%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Pillai, Sekhar
%A Brilot, Fabienne
%T Cerebrospinal fluid CD19(+) B-cell expansion in N-methyl-d-aspartate receptor encephalitis.
%B Developmental Medicine and Child Neurology
%D 2013
%C United Kingdom, United States
%I Wiley-Blackwell Publishing Ltd.
%V 55
%N 2
%P 191-193
%@ 0012-1622
%X 
%Z FOR Codes: 111403 110903 110703


%0 Journal Article
%~ PubMed
%A Sinclair, Adriane J
%A Wienholt, Louise
%A Tantsis, Esther
%A Brilot, Fabienne
%A Dale, Russell C
%T Clinical association of intrathecal and mirrored oligoclonal bands in paediatric neurology.
%B Developmental Medicine and Child Neurology
%D 2013
%C United Kingdom
%I Wiley-Blackwell Publishing Ltd.
%V 55
%N 1
%P 71-75
%@ 0012-1622
%X 
%Z FOR Codes: 111403 110703 110903


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Merheb, Vera
%A Pillai, Sekhar
%A Wang, Dongwei
%A Cantrill, Laurence
%A Murphy, Tanya K
%A Ben-Pazi, Hilla
%A Varadkar, Sophia
%A Aumann, Tim D
%A Horne, Malcolm K
%A Church, Andrew J
%A Fath, Thomas
%A Brilot, Fabienne
%T Antibodies to surface dopamine-2 receptor in autoimmune movement and psychiatric disorders.
%B Brain
%D 2012
%C United Kingdom
%I Oxford University Press
%V 135
%N Pt 11
%P 3453-3468
%@ 1460-2156
%X 
%Z FOR Codes: 110903 111403


%0 Journal Article
%A Dale, Russell
%A Banwell, Brenda
%A Bar-Or, Amit
%A Brilot-Turville, Fabienne
%T Autoantibodies against aquaporin-4 and myelin oligodendrocyte glycoprotein in paediatric CNS demyelination: Recent developments and future directions
%B Multiple Sclerosis and Related Disorders
%D 2012
%C Netherlands
%I Elsevier B. V.
%V 1
%N 3
%P 116–122
%@ 2211-0356
%X 
%Z FOR Codes: 110707


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Brilot, Fabienne
%T Autoimmune Basal Ganglia disorders.
%B Journal of Child Neurology
%D 2012
%C United States
%I Sage Publications, Inc.
%V 27
%N 11
%P 1470-1481
%@ 1708-8283
%X 
%Z FOR Codes: 111403 110903 110703


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Lang, Bethan
%A Brilot, Fabienne
%A Polfrit, Yann
%A Smith, Grahame H H
%A Wong, Melanie
%T Treatment-responsive pandysautonomia in an adolescent with ganglionic α3-AChR antibodies.
%B European Journal of Paediatric Neurology
%D 2012
%C United Kingdom
%I Elsevier Ltd
%V 16
%N 4
%P 396-398
%@ 1532-2130
%X Autoimmune autonomic ganglionopathy (AAG) is a rare disorder that presents with pandysautonomia typically in middle age and elderly patients. AAG is typically associated with serum autoantibodies that bind to the alpha-3 subunit of the ganglionic acetylcholine receptor (??3-AChR Ab). We report a 13 year old girl who presented with gut pseudo-obstruction, bladder dysfunction and dilated pupils unresponsive to pilocarpine. She had positive ??3-AChR Ab plus other autoantibodies suggesting an autoimmune diathesis. Our patient was initially resistant to steroid therapy but responded to the addition of azathioprine resulting in a near complete clinical remission. We conclude that pandysautonomia associated with ??3-AChR Ab can occur in children and has multi-organ involvement.
%Z FOR Codes: 111403


%0 Journal Article
%~ PubMed
%A Pröbstel, A K
%A Dornmair, K
%A Bittner, R
%A Sperl, P
%A Jenne, D
%A Magalhaes, S
%A Villalobos, A
%A Breithaupt, C
%A Weissert, R
%A Jacob, U
%A Krumbholz, M
%A Kuempfel, T
%A Blaschek, A
%A Stark, W
%A Gärtner, J
%A Pohl, D
%A Rostasy, K
%A Weber, F
%A Forne, I
%A Khademi, M
%A Olsson, T
%A Brilot, F
%A Tantsis, E
%A Dale, R C
%A Wekerle, H
%A Hohlfeld, R
%A Banwell, B
%A Bar-Or, A
%A Meinl, E
%A Derfuss, T
%T Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis.
%B Neurology
%D 2011
%C United States
%I Lippincott Williams & Wilkins
%V 77
%N 6
%P 580-8
%@ 1526-632X
%X To study the longitudinal dynamics of anti-myelin oligodendrocyte glycoprotein (MOG) autoantibodies in childhood demyelinating diseases.
%Z FOR Codes: 111403 110903


