Aspectos gerais da infecção pelo vírus Zika: uma revisão

Detalhes bibliográficos
Autor(a) principal: Silva, Ana Beatriz Ramalho da
Data de Publicação: 2017
Tipo de documento: Trabalho de conclusão de curso
Idioma: por
Título da fonte: Repositório Institucional da UFRN
Texto Completo: https://repositorio.ufrn.br/handle/123456789/43144
Resumo: Zika vírus (ZIKV) is an arthropod-borne virus which belongs to the family Flaviviridae, being transmitted by Aedes species mosquitoes, mainly by Aedes aegypti. The virus was discovered in 1947 in the Zika Forest, Uganda. Since its discovery, the cases were sporadic and confined to a zone across Africa and Asia until the beginning of 21st century, when the virus emerged in differents parts of the world, causing sequential outbreaks on Yap Island (2007), French Polynesia (2013) and Brazil (2015) from where the virus spreads to others American countries. Besides the vectorial transmission, the ZIKV can be transmitted by sexual intercourse, by blood transfusion and from the mother to the baby. ZIKV is a RNA virus that encodes a large polyprotein, which encode a large polyprotein that is cleaved in three structural proteins: capisid protein (C), membrane glycoprotein precursor (prM) and envelope protein (E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5). About immune response to ZIKV, researches points out that the virus elicits the activation of intracellular innate immune receptors like TLR3, RIG-I, MDA-5, resulting in the production of type I interferons (IFN-I) and proinflammatory cytokines. Moreover, the virus doesn’t induce strong stimulation of dendritric cells and active NK cells more by cytokine production than its cytotoxic function. About adaptive immune response, the ZIKV stimulates a strong humoral response with producing neutralizing antibody, activating TCD4+ cells, which induce multiple cytokine production and TCD8+ cells activation that present high level of memory cells. Likely, sequential infections by ZIKV and others flavivirus cause ADE phenomenon due cross-reactivy, however this mechanism in this disease it’s not fully clear. Regarding the clinic, the infection is commonly asymptomatic, but the symptomatic cases are self-limiting and characterized by rash, arthralgia, myalgia and mild fever. However, complications involving the nervous system, like microcephaly in newborn babies and Guillain-Barré syndrome have been associated with ZIKV infection
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spelling Silva, Ana Beatriz Ramalho daFernandes, José VeríssimoSouza, Cássio Ricardo de Medeiros2018-01-11T12:31:46Z2021-10-06T11:13:54Z2018-01-11T12:31:46Z2021-10-06T11:13:54Z2017-12-052013088824SILVA, Ana Beatriz Ramalho da. Aspectos gerais da infecção pelo vírus Zika: uma revisão. 2017. 73 f. Trabalho de Conclusão de Curso (Graduação em Biomedicina) - Departamento de Biomedicina, Centro de Biociências, Universidade Federal do Rio Grande do Norte, Natal, 2017.https://repositorio.ufrn.br/handle/123456789/43144Zika vírus (ZIKV) is an arthropod-borne virus which belongs to the family Flaviviridae, being transmitted by Aedes species mosquitoes, mainly by Aedes aegypti. The virus was discovered in 1947 in the Zika Forest, Uganda. Since its discovery, the cases were sporadic and confined to a zone across Africa and Asia until the beginning of 21st century, when the virus emerged in differents parts of the world, causing sequential outbreaks on Yap Island (2007), French Polynesia (2013) and Brazil (2015) from where the virus spreads to others American countries. Besides the vectorial transmission, the ZIKV can be transmitted by sexual intercourse, by blood transfusion and from the mother to the baby. ZIKV is a RNA virus that encodes a large polyprotein, which encode a large polyprotein that is cleaved in three structural proteins: capisid protein (C), membrane glycoprotein precursor (prM) and envelope protein (E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5). About immune response to ZIKV, researches points out that the virus elicits the activation of intracellular innate immune receptors like TLR3, RIG-I, MDA-5, resulting in the production of type I interferons (IFN-I) and proinflammatory cytokines. Moreover, the virus doesn’t induce strong stimulation of dendritric cells and active NK cells more by cytokine production than its cytotoxic function. About adaptive immune response, the ZIKV stimulates a strong humoral response with producing