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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The <span class="elsevierStyleItalic">Jornal de Pediatria</span> has published an elegant review paper entitled &#8220;Atypical manifestations of Epstein-Barr virus in children&#58; a diagnostic challenge&#8221;&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> The authors performed a literature review including the last 30 years of publications on atypical manifestations associated with an Epstein-Barr virus &#40;EBV&#41; infection&#46; However&#44; I would like to complement their review by providing a particularly important point of view related to atypical EBV infections&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">EBV is a gamma-1 herpes virus restricted to primate hosts&#44; characterized by its persistence in the B-lymphoid system&#44; and its capacity to stimulate B-cells growth by coordinating the expression of latent cycle genes&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> Most EBV-infected individuals are asymptomatic or present infectious mononucleosis syndrome with a benign course&#44; especially teenagers and young adults&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> In its normal course&#44; EBV infects B-cells and the immune system controls the virus using a complex mechanism that involves NK&#44; iNKT&#44; CD4&#44; and CD8 cells&#46; Genetic alterations leading to functional NK or T-cell impairment may lead to a failure in the EBV control mechanisms&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Primary immunodeficiencies &#40;PIDs&#41; are a group of different diseases that cause alterations in the development and&#47;or function of the immune system&#44; leading to an increased susceptibility to infections and&#44; in some cases&#44; increased incidence of autoimmune diseases and malignancies&#46; Most PID cases are genetic diseases that follow simple Mendelian patterns of inheritance&#44; while a few others are considered as complex disorders&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">4&#44;5</span></a> The advance in the genetic approaches in the last years has increased the pace at which causative genes for PIDs are being discovered&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Recently&#44; Palendira and Rickson&#44; in a educational and simple method&#44; divided PID patients into groups to explain the susceptibility to EBV infections&#58; &#40;1&#41; PIDs that are selectively susceptible to EBV&#59; &#40;2&#41; PIDs with broader virus susceptibility&#44; but frequent EBV disease&#59; &#40;3&#41; PIDs generally susceptible to viral and nonviral infections&#59; and &#40;4&#41; PIDs with an inherent susceptibility to lymphoma&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Group 1 includes the X-linked lymphoproliferative diseases type 1&#44; caused by SH2D1A gene mutations&#44; and type 2&#44; associated with XIAP gene mutations&#46; In both diseases&#44; patients could present severe infectious mononucleosis&#59; and acute disease could result in a cytokine storm that causes macrophage activation and hemophagocytic lymphohistiocytosis &#40;HLH&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4</span></a> In another review&#44; authors added three different PIDs to this group&#44; including mutations in the genes PRF1 &#40;perforin deficiency&#44; autosomal recessive &#40;AR&#41;&#41;&#44; STXBP2 &#40;munc18-2 deficiency&#44; AR&#41;&#44; and UNC13D &#40;munc13-4 deficiency&#44; AR&#41;&#44; which are also associated with HLH and the development of chronic and severe EBV disease&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Group 2 contains PIDs caused by mutations in genes CD27 &#40;CD27 deficiency&#44; AR&#41;&#44; MAGT1 &#40;XMEN syndrome&#44; X-linked&#41;&#44; ITK &#40;ITK deficiency&#44; AR&#41;&#44; CORO1A &#40;coronin-1A deficiency&#44; AR&#41;&#44; FCGR3 &#40;CD16 deficiency&#44; AR&#41;&#44; and MCM4 &#40;MCM4 deficiency&#44; AR&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> The diseases in this group showed an increased susceptibility not only to EBV&#44; but also to other herpes virus family and&#44; in some cases&#44; to HPV&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Group 3 has complex PIDs with different predispositions to several microorganisms&#44; including EBV infections&#46; The PIDs included in this group are result of mutations in genes PIK3CD &#40;Activated PI3-kinase delta syndrome&#44; autosomal dominant &#40;AD&#41;&#41;&#44; STK4 &#40;MST1 deficiency&#44; AR&#41;&#44; ZAP70 &#40;Zap-70 deficiency&#44; AR&#41;&#44; CTPS1 &#40;CTPS1 deficiency&#44; AR&#41;&#44; CARD11 &#40;CARD11 deficiency&#44; AR&#41;&#44; LRBA &#40;LRBA deficiency&#44; AR&#41;&#44; GATA2 &#40;mono MAC syndrome or GATA2 deficiency&#44; AD&#41;&#44; LYST &#40;Chediak-Higashi syndrome&#44; AR&#41;&#44; and hypomorphic mutations in ARTEMIS and DNA ligase IV&#44; both associated with Omenn syndrome&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4&#44;6</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">The PIDs in group 4 present different degrees of immune system deficiency&#44; which are also associated with increased cancer incidence and the involvement of EBV in some of these tumors&#44; especially lymphomas&#46; This group includes PIDs with mutations in genes WAS &#40;Wiskott&#8211;Aldrich syndrome&#44; X-linked&#41;&#44; ATM &#40;Ataxia telangiectasia syndrome&#44; AR&#41;&#44; and TNFRSF6 &#40;ALPS-FAS&#44; AD and AR&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4&#44;6</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The message for all pediatricians is to consider EBV as a causative agent in clinical pictures similar to those described by Bolis et al&#46; In addition to the immune system impairment associated with treatment for several diseases&#44; we must also consider these situations as a red alert for primary immunodeficiencies in pediatric patients&#46; Recognizing PIDs may be essential to achieve a better management for patients with atypical EBV infections&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0050" class="elsevierStylePara elsevierViewall">C&#46;H&#46;I&#46;L&#46;D&#46;R&#46;E&#46;N&#46; initiative for primary immunodeficiency research of the <span class="elsevierStyleGrantSponsor" id="gs1">Jeffrey Modell Foundation</span>&#59; Postdoctoral Fellow abroad through Coordena&#231;&#227;o de Aperfei&#231;oamento de Pessoal de N&#237;vel Superior &#8211; CAPES &#40;Higher Education Personnel Improvement Coordination&#41;&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">The author declares no conflicts of interest&#46;</p></span></span>"
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Letter to the Editor
Atypical manifestations of Epstein-Barr virus: red alert for primary immunodeficiencies
Manifestações atípicas do vírus de Epstein-Barr: alerta vermelho para imunodeficiências primárias
Gesmar R.S. Segundo
Universidade Federal de Uberlândia (UFU), Departamento de Pediatria, Uberlândia, MG, Brazil
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The <span class="elsevierStyleItalic">Jornal de Pediatria</span> has published an elegant review paper entitled &#8220;Atypical manifestations of Epstein-Barr virus in children&#58; a diagnostic challenge&#8221;&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> The authors performed a literature review including the last 30 years of publications on atypical manifestations associated with an Epstein-Barr virus &#40;EBV&#41; infection&#46; However&#44; I would like to complement their review by providing a particularly important point of view related to atypical EBV infections&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">EBV is a gamma-1 herpes virus restricted to primate hosts&#44; characterized by its persistence in the B-lymphoid system&#44; and its capacity to stimulate B-cells growth by coordinating the expression of latent cycle genes&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> Most EBV-infected individuals are asymptomatic or present infectious mononucleosis syndrome with a benign course&#44; especially teenagers and young adults&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> In its normal course&#44; EBV infects B-cells and the immune system controls the virus using a complex mechanism that involves NK&#44; iNKT&#44; CD4&#44; and CD8 cells&#46; Genetic alterations leading to functional NK or T-cell impairment may lead to a failure in the EBV control mechanisms&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Primary immunodeficiencies &#40;PIDs&#41; are a group of different diseases that cause alterations in the development and&#47;or function of the immune system&#44; leading to an increased susceptibility to infections and&#44; in some cases&#44; increased incidence of autoimmune diseases and malignancies&#46; Most PID cases are genetic diseases that follow simple Mendelian patterns of inheritance&#44; while a few others are considered as complex disorders&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">4&#44;5</span></a> The advance in the genetic approaches in the last years has increased the pace at which causative genes for PIDs are being discovered&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Recently&#44; Palendira and