Almeida Gabriel Magno de Freitas, de Oliveira Danilo Bretas, Magalhães Cintia Lopes de Brito, Bonjardim Cláudio Antônio, Ferreira Paulo César Peregrino, Kroon Erna Geessien
Laboratório de Vírus, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos, 6627 Pampulha, Belo Horizonte CEP 31270-901, MG, Brazil.
Antiviral Res. 2008 Dec;80(3):302-8. doi: 10.1016/j.antiviral.2008.06.016. Epub 2008 Jul 25.
Interferons (IFNs) are cytokines with important immunomodulatory activity in vertebrates. Although type I IFNs and interleukins (IL) 29 and 28a (type III IFNs) bind to different cellular receptors and have distinct structures, most of their biological activities are redundant. Apeu virus (APEUV) is a member of the Bunyaviridae family isolated from the Brazilian rain forest. In this paper we evaluated the antiviral activity of type I and type III IFNs against APEUV. All tested IFNs were able to induce an antiviral state against the virus in a dose-dependent way. The activity of type III IFNs did not need the presence of type I IFNs. Mixing both types of IFNs did not improve the biological activity of each type alone. The tested IFNs were also able to protect human peripheral blood mononuclear cells from infection. IFN alpha2, IFN beta, IL-29 and IL-28a induced the expression of 2',5'-oligoadenylate synthetase (2'5'OAS) and 6-16 genes. Although MxA gene was related to antiviral activity against Bunyaviruses, there was no induction of MxA in our model. We were able to show activity of type I and type III IFNs against a RNA virus, and that this activity is not dependent on MxA gene.
干扰素（IFNs）是脊椎动物中具有重要免疫调节活性的细胞因子。虽然I型干扰素和白细胞介素（IL）29及28a（III型干扰素）与不同的细胞受体结合且结构不同，但它们的大多数生物学活性是冗余的。阿佩乌病毒（APEUV）是从巴西雨林分离出的布尼亚病毒科成员。在本文中，我们评估了I型和III型干扰素对APEUV的抗病毒活性。所有测试的干扰素都能够以剂量依赖的方式诱导针对该病毒的抗病毒状态。III型干扰素的活性不需要I型干扰素的存在。将两种类型的干扰素混合并不能提高每种类型单独的生物学活性。测试的干扰素还能够保护人外周血单核细胞免受感染。干扰素α2、干扰素β、IL - 29和IL - 28a诱导了2',5'-寡腺苷酸合成酶（2'5'OAS）和6 - 16基因的表达。虽然Mx A基因与针对布尼亚病毒的抗病毒活性有关，但在我们的模型中没有诱导出Mx A。我们能够证明I型和III型干扰素对一种RNA病毒具有活性，并且这种活性不依赖于Mx A基因。