%0 Journal Article
%~ PubMed
%A Brilot, F
%A Merheb, V
%A Ding, A
%A Murphy, T
%A Dale, R C
%T Antibody binding to neuronal surface in Sydenham chorea, but not in PANDAS or Tourette syndrome.
%B Neurology
%D 2011
%C United States
%I Lippincott Williams & Wilkins
%V 76
%N 17
%P 1508-13
%@ 1526-632X
%X To test the hypothesis that Sydenham chorea (SC) immunoglobulin G (IgG) autoantibodies bind to specific neuronal surface proteins, whereas IgG from patients with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) or Tourette syndrome (TS) do not bind to neuronal surface proteins.
%Z FOR Codes: 1109 1114


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Yin, Katie
%A Ding, Alice
%A Merheb, Vera
%A Varadkhar, Sophie
%A McKay, Damien
%A Singh-Grewal, Davinder
%A Brilot, Fabienne
%T Antibody binding to neuronal surface in movement disorders associated with lupus and antiphospholipid antibodies.
%B Developmental Medicine and Child Neurology
%D 2011
%C United Kingdom, United States
%I Mac Keith Press
%V 53
%N 6
%P 522-528
%@ 0012-1622
%X Aim??? Systemic lupus erythematosus is a multi-organ autoimmune disorder associated with autoantibodies of complex diversity. Antiphospholipid antibodies (aPL), which are commonly associated with lupus, create a pro-thrombotic tendency, but are also associated with non-thrombotic neurological features. Movement disorders are rare neuropsychiatric complications of lupus and antiphospholipid syndrome, and autoimmune and thromboembolic disease mechanisms have been proposed. Method??? We describe the clinical features, investigation findings, treatment, and outcome of six paediatric participants with movement disorders associated with lupus and/or aPL (six females, median age 13y, range 8-15). To examine the autoantibody hypothesis, we used a neuronal cell line with dopaminergic characteristics and measured serum antibody binding to neuronal cell-surface antigens using flow cytometry. For comparison with the six participants, we used serum from healthy individuals (n=12, six females, median age 11y, range 9-13) and children with other neurological diseases (n=13, seven females, median age 7y, range 2-15). Results??? Of the six participants, two had lupus only, two had lupus with aPL, and two had aPL only. The movement disorder was chorea in four and parkinsonism in two. All four participants with chorea had aPL and movement disorder relapses. The two participants with parkinsonism did not have aPL, but had a progressive course until rituximab or plasma exchange resulted in neuropsychiatric remission. All six participants demonstrated elevated serum antibody binding to neuronal cell-surface antigens compared with healthy individuals and those with other neurological diseases. Interpretation??? This report supports the association of chorea with aPL, but suggests a different autoimmune mechanism operates in lupus parkinsonism. The presence of antibody binding to neuronal cell-surface antigens supports a possible direct action of autoantibodies on neurons in patients with movement disorders associated with lupus and aPL.
%Z FOR Codes: 111403 110903


