Interação de acanthamoeba polyphaga mimivirus com o sistema interferon humano em células mononucleares do sangue periférico (PBMC)

• Ano de defesa: 2013
• Autor(a) principal: Lorena Christine Ferreira da Silva
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Interferons; Acanthamoeba polyphaga mimivirus; PBMC; Microbiologia; Células mononucleares do sangue periférico; Acanthamoeba polyphaga; Interferon
• Link de acesso: http://hdl.handle.net/1843/BUBD-9UKJ3B

Acanthamoeba polyphaga mimivirus (APMV) is a giant, double-stranded virus of the Mimiviridae family that was discovered in 2003. This virus presents high structural and genetic complexity. Although free-living amoebas are hosts for the APMV, recent studies have shown that this virus is able to replicate in phagocytes and it is believed that might be a human pathogen that causes pneumonia. In the present study, were investigated how some components of the interferon (IFN) system are stimulated by APMV in human peripheral blood mononuclear cells (PBMC) and how APMV replication is affected by IFN treatment. The results demonstrated that APMV is able to replicate in human total PBMC, inducing type I Interferons (IFN) in these cells but inhibiting interferon stimulated genes (ISG) induction by viroceptor and STAT dephosphorylation independent mechanisms. Were also showed that APMV is resistant to the antiviral action of interferon-alpha2 (IFNA2) but is sensitive to the antiviral action of interferon-beta (IFNB1). The results confirm those obtained in previous studies, which demonstrated the productive infection of professional phagocytes with APMV, and expands them by showing that this virus is recognized by the immune system of vertebrates and inhibits it. Thus, were provided the first data regarding APMV and the IFN system interaction and raised new and relevant evolutional questions about the relationship between APMV and vertebrate hosts.