Viral regulation of host cell biology by hijacking of the nucleolar DNA-damage response

Rawlinson, Stephen M.; Zhao, Tianyue; Rozario, Ashley M.; Rootes, Christina L.; McMillan, Paul J.; Purcell, Anthony W.; Woon, Amanda P.; Marsh, Glenn A.; Lieu, Kim G.; Wang, Lin‐Fa; Netter, Hans; Bell, Toby D. M.; Stewart, Cameron R.; Moseley, Gregory W.

doi:10.1038/s41467-018-05354-7

Cited by 39 publications

(95 citation statements)

References 50 publications

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“…Recently, viral regulation of host cell machinery has been revealed to target nucleolar DNA-damage response (DDR) pathway by causing inhibition of nucleolar Treacle protein that increases Henipavirus (Hendra and Nipha virus) production (Rawlinson et al. 2018). A diagrammatic structure of Nipah virus is depicted in Figure 1.…”

Section: Nipah Virusmentioning

confidence: 99%

Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies – a comprehensive review

Singh

Dhama

Chakraborty³

et al. 2019

Veterinary Quarterly

168

125

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Nipah (Nee-pa) viral disease is a zoonotic infection caused by Nipah virus (NiV), a paramyxovirus belonging to the genus Henipavirus of the family Paramyxoviridae. It is a biosafety level-4 pathogen, which is transmitted by specific types of fruit bats, mainly Pteropus spp. which are natural reservoir host. The disease was reported for the first time from the Kampung Sungai Nipah village of Malaysia in 1998. Human-to-human transmission also occurs. Outbreaks have been reported also from other countries in South and Southeast Asia. Phylogenetic analysis affirmed the circulation of two major clades of NiV as based on currently available complete N and G gene sequences. NiV isolates from Malaysia and Cambodia clustered together in NiV-MY clade, whereas isolates from Bangladesh and India clusterered within NiV-BD clade. NiV isolates from Thailand harboured mixed population of sequences. In humans, the virus is responsible for causing rapidly progressing severe illness which might be characterized by severe respiratory illness and/or deadly encephalitis. In pigs below six months of age, respiratory illness along with nervous symptoms may develop. Different types of enzyme-linked immunosorbent assays along with molecular methods based on polymerase chain reaction have been developed for diagnostic purposes. Due to the expensive nature of the antibody drugs, identification of broad-spectrum antivirals is essential along with focusing on small interfering RNAs (siRNAs). High pathogenicity of NiV in humans, and lack of vaccines or therapeutics to counter this disease have attracted attention of researchers worldwide for developing effective NiV vaccine and treatment regimens.

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Section: Nipah Virusmentioning

confidence: 99%

Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies – a comprehensive review

Singh

Dhama

Chakraborty³

et al. 2019

Veterinary Quarterly

168

125

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“…Thus, VP24 nucleocytoplasmic trafficking might provide regulation of the replication-assembly switch, similar to mechanisms proposed for dynamic nucleocytoplasmic localisation of matrix proteins of paramyxoviruses (31). Many matrix proteins of henipaviruses have also recently been shown to have specific intranuclear functions through interaction with nuclear/nucleolar proteins (36,37). In light of our finding that VP24 undergoes nucleocytoplasmic trafficking, it is intriguing that mass spectrometry analysis identified a large number of proteins in the VP24 interactome with functions related to the nucleus (39), consistent with possible intranuclear functions of VP24.…”

Section: Discussionmentioning

confidence: 74%

“…Defective nuclear export of P1 correlates with impaired IFN antagonism and viral attenuation (32)(33)(34). Many proteins of cytoplasmic viruses also form intranuclear interactions/functions, including isoforms of RABV P protein and the matrix proteins of Nipah and Hendra viruses, enabling cytoplasmic viruses to modulate intranuclear processes (35)(36)(37).…”

mentioning

confidence: 99%

The Ebola virus interferon antagonist VP24 undergoes active nucleocytoplasmic trafficking

Harrison

Moseley

2020

Preprint

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Viral interferon (IFN) antagonist proteins mediate evasion of IFN-mediated innate immunity and are often multifunctional, having distinct roles in viral replication processes. Functions of the Ebola virus (EBOV) IFN antagonist VP24 include nucleocapsid assembly during cytoplasmic replication and inhibition of IFN-activated signalling by STAT1. For the latter, VP24 prevents STAT1 nuclear import via competitive binding to nuclear import receptors (karyopherins). Many viral proteins, including proteins from viruses with cytoplasmic replication cycles, interact with the trafficking machinery to undergo nucleocytoplasmic transport, with key roles in pathogenesis. Despite established karyopherin interaction, the nuclear trafficking profile of VP24 has not been investigated. We find that VP24 becomes strongly nuclear following overexpression of karyopherin or inhibition of nuclear export pathways. Molecular mapping indicates that cytoplasmic localisation of VP24 depends on a CRM1-dependent nuclear export sequence at the VP24 C-terminus. Nuclear export is not required for STAT1 antagonism, consistent with competitive karyopherin binding being the principal antagonistic mechanism while export mediates return of nuclear VP24 to the cytoplasm for replication functions. Thus, nuclear export of VP24 might provide novel targets for antiviral approaches.

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“…Key SRM applications for DNA damage detection can be found here in [99][100][101][102][103][104][105][106].…”

Section: Super Resolution Microscopy (Srm)mentioning

confidence: 99%

In Situ Detection of Complex DNA Damage Using Microscopy: A Rough Road Ahead

Nikitaki

Pariset

Sudar

et al. 2020

Cancers

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Complexity of DNA damage is considered currently one if not the primary instigator of biological responses and determinant of short and long-term effects in organisms and their offspring. In this review, we focus on the detection of complex (clustered) DNA damage (CDD) induced for example by ionizing radiation (IR) and in some cases by high oxidative stress. We perform a short historical perspective in the field, emphasizing the microscopy-based techniques and methodologies for the detection of CDD at the cellular level. We extend this analysis on the pertaining methodology of surrogate protein markers of CDD (foci) colocalization and provide a unique synthesis of imaging parameters, software, and different types of microscopy used. Last but not least, we critically discuss the main advances and necessary future direction for the better detection of CDD, with important outcomes in biological and clinical setups.

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Viral regulation of host cell biology by hijacking of the nucleolar DNA-damage response

Cited by 39 publications

References 50 publications

Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies – a comprehensive review

Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies – a comprehensive review

The Ebola virus interferon antagonist VP24 undergoes active nucleocytoplasmic trafficking

In Situ Detection of Complex DNA Damage Using Microscopy: A Rough Road Ahead

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