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Tantsis, Esther
%A Merheb, Vera
%A Brilot, Fabienne
%T Cerebrospinal fluid B-cell expansion in longitudinally extensive transverse myelitis associated with neuromyelitis optica immunoglobulin G.
%B Developmental medicine and child neurology
%D 2011
%C United Kingdom, United States
%I Mac Keith Press
%V 53
%N 9
%P 856-60
%@ 0012-1622
%X A first episode of central nervous system (CNS) demyelination may represent heterogeneous entities such as acute disseminated encephalomyelitis, clinically isolated syndrome, neuromyelitis optica (NMO), or multiple sclerosis. As new immune therapies become available, it is increasingly important to make an early diagnosis. Autoantibodies such as NMO immunoglobulin G (IgG) and myelin oligodendrocyte glycoprotein IgG are increasingly being employed to define subgroups of CNS demyelination or guide treatment. Similarly, cerebrospinal fluid (CSF) immunophenotyping can demonstrate B-lymphocyte subpopulation expansion, which has been used to guide therapy in other autoimmune CNS disorders. We present a report on a 15-year-old male with longitudinally extensive transverse myelitis with magnetic resonance imaging findings of oedema, cavitation, and gadolinium enhancement. NMO-IgG and aquaporin 4 IgG were positive; thus, we diagnosed a limited form of NMO. Acute CSF immunophenotyping revealed a 3.6% expansion of CD19 B-cell populations, whereas a comparison group of five children (4 males, age range 2-15y; mean age 7y) with other neurological disorders showed only a 0.51% expansion (SD 0.25%). In view of the diagnosis of a ''limited form of neuromyelitis optica'', we therefore elected to treat him aggressively from the outset with a prolonged steroid regimen and mycophenylate mofetil. This case demonstrates a correlation between autoantibody production and CSF B lymphocyte expansion in an individual with CNS demyelination. These approaches could be used in individuals with a first episode of CNS demyelination to help delineate immunological subgroups and guide treatment.
%Z FOR Codes: 111403 110903


%0 Journal Article
%~ PubMed
%A Suleiman, Jehan
%A Brenner, Tanja
%A Gill, Deepak
%A Troedson, Christopher
%A Sinclair, Adriane J
%A Brilot, Fabienne
%A Vincent, Angela
%A Lang, Bethan
%A Dale, Russell C
%T Immune-mediated steroid-responsive epileptic spasms and epileptic encephalopathy associated with VGKC-complex antibodies.
%B Developmental medicine and child neurology
%D 2011
%C United Kingdom, United States
%I Mac Keith Press
%V 53
%N 11
%P 1058-60
%@ 0012-1622
%X Autoantibodies that bind to voltage-gated potassium-channel complex proteins (VGKC-complex antibodies) occur frequently in adults with limbic encephalitis presenting with cognitive impairment and seizures. Recently, VGKC-complex antibodies have been described in a few children with limbic encephalitis, and children with unexplained encephalitis presenting with status epilepticus. We report a case of infantile-onset epileptic spasms and developmental delay compatible with epileptic encephalopathy. Our patient was a female infant, aged 4 months at presentation. She had evidence of immune activation in the central nervous system with elevated cerebrospinal fluid neopterin and mirrored oligoclonal bands, which prompted testing for autoantibodies. VGKC-complex antibodies were elevated (201 pmol/L, normal<100), but extended antibody testing, including leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein 2 (CASPR2), was negative. The patient showed a partial response to steroid treatment, which was started late in the disease course. On review at 13 months of age, her development was consistent with an age of 5 to 6 months. These results suggest that VGKC-complex antibodies might represent a marker of immune therapy responsiveness in a subgroup of patients with infantile epileptic encephalopathy.
%Z FOR Codes: 111403 110903


%0 Journal Article
%~ PubMed
%A Suleiman, J
%A Brenner, T
%A Gill, D
%A Brilot, F
%A Antony, J
%A Vincent, A
%A Lang, B
%A Dale, R C
%T VGKC antibodies in pediatric encephalitis presenting with status epilepticus.
%B Neurology
%D 2011
%C United States
%I Lippincott Williams & Wilkins
%V 76
%N 14
%P 1252-1255
%@ 1526-632X
%X Voltage-gated potassium channel antibodies (VGKC Ab) are associated with limbic encephalitis and neuromyotonia in adults. There have been no systematic investigations in children to date.
%Z FOR Codes: 110903


%0 Journal Article
%~ PubMed
%A Selter, R C
%A Brilot, F
%A Grummel, V
%A Kraus, V
%A Cepok, S
%A Dale, R C
%A Hemmer, B
%T Antibody responses to EBV and native MOG in pediatric inflammatory demyelinating CNS diseases.
%B Neurology
%D 2010
%C United States
%I Lippincott Williams & Wilkins
%V 74
%N 21
%P 1711-5
%@ 1526-632X
%X Epstein-Barr virus (EBV) has been discussed as a possible causative agent in inflammatory demyelinating diseases of the CNS. Cross-reactivity between EBV and myelin proteins has been proposed as a potential mechanism by which EBV could elicit an autoimmune response targeting the CNS. Recently, high antibody titers to native myelin oligodendrocyte glycoprotein (nMOG) were found in children affected by the first inflammatory demyelinating event. The relation between antibody responses to EBV and nMOG has not been addressed in children so far.
%Z FOR Codes: 110903


