African swine fever virus replication events and cell nucleus: New insights and perspectives
•Early intranuclear ASFV genome replication, modification of host nuclear landscape and epigenetic signatures.•ASFV-A104R histone-like protein is needed for viral progeny production.•AFSV encodes for an E2 ubiquitin-conjugating enzyme that is required for viral replication cycle.•In vitro inhibition...
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Published in | Virus research Vol. 270; p. 197667 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.09.2019
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Subjects | |
Online Access | Get full text |
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Summary: | •Early intranuclear ASFV genome replication, modification of host nuclear landscape and epigenetic signatures.•ASFV-A104R histone-like protein is needed for viral progeny production.•AFSV encodes for an E2 ubiquitin-conjugating enzyme that is required for viral replication cycle.•In vitro inhibition of the ASFV-topoisomerase II disrupts viral replication.•ASFV-QP509 L and Q706 L RNA helicases have non-redundant and essential activities.
African swine fever (ASF) is currently matter for major concerns in global swine industry as it is highly contagious and causes acute fatal haemorrhagic fever in domestic pigs and wild boar. The absence of effective vaccines and treatments pushes ASF control to relay on strict sanitary and stamping out measures with costly socio-economic impacts. The current epidemic scenario of fast spreading throughout Asiatic countries impels further studies on prevention and combat strategies against ASF.
Herein we review knowledge on African Swine Fever Virus (ASFV) interactions with the host cell nucleus and on the functional properties of different viral DNA-replication related proteins. This entails, the confirmation of an intranuclear viral DNA replication phase, the characterization of cellular DNA damage responses (DDR), the subnuclear compartments disruption due to viral modulation, and the unravelling of the biological role of several viral proteins (A104R, I215 L, P1192R, QP509 L and Q706 L), so to contribute to underpin rational strategies for vaccine candidates development. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0168-1702 1872-7492 |
DOI: | 10.1016/j.virusres.2019.197667 |