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v. 2 n. 2 (2021): Edição Especial: Anais de Eventos
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Anais do I Congresso Nacional de Microbiologia Clínica On-Line
MECANISMOS DE MANUTENÇÃO DA LATÊNCIA DO VÍRUS VARICELA ZÓSTER: UMA ADAPTAÇÃO NECESSÁRIA
Autores
Raniery Augusto dos Santos Beserra Nogueira
Ana Beatriz Silva Barbosa
Francisco Das Chagas Diassis Jácome Valentim
Sâmya Pires Batista De Azevêdo
Jamile Rodrigues Cosme De Holanda
Palavras-chave:
APOPTOSE, FASES DE LEITURA ABERTA, GENOMA VIRAL, HERPES ZOSTER, LATÊNCIA VIRAL
Resumo
Introdução: O Vírus Varicela Zóster pertence à subfamília α-herpesviridae e é um DNA-vírus de fita dupla, possuindo 68 Fases de Leitura Aberta (ORF) únicas. Sendo responsável por varicela, em um primeiro contato, o vírus mantém-se latente por um longo período em gânglios das raízes dorsais e de nervos cranianos, disseminando-se por essas estruturas após décadas, quando reativado, configurando Herpes Zóster, cujas complicações prejudicam a qualidade de vida dos pacientes. Posteriormente à infecção primária, o vírus classifica-se como neurotrópico e seus meios de sobrevida em neurônios, ainda não são claros. Objetivo: Este estudo busca elucidar os mecanismos de latência desse patógeno, visando ao desenvolvimento do conhecimento científico no assunto. Material e Métodos: Utilizando-se da plataforma online PubMed, foram pesquisados os descritores “varicella zoster virus”, em adição a “apoptosis”, e “herpes zoster infection”, com o operador booleano “AND” tendo como filtro a delimitação temporal entre 01/01/2018 e 01/05/2021. Resultados: Ao longo do período de latência, o DNA viral é encontrado em células neuronais, estando em forma não-integrada (cita-se epissoma infinito ou comprimento concateméro) e sua transcrição é fortemente restrita. Em meio ao genoma viral, o ORF63 mostrou-se de grande relevância na proteção de neuronal em humanos. Durante monitorização, foi-se percebido a migração da proteína OFR63 quando se induz apoptose na célula, tornando-se mais citoplasmática. A partir disso, percebeu-se interação inibitória entre a proteína ORF63 e a estaurosporina, molécula indutora da apoptose. O que até então se mostrava como hipótese, foi melhor embasado pela redução dos níveis de caspase-3, marcador apoptótico celular, em neurônios infectados pelo VVZ quando comparados a outras células (infectadas ou não). Conclusão: Diante de todas as questões, ainda cientificamente obscuras, acerca da capacidade desse vírus de sobreviver durante décadas nos gânglios nervosos, ressalta-se a necessidade de mais pesquisas na área, para que se tenha melhor manejo de pacientes infectados com o Vírus Varicela Zóster. Ademais, não se pode negar que a inibição da apoptose é uma evolução adaptativa muito favorável ao microrganismo, já que as células neuronais são hospedeiras senescentes e seu aumento de vida significa aumento de vida do patógeno.
Como Citar
Nogueira, R. A. dos S. B. ., Barbosa, A. B. S., Valentim, F. D. C. D. J., Azevêdo, S. P. B. D. ., & Holanda, J. R. C. D. (2021). MECANISMOS DE MANUTENÇÃO DA LATÊNCIA DO VÍRUS VARICELA ZÓSTER: UMA ADAPTAÇÃO NECESSÁRIA. Revista Multidisciplinar Em Saúde , 2 (2), 25. https://doi.org/10.51161/rems/1182
Seção
Anais do I Congresso Nacional de Microbiologia Clínica On-Line
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