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Paving the way towards understanding the inflammatory pathways triggered by giant viruses in mammalian cells: effect of mimivirus-cell interactions on IκBα degradation
bioRxiv - Microbiology Pub Date : 2021-09-16 , DOI: 10.1101/2021.09.16.460633
Juliana dos Santos Oliveira , Dahienne Ferreira Oliveira , Victor Alejandro Essus , Gabriel Henrique Pereira Nunes , Leandro Honorato , Leandro Oliveira , Leonardo Nimrichter , José Mauro Peralta , Allan Jefferson Guimaraes , Debora Foguel , Juliana Reis Cortines

Even after two decades since the identification of the first giant virus, the Acanthamoeba polyphaga mimivirus (APMV), it still elude scientists. Their gigantic size and genome are unique in the whole virosphere, and many aspects of their biology are still unknown, including their possible hosts. They are cultivated in laboratories using Acanthamoeba cells as hosts, but little is known about the infectivity of these giant viruses in vertebrate cells. However, there is evidence of the possible involvement of APMV in pneumonia and activation of inflammatory pathways. Among the hundreds of prospected giant viruses members is Tupanvirus, isolated in Brazil. Its particles have a characteristically large size varying between 1.2 to 2 μm and are covered by fibrils. In the present work, we aim to study the consequences of the incubation of APMV and Tupanvirus with mammalian cells. These cells express Toll-like receptors (TLR) that are capable of recognizing lipopolysaccharides, favoring the internalization of the antigen and activation of the inflammatory system. We used a lineage of human lung adenocarcinoma cells (A549) to evaluate possible effects of TLR activation by the giant viruses and if we could detect the probable cause of the said giant-virus dependent pneumonia. Our results show that APMV and Tupanvirus (TPV) activate cellular receptors related to the Toll-like 4 type-induced inflammatory response and that the A549 cells are capable of internalizing the latter virus. Therefore, this study brings new insights into the possible interactions established between mimiviruses (here represented by APMV and Tupanvirus) and members of the innate cellular immune response.

中文翻译:

为了解哺乳动物细胞中巨型病毒引发的炎症途径铺平道路:拟菌病毒-细胞相互作用对 IκBα 降解的影响

即使在发现第一个巨型病毒——拟多食棘阿米巴病毒 (APMV) 后的二十年里,科学家们仍然没有发现它。它们巨大的体型和基因组在整个病毒圈中都是独一无二的,它们生物学的许多方面仍然未知,包括它们可能的宿主。它们在实验室中使用棘阿米巴进行培养细胞作为宿主,但对这些巨型病毒在脊椎动物细胞中的感染性知之甚少。然而,有证据表明 APMV 可能参与肺炎和炎症通路的激活。在数百个潜在的巨型病毒成员中,有在巴西分离的图潘病毒。其颗粒具有特征性的大尺寸,在 1.2 至 2 μm 之间变化,并被原纤维覆盖。在目前的工作中,我们的目标是研究 APMV 和 Tupanvirus 与哺乳动物细胞孵育的后果。这些细胞表达能够识别脂多糖的 Toll 样受体 (TLR),有利于抗原的内化和炎症系统的激活。我们使用人类肺腺癌细胞谱系 (A549) 来评估巨病毒激活 TLR 的可能影响,以及我们是否能够检测到所述巨病毒依赖性肺炎的可能原因。我们的结果表明 APMV 和 Tupanvirus (TPV) 激活与 Toll 样 4 型诱导的炎症反应相关的细胞受体,并且 A549 细胞能够内化后者病毒。因此,这项研究为拟菌病毒(此处由 APMV 和 Tupanvirus 表示)与先天细胞免疫反应的成员之间可能建立的相互作用带来了新的见解。我们的结果表明 APMV 和 Tupanvirus (TPV) 激活与 Toll 样 4 型诱导的炎症反应相关的细胞受体,并且 A549 细胞能够内化后一种病毒。因此,这项研究为拟菌病毒(此处由 APMV 和 Tupanvirus 表示)与先天细胞免疫反应的成员之间可能建立的相互作用带来了新的见解。我们的结果表明 APMV 和 Tupanvirus (TPV) 激活与 Toll 样 4 型诱导的炎症反应相关的细胞受体,并且 A549 细胞能够内化后者病毒。因此,这项研究为拟菌病毒(此处由 APMV 和 Tupanvirus 表示)与先天细胞免疫反应的成员之间可能建立的相互作用带来了新的见解。
更新日期:2021-09-19
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