neutralizing antibody, activating TCD4+ cells, which induce multiple cytokine production and TCD8+ cells activation that present high level of memory cells. Likely, sequential infections by ZIKV and others flavivirus cause ADE phenomenon due cross-reactivy, however this mechanism in this disease it’s not fully clear. Regarding the clinic, the infection is commonly asymptomatic, but the symptomatic cases are self-limiting and characterized by rash, arthralgia, myalgia and mild fever. However, complications involving the nervous system, like microcephaly in newborn babies and Guillain-Barré syndrome have been associated with ZIKV infectionO vírus Zika (ZIKV) é um arbovírus pertencente à família Flaviviridae, sendo transmitido por mosquitos do gênero Aedes, especialmente pela espécie Aedes aegypti. Sua descoberta se deu em 1947 na floresta Zika, em Uganda. Desde então, casos esporádicos foram relatados e confinados às regiões da África e da Ásia até que, no início século XXI o vírus emergiu em diferentes lugares do globo, causando três grandes surtos consecutivos na Ilha de Yap (2007), na Polinésia Francesa (2013) e no Brasil (2015), de onde se espalhou para outros países do continente americano. Além da transmissão vetorial, pode haver a transmissão vertical, por contato sexual ou transfusão de sangue. O ZIKV é um vírus de RNA que codifica uma poliproteína precursora, a qual é posteriormente processada em três proteínas estruturais: proteína do capsídeo (C), proteína precursora de membrana (prM), proteína do envelope (E) e 7 proteínas não estruturais (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5). Sobre a resposta imune ao ZIKV, estudos apontam que o vírus promove a ativação de receptores intracelulares da imunidade inata tais como o TLR3, RIG-1 e MDA-5, resultando na produção de interferon do tipo I (IFN-I) e citocinas pró-inflamatórias. Além disso, o vírus não induz uma forte estimulação de células dendríticas e acionam as células NK mais pela produção de citocinas do que por sua ação citotóxica. Sobre a resposta imune adaptativa, o ZIKV estimula uma forte resposta humoral, com produção de anticorpos neutralizantes, e promove a ativação tanto dos linfócitos TCD4+, os quais induzem uma produção múltipla de citocinas, como dos linfócitos TCD8+ que apresentam elevada proporção de células de memória. É provável que infecções sequenciais pelo ZIKV e outros flavivírus possam resultar no fenômeno ADE em decorrência da reatividade cruzada, entretanto tal mecanismo nessa virose não está totalmente esclarecido. Quanto à clínica, a infecção pelo ZIKV é frequentemente assintomática, mas os casos sintomáticos são de natureza autolimitada e caracterizados pelo aparecimento de exantema maculopapular, hiperemia conjuntival, mialgia, atralgia e febre branda. Entretanto, complicações envolvendo o sistema nervoso, como a Síndrome de Guillain-Barré (SGB) e a microcefalia em recém-nascidos, tem sido associadas à infecção pelo ZIKVUniversidade Federal do Rio Grande do NorteUFRNBrasilCurso de Bacharelado em BiomedicinaVírus ZikaResposta imunePatogeniaAspectos gerais da infecção pelo vírus Zika: uma revisãoinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/bachelorThesisinfo:eu-repo/semantics/openAccessporreponame:Repositório Institucional da UFRNinstname:Universidade Federal do Rio Grande do Norte (UFRN)instacron:UFRNTEXTInfecçaoVirusZika_Silva_2017.pdf.txtExtracted texttext/plain135221https://repositorio.ufrn.br/bitstream/123456789/43144/1/Infec%c3%a7aoVirusZika_Silva_2017.pdf.txtf49219e68285b8f129754db1a970ebcfMD51AspectosGeraisInfeccao_Silva_2017.pdf.txtExtracted texttext/plain135221https://repositorio.ufrn.br/bitstream/123456789/43144/2/AspectosGeraisInfeccao_Silva_2017.pdf.txtf49219e68285b8f129754db1a970ebcfMD52ORIGINALAspectosGeraisInfeccao_Silva_2017.pdfMonografiaapplication/pdf2109785https://repositorio.ufrn.br/bitstream/123456789/43144/3/AspectosGeraisInfeccao_Silva_2017.pdf92f9024c57fa6c143d3aa4e049bd71e3MD53CC-LICENSElicense_urlapplication/octet-stream49https://repositorio.ufrn.br/bitstream/123456789/43144/4/license_url4afdbb8c545fd630ea7db775da747b2fMD54license_textapplication/octet-stream0https://repositorio.ufrn.br/bitstream/123456789/43144/5/license_textd41d8cd98f00b204e9800998ecf8427eMD55license_rdfapplication/octet-stream0https://repositorio.ufrn.br/bitstream/123456789/43144/6/license_rdfd41d8cd98f00b204e9800998ecf8427eMD56LICENSElicense.txttext/plain756https://repositorio.ufrn.br/bitstream/123456789/43144/7/license.txta80a9cda2756d355b388cc443c3d8a43MD57123456789/431442021-10-06 08:13:54.313oai:https://repositorio.ufrn.br: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ório de PublicaçõesPUBhttp://repositorio.ufrn.br/oai/opendoar:2021-10-06T11:13:54Repositório Institucional da UFRN - Universidade Federal do Rio Grande do Norte (UFRN)false
