Comment on:
A Variegated Squirrel Bornavirus Associated with Fatal Human Encephalitis. [N Engl J Med. 2015]
Bornavirus Associated with Fatal Human Encephalitis. [N Engl J Med. 2015

Beer, Martin

Schmidt-Chanasit, J.

Tappe, D.

English

OA OpenAgrar repository

T h e  n e w  e ngl a nd  j o u r na l  o f  m e dic i n en engl j med 373;19 nejm.org november 5, 201518804. Thorsen LB, Thomsen MS, Berg M, et al. CT-planned inter-nal mammary node radiotherapy in the DBCG-IMN study: ben-efit versus potentially harmful effects. Acta Oncol 2014;53:1027-34.5. Grantzau T, Thomsen MS, Væth M, Overgaard J. Risk of sec-ond primary lung cancer in women after radiotherapy for breast cancer. Radiother Oncol 2014;111:366-73.DOI: 10.1056/NEJMc1510505Bornavirus Associated with Fatal Human EncephalitisTo the Editor: Hoffmann et al. (July 9 issue)1 describe three patients with a new form of en-cephalitis caused by variegated squirrel 1 borna-virus (VSBV-1). This finding is interesting, since the cause of up to 37% of cases of encephalitis remains undetermined, despite extensive infec-tious, autoimmune, and paraneoplastic testing.2 I was surprised by the fact that Patient 1 had a highly positive anti-Yo (Purkinje cell) autoanti-body in the cerebrospinal f luid. Anti-Yo auto-antibodies are well-characterized onconeural antibodies (together with anti-Hu, anti-CV2, anti-Ri, anti-Ma2, and amphiphysin), which are usu-ally associated with a paraneoplastic form of cer-ebellar degeneration.3 Any patient who presents with a neurologic syndrome (classic or not) and harbors well-characterized onconeural antibod-ies, even in the absence of a tumor, fulfills the diagnostic criteria for a definite paraneoplastic neurologic syndrome.3 The authors ruled out the presence of cancer using full-body computed to-mography. One intriguing explanation could be that the infection triggered the antibody synthe-sis through the release of antigens by viral neu-ronal lysis or molecular mimicry, as proposed for autoimmune neurologic relapses after herpes simplex encephalitis.4Alberto Vogrig, M.D.University of Verona Verona, ItalyNo potential conflict of interest relevant to this letter was re-ported.1. Hoffmann B, Tappe D, Höper D, et al. A variegated squirrel bornavirus associated with fatal human encephalitis. N Engl J Med 2015;373:154-62.2. Granerod J, Ambrose HE, Davies NW, et al. Causes of  encephalitis and differences in their clinical presentations in England: a multicentre, population-based prospective study. Lancet Infect Dis 2010;10:835-44.3. Graus F, Delattre JY, Antoine JC, et al. Recommended diag-nostic criteria for paraneoplastic neurological syndromes. J Neurol Neurosurg Psychiatry 2004;75:1135-40.4. Armangue T, Leypoldt F, Málaga I, et al. Herpes simplex virus encephalitis is a trigger of brain autoimmunity. Ann Neurol 2014;75:317-23.DOI: 10.1056/NEJMc1510342The authors reply: In Patient 1 in our report, anti-Yo antibodies were detected in high titers in cerebrospinal fluid but not in serum. According to proposed diagnostic criteria1 for paraneoplas-tic neurologic syndromes, such a syndrome would indeed be diagnosed in this patient. We agree that the anti-Yo antibodies might have been in-duced by the viral infection. The cytoplasmic Yo antigen, which is found in several parts of the brain,2 might become exposed to the immune system after neuron disintegration during infec-tion. This possibility is underlined by the absence of nonpathogenic anti-Yo antibodies in the pa-tient’s serum, contrasting with their presence in serum samples obtained from patients with para-neoplastic neurologic syndromes.1 Thus, in our patient, we might rather call the epiphenomenon of anti-Yo antibodies parainfectious and not paraneoplastic. It was reported that cancer was not found in 2% of patients with anti-Yo antibod-ies1; a subgroup of these cases might be virus-induced. It was suggested that in patients with herpes simplex encephalitis, molecular mimicry or antigen release by viral neuronal lysis and in-flammation might induce pathogenic antibodies against neuronal surface N-methyl-d-aspartate receptor (NMDAR).3,4 Such antibodies probably led to cell-surface or synaptic autoimmunity with clinical symptoms.Dennis Tappe, M.D. Jonas Schmidt-Chanasit, M.D.Bernhard Nocht Institute for Tropical Medicine Hamburg, GermanyMartin Beer, D.V.M.Friedrich-Loeffler-Institut Greifswald-Insel Riems, Germany martin.beer@fli.bund.deSince publication of their article, the authors report no fur-ther potential conflict of interest.1. Graus F, Delattre JY, Antoine JC, et al. Recommended diag-nostic criteria for paraneoplastic neurological syndromes. J Neurol Neurosurg Psychiatry 2004;75:1135-40.2. Hasadsri L, Lee J, Wang BH, Yekkirala L, Wang M. Anti-Yo associated paraneoplastic cerebellar degeneration in a man with The New England Journal of Medicine Downloaded from nejm.org on April 13, 2016. For personal use only. No other uses without permission.  