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Brilot, Fabienne
%T Biomarkers of inflammatory and auto-immune central nervous system disorders.
%B Current opinion in pediatrics
%D 2010
%C United States
%I Lippincott Williams & Wilkins
%V 22
%N 6
%P 718-25
%@ 1040-8703
%X Inflammatory and auto-immune disorders of the central nervous system are a heterogeneous group of disorders. Many of these disorders are potentially treatable with immune therapies that can reduce disability or prevent death. We review the clinical value of biomarkers which can aid in the diagnosis of paediatric inflammatory and auto-immune central nervous system (CNS) disorders.
%Z FOR Codes: 110903


%0 Book Section
%A Brilot-Turville, Fabienne
%T Inflammation and Autoimmunity: A Nervous System Perspective
%B Inflammatory and Autoimmune Disorders of the Nervous System in Children
%D 2010
%C London,  UK
%I MacKeith Press
%V 
%N 
%P 1-13
%@ 9781989683667
%E Vincent, Angela
%E Dale, Russell
%X 
%Z FOR Codes: 110904


%0 Journal Article
%~ PubMed
%A Evesson, Frances J
%A Peat, Rachel A
%A Lek, Angela
%A Brilot, Fabienne
%A Lo, Harriet P
%A Dale, Russell C
%A Parton, Robert G
%A North, Kathryn N
%A Cooper, Sandra T
%T Reduced plasma membrane expression of dysferlin mutants is due to accelerated endocytosis via a syntaxin-4 associated pathway.
%B The Journal of biological chemistry
%D 2010
%C United States
%I American Society for Biochemistry and Molecular Bi
%V 285
%N 37
%P 28529-39
%@ 1083-351X
%X Ferlins are an ancient family of C2 domain-containing proteins, with emerging roles in vesicular trafficking and human disease. Dysferlin mutations cause inherited muscular dystrophy, and dysferlin also shows abnormal plasma membrane expression in other forms of muscular dystrophy. We establish dysferlin as a short-lived (protein half-life approximately 4-6 h) and transitory transmembrane protein (plasma membrane half-life approximately 3 h), with a propensity for rapid endocytosis when mutated, and an association with a syntaxin-4 endocytic route. Dysferlin plasma membrane expression and endocytic rate is regulated by the C2B-FerI-C2C motif, with a critical role identified for C2C. Disruption of C2C dramatically reduces plasma membrane dysferlin (by 2.5-fold), due largely to accelerated endocytosis (by 2.5-fold). These properties of reduced efficiency of plasma membrane expression due to accelerated endocytosis are also a feature of patient missense mutant L344P (within FerI, adjacent to C2C). Importantly, dysferlin mutants that demonstrate accelerated endocytosis also display increased protein lability via endosomal proteolysis, implicating endosomal-mediated proteolytic degradation as a novel basis for dysferlin-deficiency in patients with single missense mutations. Vesicular labeling studies establish that dysferlin mutants rapidly transit from EEA1-positive early endosomes through to dextran-positive lysosomes, co-labeled by syntaxin-4 at multiple stages of endosomal transit. In summary, our studies define a transient biology for dysferlin, relevant to emerging patient therapeutics targeting dysferlin replacement. We introduce accelerated endosomal-directed degradation as a basis for lability of dysferlin missense mutants in dysferlinopathy, and show that dysferlin and syntaxin-4 similarly transit a common endosomal pathway in skeletal muscle cells.
%Z FOR Codes: 110904


%0 Journal Article
%~ PubMed
%A Brilot, Fabienne
%A Dale, Russell C
%A Selter, Rebecca C
%A Grummel, Verena
%A Reddy Kalluri, Sudhakar
%A Aslam, Muhammad
%A Busch, Verena
%A Zhou, Dun
%A Cepok, Sabine
%A Hemmer, Bernhard
%T Antibodies to native myelin oligodendrocyte glycoprotein in children with inflammatory demyelinating central nervous system disease.
%B Annals of neurology
%D 2009
%C United States
%I John Wiley & Sons, Inc.
%V 66
%N 6
%P 833-42
%@ 1531-8249
%X Myelin oligodendrocyte glycoprotein (MOG) is a candidate target antigen in demyelinating diseases of the central nervous system (CNS). Although MOG is encephalitogenic in different animal models, the relevance of this antigen in human autoimmune diseases of the CNS is still controversial.
%Z FOR Codes: 110903


