Adenovirus sensing by the immune system

• Type of Material: Article
• Authors: Svetlana Atasheva, Emory University; Dmitry Shayakhmetov, Emory University
• Language: English
• Date: 2016-12-01
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2016 Elsevier B.V. All rights reserved.
• Final Published Version (URL): http://dx.doi.org/10.1016/j.coviro.2016.08.017
• Title of Journal or Parent Work: Current Opinion in Virology
• ISSN: 1879-6257
• Volume: 21
• Start Page: 109
• End Page: 113
• Grant/Funding Information: This work was supported by the funds from the US National Institutes of Health grants AI065429, AI107960, AI126816, and funds from the Children’s Healthcare of Atlanta Research Trust to D.M.S.
• Keywords: TRIGGERS; DISEASE; RECEPTOR; Virology; RESPONSES; INNATE IMMUNITY; Life Sciences & Biomedicine; DNA; LIVER; Science & Technology; KUPFFER CELLS; VECTORS; IN-VIVO
• Research Categories: Biology, Virology; Biology, Microbiology; Health Sciences, Immunology

Abstract

The host immune system developed multiple ways for recognition of viral pathogens. Upon disseminated adenovirus infection, the immune system senses adenovirus invasion from the moment it enters the bloodstream. The soluble blood factors, FX, antibodies, and complement, can bind and activate plethora of host-protective immune responses. Adenovirus binding to the cellular β3 integrin and endosomal membrane rupture trigger activation of IL-1α/IL-1R1 proinflammatory cascade leading to attraction of cytotoxic immune cells to the site of infection. Upon cell entry, adenovirus exposes its DNA genome in the cytoplasm and triggers DNA sensors signaling. Even when inside the nucleus, the specialized cellular machinery that recognizes the double-strand DNA breaks become activated and triggers viral DNA replication arrest. Thus, the host employs very diverse mechanisms to prevent viral dissemination.