dc.title.pr_BR.fl_str_mv Aspectos gerais da infecção pelo vírus Zika: uma revisão
title Aspectos gerais da infecção pelo vírus Zika: uma revisão
spellingShingle Aspectos gerais da infecção pelo vírus Zika: uma revisão
Silva, Ana Beatriz Ramalho da
Vírus Zika
Resposta imune
Patogenia
title_short Aspectos gerais da infecção pelo vírus Zika: uma revisão
title_full Aspectos gerais da infecção pelo vírus Zika: uma revisão
title_fullStr Aspectos gerais da infecção pelo vírus Zika: uma revisão
title_full_unstemmed Aspectos gerais da infecção pelo vírus Zika: uma revisão
title_sort Aspectos gerais da infecção pelo vírus Zika: uma revisão
author Silva, Ana Beatriz Ramalho da
author_facet Silva, Ana Beatriz Ramalho da
author_role author
dc.contributor.referees1.none.fl_str_mv Fernandes, José Veríssimo
dc.contributor.referees2.none.fl_str_mv Souza, Cássio Ricardo de Medeiros
dc.contributor.author.fl_str_mv Silva, Ana Beatriz Ramalho da
dc.subject.pr_BR.fl_str_mv Vírus Zika
Resposta imune
Patogenia
topic Vírus Zika
Resposta imune
Patogenia
description Zika vírus (ZIKV) is an arthropod-borne virus which belongs to the family Flaviviridae, being transmitted by Aedes species mosquitoes, mainly by Aedes aegypti. The virus was discovered in 1947 in the Zika Forest, Uganda. Since its discovery, the cases were sporadic and confined to a zone across Africa and Asia until the beginning of 21st century, when the virus emerged in differents parts of the world, causing sequential outbreaks on Yap Island (2007), French Polynesia (2013) and Brazil (2015) from where the virus spreads to others American countries. Besides the vectorial transmission, the ZIKV can be transmitted by sexual intercourse, by blood transfusion and from the mother to the baby. ZIKV is a RNA virus that encodes a large polyprotein, which encode a large polyprotein that is cleaved in three structural proteins: capisid protein (C), membrane glycoprotein precursor (prM) and envelope protein (E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5). About immune response to ZIKV, researches points out that the virus elicits the activation of intracellular innate immune receptors like TLR3, RIG-I, MDA-5, resulting in the production of type I interferons (IFN-I) and proinflammatory cytokines. Moreover, the virus doesn’t induce strong stimulation of dendritric cells and active NK cells more by cytokine production than its cytotoxic function. About adaptive immune response, the ZIKV stimulates a strong humoral response with producing neutralizing antibody, activating TCD4+ cells, which induce multiple cytokine production and TCD8+ cells activation that present high level of memory cells. Likely, sequential infections by ZIKV and others flavivirus cause ADE phenomenon due cross-reactivy, however this mechanism in this disease it’s not fully clear. Regarding the clinic, the infection is commonly asymptomatic, but the symptomatic cases are self-limiting and characterized by rash, arthralgia, myalgia and mild fever. However, complications involving the nervous system, like microcephaly in newborn babies and Guillain-Barré syndrome have been associated with ZIKV infection
publishDate 2017
dc.date.issued.fl_str_mv 2017-12-05
dc.date.accessioned.fl_str_mv 2018-01-11T12:31:46Z
2021-10-06T11:13:54Z
dc.date.available.fl_str_mv 2018-01-11T12:31:46Z
2021-10-06T11:13:54Z
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dc.identifier.citation.fl_str_mv SILVA, Ana Beatriz Ramalho da. Aspectos gerais da infecção pelo vírus Zika: uma revisão. 2017. 73 f. Trabalho de Conclusão de Curso (Graduação em Biomedicina) - Departamento de Biomedicina, Centro de Biociências, Universidade Federal do Rio Grande do Norte, Natal, 2017.
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identifier_str_mv 2013088824
SILVA, Ana Beatriz Ramalho da. Aspectos gerais da infecção pelo vírus Zika: uma revisão. 2017. 73 f. Trabalho de Conclusão de Curso (Graduação em Biomedicina) - Departamento de Biomedicina, Centro de Biociências, Universidade Federal do Rio Grande do Norte, Natal, 2017.
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