that BDV can establish a nonlytic chronic infection in primary cortical feline astrocytes that is associated with a severe impairment in the astrocytes' ability to uptake glutamate. In contrast, the astrocytes' ability to uptake glucose, as well as their protein synthesis, viability, and rate of proliferation, was not affected by BDV infection. These findings suggest that, in vivo, BDV could also affect an important astrocyte function required to prevent neuronal excitotoxicity. This, in turn, might contribute to the neuropathogenesis of BDV.Borna disease (BD) virus (BDV) causes central nervous system (CNS) disease in a broad range of vertebrate species (36,43,48,63,65). BDV has a nonsegmented, negative-strand (NNS) RNA genome (9, 17). Based on its unique genetic and biological features, BDV is considered to be the prototypic member of a new virus family, Bornaviridae, within the order Mononegavirales (19,68).Naturally occurring BDV infections were thought to be mainly restricted to horses and sheep within certain geographic regions of central Europe. Current evidence, however, indicates that the natural host range, geographic distribution, and prevalence of BDV are much broader than previously considered (36,43,63,65). The genetics, immune status, and age of the host, as well as viral factors, contribute to a high degree of heterogeneity in disease symptoms and pathological manifestations associated with BDV infection. Clinical manifestations can range from dramatic to subtle or even been unapparent (32,36,43,63,65). Nevertheless, all known BDV isolates are noncytolytic and highly neurotropic (43,48,65). Heightened viral gene expression in limbic system structures and neuronal structural alterations within the hippocampal formation are the main histopathological hallmarks of BDV infection (32,34,35). Immune cell infiltrates are frequently, but not always, observed in the CNS of BDV-infected animals, and immunemediated neuronal damage is thought to be responsible for the clinical symptoms associated with classic BD (5,48,65,71). BDV affects the postnata...

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“…of BDV by intracerebral (i.c.) inoculation, the first symptoms may arise 2 weeks p.i., but it may take up to 2.5 months or a cat may remain asymptomatic for at least 6 months, regardless of the strain used (V or a feline isolate; Lundgren et al, 1997). Ponies infected experimentally with 1610 3 -2610 4 TCID 50 (median tissue culture infective dose) of BDV strain CRP3 by i.c.…”

Section: Infection and Disease Of Production And Companion Animalsmentioning

confidence: 99%

Epidemiology and host spectrum of Borna disease virus infections

Kinnunen

Palva

Vaheri

et al. 2013

Journal of General Virology

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Borna disease virus (BDV) has gained lot of interest because of its zoonotic potential, ability to introduce cDNA of its RNA transcripts into host genomes, and ability to cause severe neurobehavioural diseases. Classical Borna disease is a progressive meningoencephalomyelitis in horses and sheep, known in central Europe for centuries. According to current knowledge, BDV or a close relative also infects several other species, including humans at least occasionally, in central Europe and elsewhere, but the existence of potential ‘human Borna disease’ with its suspected neuropsychiatric symptoms is highly controversial. The recent detection of endogenized BDV-like genes in primate and various other vertebrate genomes confirms that at least ancient bornaviruses did infect our ancestors. The epidemiology of BDV is largely unknown, but accumulating evidence indicates vectors and reservoirs among small wild mammals. The aim of this review is to bring together the current knowledge on epidemiology of BDV infections. Specifically, geographical and host distribution are addressed and assessed in the critical light of the detection methods used. We also review some salient clinical aspects.

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Neurological disease and encephalitis in cats experimentally infected with Borna disease virus

Cited by 38 publications

References 30 publications

Prevalence of Circulating Antibodies to p10, a Non-structural Protein of the Borna Disease Virus in Cats with Ataxia.

Prevalence of Circulating Antibodies to p10, a Non-structural Protein of the Borna Disease Virus in Cats with Ataxia.

Borna Disease Virus Persistence Causes Inhibition of Glutamate Uptake by Feline Primary Cortical Astrocytes

Epidemiology and host spectrum of Borna disease virus infections

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