Rickson&#44; in a educational and simple method&#44; divided PID patients into groups to explain the susceptibility to EBV infections&#58; &#40;1&#41; PIDs that are selectively susceptible to EBV&#59; &#40;2&#41; PIDs with broader virus susceptibility&#44; but frequent EBV disease&#59; &#40;3&#41; PIDs generally susceptible to viral and nonviral infections&#59; and &#40;4&#41; PIDs with an inherent susceptibility to lymphoma&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Group 1 includes the X-linked lymphoproliferative diseases type 1&#44; caused by SH2D1A gene mutations&#44; and type 2&#44; associated with XIAP gene mutations&#46; In both diseases&#44; patients could present severe infectious mononucleosis&#59; and acute disease could result in a cytokine storm that causes macrophage activation and hemophagocytic lymphohistiocytosis &#40;HLH&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4</span></a> In another review&#44; authors added three different PIDs to this group&#44; including mutations in the genes PRF1 &#40;perforin deficiency&#44; autosomal recessive &#40;AR&#41;&#41;&#44; STXBP2 &#40;munc18-2 deficiency&#44; AR&#41;&#44; and UNC13D &#40;munc13-4 deficiency&#44; AR&#41;&#44; which are also associated with HLH and the development of chronic and severe EBV disease&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Group 2 contains PIDs caused by mutations in genes CD27 &#40;CD27 deficiency&#44; AR&#41;&#44; MAGT1 &#40;XMEN syndrome&#44; X-linked&#41;&#44; ITK &#40;ITK deficiency&#44; AR&#41;&#44; CORO1A &#40;coronin-1A deficiency&#44; AR&#41;&#44; FCGR3 &#40;CD16 deficiency&#44; AR&#41;&#44; and MCM4 &#40;MCM4 deficiency&#44; AR&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> The diseases in this group showed an increased susceptibility not only to EBV&#44; but also to other herpes virus family and&#44; in some cases&#44; to HPV&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">4</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Group 3 has complex PIDs with different predispositions to several microorganisms&#44; including EBV infections&#46; The PIDs included in this group are result of mutations in genes PIK3CD &#40;Activated PI3-kinase delta syndrome&#44; autosomal dominant &#40;AD&#41;&#41;&#44; STK4 &#40;MST1 deficiency&#44; AR&#41;&#44; ZAP70 &#40;Zap-70 deficiency&#44; AR&#41;&#44; CTPS1 &#40;CTPS1 deficiency&#44; AR&#41;&#44; CARD11 &#40;CARD11 deficiency&#44; AR&#41;&#44; LRBA &#40;LRBA deficiency&#44; AR&#41;&#44; GATA2 &#40;mono MAC syndrome or GATA2 deficiency&#44; AD&#41;&#44; LYST &#40;Chediak-Higashi syndrome&#44; AR&#41;&#44; and hypomorphic mutations in ARTEMIS and DNA ligase IV&#44; both associated with Omenn syndrome&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4&#44;6</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">The PIDs in group 4 present different degrees of immune system deficiency&#44; which are also associated with increased cancer incidence and the involvement of EBV in some of these tumors&#44; especially lymphomas&#46; This group includes PIDs with mutations in genes WAS &#40;Wiskott&#8211;Aldrich syndrome&#44; X-linked&#41;&#44; ATM &#40;Ataxia telangiectasia syndrome&#44; AR&#41;&#44; and TNFRSF6 &#40;ALPS-FAS&#44; AD and AR&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4&#44;6</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The message for all pediatricians is to consider EBV as a causative agent in clinical pictures similar to those described by Bolis et al&#46; In addition to the immune system impairment associated with treatment for several diseases&#44; we must also consider these situations as a red alert for primary immunodeficiencies in pediatric patients&#46; Recognizing PIDs may be essential to achieve a better management for patients with atypical EBV infections&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Funding</span><p id="par0050" class="elsevierStylePara elsevierViewall">C&#46;H&#46;I&#46;L&#46;D&#46;R&#46;E&#46;N&#46; initiative for primary immunodeficiency research of the <span class="elsevierStyleGrantSponsor" id="gs1">Jeffrey Modell Foundation</span>&#59; Postdoctoral Fellow abroad through Coordena&#231;&#227;o de Aperfei&#231;oamento de Pessoal de N&#237;vel Superior &#8211; CAPES &#40;Higher Education Personnel Improvement Coordination&#41;&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Conflicts of interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">The author declares no conflicts of interest&#46;</p></span></span>"
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Article information
ISSN: 00217557
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