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. 2018 Feb 22;8:3471. doi: 10.1038/s41598-018-21872-2

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Proposed working model of the role of pI215L during ASFV infection. Once ASFV enters the host cell, different host mechanisms are subverted in other to generate a productive infection. By encoding an E2 ubiquitin-conjugating enzyme (pI215L), ASFV hijacks the cellular ubiquitin-proteasome system modulating the function and subcellular localization of host proteins and its own proteins. By controlling the ubiquitination status of the cellular proteins, viruses are able to evade host antiviral responses by targeting proteins to proteasomal degradation and to modulate the activity of viral proteins in different mechanisms. Our model suggests that by downregulating I215L expression, a reduction in the abundance of ubiquitin-tagged proteins occurs and consequently causes an inhibition of several crucial viral processes (e.g. genome replication, gene transcription, translation, egress), as well as host pathways (e.g. antiviral immune response, apoptosis).