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Brilot, Fabienne
%A Fagan, Elizabeth
%A Earl, John
%T Cerebrospinal fluid neopterin in paediatric neurology: a marker of active central nervous system inflammation.
%B Developmental Medicine and Child Neurology
%D 2009
%C United Kingdom, Unit
%I Mac Keith Press
%V 51
%N 4
%P 317-323
%@ 0012-1622
%X AIM: Cerebrospinal fluid (CSF) neopterin production is increased by interferon-gamma stimulation and appears to act as a marker of intrathecal immune activation. We aimed to test the usefulness of elevated CSF neopterin as a biological marker of central nervous system (CNS) inflammation. METHOD: We retrospectively reviewed CSF neopterin in 158 children (89 males, 69 females, mean age 4y 1mo, SD 3y 11mo, range 1mo-15y). RESULTS: CSF neopterin levels in children with chronic static CNS disorders (n=105) were predominantly low, suggesting that inflammation is rare in these patients. We created an upper value of normal (chronic static group 95th centile 27.4 nmol/l). CSF neopterin was elevated in all 10 patients with acute encephalitis and in 10 of 12 patients with other acute inflammatory CNS disorders (demyelination, post-infectious ataxia, myelitis). CSF neopterin was also significantly elevated in patients with chronic progressive disorders of inflammatory origin. Interestingly, CSF neopterin was elevated in four of six patients with chronic static disorders who were tested during a febrile exacerbation of seizures or dystonia, suggesting that intrathecal immune activation may be important in this setting. INTERPRETATION: Neopterin has a short half-life and was useful for monitoring inflammation activity in a patient with relapsing-remitting encephalitis. CSF neopterin is a useful marker of inflammation in a broad range of acute and chronic CNS disorders, and is a significantly more sensitive marker of inflammation than CSF pleocytosis.
%Z FOR Codes: 60104 110903 110707


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Irani, Sarosh R
%A Brilot, Fabienne
%A Pillai, Sekhar
%A Webster, Richard
%A Gill, Deepak
%A Lang, Bethan
%A Vincent, Angela
%T N-methyl-D-aspartate receptor antibodies in pediatric dyskinetic encephalitis lethargica.
%B Annals of neurology
%D 2009
%C United States
%I John Wiley & Sons, Inc.
%V 66
%N 5
%P 704-9
%@ 1531-8249
%X Encephalitis lethargica (EL) describes an encephalitis with psychiatric, sleep, and extrapyramidal movement disorders. Dyskinetic and parkinsonian forms have been described. EL shares clinical features with the anti-N-methyl-D-aspartate receptor (NMDAR-Ab) encephalitis. We studied 20 sera from pediatric patients with contemporary EL. Ten sera (from 2 males and 8 females, aged 1.3-13 years) and 6/6 cerebrospinal fluid samples were positive for NMDAR-Ab. NMDAR-Ab-positive patients had dyskinesias, agitation, seizures, and insomnia, whereas parkinsonism and somnolence dominated in the NMDAR-Ab-negative children. We were unable to identify any tumors. The dyskinetic form of EL is an NMDAR-Ab encephalitis and can affect very young children.
%Z FOR Codes: 110903


%0 Journal Article
%~ PubMed
%A Dale, Russell C
%A Brilot, Fabienne
%A Banwell, Brenda
%T Pediatric central nervous system inflammatory demyelination:  acute disseminated encephalomyelitis, clinically isolated  syndromes, neuromyelitis optica, and multiple sclerosis.
%B Current Opinion in Neurology
%D 2009
%C United States
%I Lippincott Williams & Wilkins
%V 22
%N 3
%P 233-240
%@ 1473-6551
%X PURPOSE OF REVIEW: We review the recent consensus definitions for acute disseminated encephalomyelitis,clinically isolated syndromes, neuromyelitis optica, and multiple sclerosis (MS) in children. We also discuss the importance of clinically defined consistency, the need for biomarker-based patient delineation, the likelihood of subsequent MS diagnosis following acute demyelination, and current therapeutic options. RECENT FINDINGS: Studies of children after a first episode of demyelination have identified disease onset in adolescence, intrathecal oligoclonal bands and optic neuritis as associated with a higher MS risk, whereas prepubertal onset, presence of polyfocal features with encephalopathy, and transverse myelitis have been associated with a lower risk of subsequent MS. The relapsing-remitting form of MS accounts for over 96% of all MS in children. Neuromyelitis optica appears to be a distinct clinical and biological entity for which neuromyelitis optica IgG provides a high degree of specificity. Neuroimaging plays a key role in the diagnosis of acute demyelination, and serial imaging can provide evidence of lesion dissemination in time that can confirm a diagnosis of MS even in the absence of clinical relapse. SUMMARY: Although clinical definitions, increased awareness, and MRI have contributed to the increasing identification of acute demyelination and MS in children, challenges remain in predicting MS risk. Identification of reliable biomarkers or application of more advanced neuroimaging techniques would serve as invaluable tools to distinguish monophasic demyelination from the first attack of MS.
%Z FOR Codes: 110903 110701