Copyright © 2015 Massachusetts Medical Society. All rights reserved. correspondencen engl j med 373;19 nejm.org november 5, 2015 1881large cell cancer of the lung. Case Rep Neurol Med 2013;2013: 725936.3. Armangue T, Leypoldt F, Málaga I, et al. Herpes simplex vi-rus encephalitis is a trigger of brain autoimmunity. Ann Neurol 2014;75:317-23.4. Prüss H, Finke C, Höltje M, et al. N-methyl-D-aspartate re-ceptor antibodies in herpes simplex encephalitis. Ann Neurol 2012;72:902-11.DOI: 10.1056/NEJMc1510342Chagas’ DiseaseTo the Editor: We would like to address some key points related to the article by Bern (July 30 issue)1 on the basis of our everyday experience in clinical and surgical practice. Bern did not men-tion precordial chest pain in the clinical picture of patients with chronic Chagas’ disease. Precor-dial chest pain affects up to 15% of patients with this condition and may simulate acute coronary syndromes in the absence of obstructive coro-nary artery disease.2 Abnormalities in left ven-tricular wall motion have prognostic value in pa-tients with chronic Chagas’ disease because these abnormalities are a marker of disease progres-sion to chronic cardiomyopathy.3 Fever is not routinely observed in heart-transplant recipients in whom there has been reactivation of Trypano-soma cruzi infection. Rather, the diagnosis of Cha-gas’ disease should be suspected in patients with symptoms resembling those of acute cellular re-jection despite the administration of proper im-munosuppressive therapy, since the parasite is seldom seen in myocardial tissue.4 Amiodarone increases the risk of death among patients with chronic Chagas’ disease and chronic heart fail-ure. Consequently, this drug should only be given to patients with symptomatic, life-threatening ventricular arrhythmias.5Reinaldo B. Bestetti, M.D., Ph.D. Marcelo E. Garcia, M.D., Ph.D. Carolina B.A. Restini, Pharm.D., Ph.D.University of Ribeirão Preto Ribeirão Preto, Brazil rbestetti44@gmail.comNo potential conflict of interest relevant to this letter was re-ported.1. Bern C. Chagas’ disease. N Engl J Med 2015;373:456-66.2. Bestetti RB, Restini CB. Precordial chest pain in patients with chronic Chagas disease. Int J Cardiol 2014;176:309-14.3. Bestetti RB, Cardinalli-Neto A. Antitrypanosomal therapy for chronic Chagas’ disease. N Engl J Med 2011;365:1258-9.4. Theodoropoulos TA, Silva AG, Bestetti RB. Eosinophil blood count and anemia are associated with Trypanosoma cruzi infec-tion reactivation in Chagas’ heart transplant recipients. Int J Cardiol 2010;145:55-6.5. Ayub-Ferreira SM, Mangini S, Issa VS, et al. Mode of death on Chagas heart disease: comparison with other etiologies: a sub-analysis of the REMADHE prospective trial. PLoS Negl Trop Dis 2013;7(4):e2176.DOI: 10.1056/NEJMc1510996To the Editor: Bern points out the lack of data available for mapping the estimated prevalence of Chagas’ disease at the subnational level. Never-theless, Argentina is a large country that includes diverse climatic regions, and this fact limits the circulation of the vector for T. cruzi. Therefore, the provinces of Chaco, Catamarca, Formosa, Santi-ago del Estero, San Juan, and Mendoza had a re-emergence of vectorial transmission, whereas there was only a minor risk of vectorial transmis-sion in the rural areas of Córdoba, Corrientes, La Rioja, Salta, and Tucumán.1 The conditions that increase the risk of contracting the disease are the presence of straw houses, earthen floors, and tropical weather. For these reasons, an area in Chaco known as Monte Impenetrable, a forest with an area of 3000 km2, has the highest rate of vectorial circulation in Argentina. However, the provinces of San Luis, Misiones, and Santa Fé managed to break vector circulation by imple-menting prevention programs. In the remaining provinces, such as Buenos Aires, all the new cas-es correspond with the vertical transmission of Chagas’ disease, which is particularly influenced by national and international migrations.2Debora Pellegrini, M.D. Rosana Jordan, M.D. Julio E. Bruetman, M.D.British Hospital of Buenos Aires Buenos Aires, Argentina debopellegrini@hotmail.comNo potential conflict of interest relevant to this letter was re-ported.1. Programa Nacional de Chagas. Diagnóstico de situación. Buenos Aires: Ministerio de Salud, 2013 (http://www.msal.gov.ar/chagas/index.php/institucional/diagnostico).2. Moscatelli G, García Bournissen F, Freilij H, et al. Impact of The New England Journal of Medicine Downloaded from nejm.org on April 13, 2016. For personal use only. No other uses without permission.  Copyright © 2015 Massachusetts Medical Society. All rights reserved. 

Bornavirus Associated with Fatal Human Encephalitis

https://www.openagrar.de/servlets/MCRFileNodeServlet/Document_derivate_00014309/SD2015520.pdf

Bornavirus Associated with Fatal Human Encephalitis

Abstract

Similar works

Full text

Available Versions

OA OpenAgrar repository