%0 Journal Article
%~ PubMed
%A Brilot, Fabienne
%A Strowig, Till
%A Roberts, Susanne M
%A Arrey, Frida
%A Münz, Christian
%T NK cell survival mediated through the regulatory synapse with human DCs requires IL-15Ralpha.
%B The Journal of clinical investigation
%D 2007
%C US
%I Amer Soc Clinical Investigation Inc
%V 117
%N 11
%P 3316-3329
%@ 0021-9738
%X DCs activate NK cells during innate immune responses to viral infections. However, the composition and kinetics of the immunological synapse mediating this interaction are largely unknown. Here, we report the rapid formation of an immunological synapse between human resting NK cells and mature DCs. Although inhibitory NK cell receptors were polarized to this synapse, where they are known to protect mature DCs from NK cell lysis, the NK cell also received activation signals that induced mobilization of intracellular calcium and CD69 upregulation. The high-affinity component of the receptor for IL-15, IL-15Ralpha, accumulated at the synapse center on NK cells, and blocking of IL-15Ralpha increased NK cell apoptosis and diminished NK cell survival during their interaction with DCs. Furthermore, IL-15Ralpha-deficient NK cells, obtained from donors with a history of infectious mononucleosis, showed diminished survival in culture with DCs. Synapse formation was required for IL-15Ralpha-mediated NK cell survival, because synapse disruption by adhesion molecule blocking decreased DC-induced NK cell survival. These results identify what we believe to be a novel regulatory NK cell synapse with hallmarks of spatially separated inhibitory and activating interactions at its center. We suggest that this synapse formation enables optimal NK cell activation by DCs during innate immune responses.
%Z FOR Codes: 110199


%0 Book Section
%A Brilot-Turville, Fabienne
%A Geenen, Vincent
%A Hober, Didier
%T Coxsackievirus B4 and Type I Diabetes
%B Progress in Virus Research
%D 2006
%C United States
%I Nova Publishers
%V 
%N 
%P 169-190
%@ 1594544387
%E Thebault, Sabine
%X 
%Z FOR Codes: 110804


%0 Journal Article
%~ PubMed
%A Jaïdane, Hela
%A Gharbi, Jawhar
%A Lobert, Pierre-Emmanuel
%A Lucas, Bernadette
%A Hiar, Raïda
%A M'hadheb, Manel Ben
%A Brilot, Fabienne
%A Geenen, Vincent
%A Aouni, Mahjoub
%A Hober, Didier
%T Prolonged viral RNA detection in blood and lymphoid tissues from coxsackievirus B4 E2 orally-inoculated Swiss mice.
%B Microbiology and immunology
%D 2006
%C Australia
%I Wiley-Blackwell
%V 50
%N 12
%P 971-974
%@ 0385-5600
%X The spreading of viral RNA within Swiss Albino mice orally inoculated with coxsackievirus B4 E2 strain (CVB4 E2) was studied by using RT-PCR and semi-nested-RT-PCR methods. Viral RNA was detected in various organs: pancreas, heart, small intestine, spleen, thymus, and blood at various postinfectious (p.i.) times ranging from 8 hr to 150 days. Our results show that (i) outbred mice can be infected with CVB4 E2 following an oral inoculation, which results in systemic spreading of viral RNA, (ii) CVB4 E2 infection can be associated with a prolonged detection of viral RNA in spleen, thymus and blood, up to 70 days p.i. and further in other organ tissues.
%Z FOR Codes: 110704