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Nuclear domain 10 components upregulated via interferon during human cytomegalovirus infection potently regulate viral infection.

Abstract Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that causes life-threatening disease in immunocompromised and immunonaïve individuals. Type I interferons (IFNs) are crucial molecules in the innate immune response to HCMV and are also known to upregulate several components of the interchromosomal multiprotein aggregates collectively referred to as nuclear domain 10 (ND10). In the context of herpesvirus infection, ND10 components are known to restrict gene expression. This raises the question as to whether key ND10 components (PML, Sp100 and hDaxx) act as anti-viral IFN-stimulated genes (ISGs) during HCMV infection. In this study, analysis of ND10 component transcription during HCMV infection demonstrated that PML and Sp100 were significantly upregulated whilst hDaxx expression remained unchanged. In cells engineered to block the production of, or response to, type I IFNs, upregulation of PML and Sp100 was not detected during HCMV infection. Furthermore, pre-treatment with an IFN-β neutralizing antibody inhibited upregulation of PML and Sp100 during both infection and treatment with HCMV-infected cell supernatant. The significance of ND10 components functioning as anti-viral ISGs during HCMV infection was determined through knockdown of PML, Sp100 and hDaxx. ND10 knockdown cells were significantly more permissive to HCMV infection, as previously described but, in contrast to control cells, could support HCMV plaque formation following IFN-β pre-treatment. This ability of HCMV to overcome the potently anti-viral effects of IFN-β in ND10 expression deficient cells provides evidence that ND10 component upregulation is a key mediator of the anti-viral activity of IFN-β.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title the journal of general virology
Publication Year Start




PMID- 28745271
OWN - NLM
STAT- MEDLINE
DA  - 20170726
DCOM- 20170804
LR  - 20170804
IS  - 1465-2099 (Electronic)
IS  - 0022-1317 (Linking)
VI  - 98
IP  - 7
DP  - 2017 Jul
TI  - Nuclear domain 10 components upregulated via interferon during human
      cytomegalovirus infection potently regulate viral infection.
PG  - 1795-1805
LID - 10.1099/jgv.0.000858 [doi]
AB  - Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that causes
      life-threatening disease in immunocompromised and immunonaive individuals. Type I
      interferons (IFNs) are crucial molecules in the innate immune response to HCMV
      and are also known to upregulate several components of the interchromosomal
      multiprotein aggregates collectively referred to as nuclear domain 10 (ND10). In 
      the context of herpesvirus infection, ND10 components are known to restrict gene 
      expression. This raises the question as to whether key ND10 components (PML,
      Sp100 and hDaxx) act as anti-viral IFN-stimulated genes (ISGs) during HCMV
      infection. In this study, analysis of ND10 component transcription during HCMV
      infection demonstrated that PML and Sp100 were significantly upregulated whilst
      hDaxx expression remained unchanged. In cells engineered to block the production 
      of, or response to, type I IFNs, upregulation of PML and Sp100 was not detected
      during HCMV infection. Furthermore, pre-treatment with an IFN-beta neutralizing
      antibody inhibited upregulation of PML and Sp100 during both infection and
      treatment with HCMV-infected cell supernatant. The significance of ND10
      components functioning as anti-viral ISGs during HCMV infection was determined
      through knockdown of PML, Sp100 and hDaxx. ND10 knockdown cells were
      significantly more permissive to HCMV infection, as previously described but, in 
      contrast to control cells, could support HCMV plaque formation following IFN-beta
      pre-treatment. This ability of HCMV to overcome the potently anti-viral effects
      of IFN-beta in ND10 expression deficient cells provides evidence that ND10
      component upregulation is a key mediator of the anti-viral activity of IFN-beta.
FAU - Ashley, Caroline L
AU  - Ashley CL
AD  - 1Discipline of Infectious Diseases and Immunology, Sydney Medical School, Charles
      Perkins Centre, University of Sydney, Camperdown, New South Wales 2050,
      Australia.
FAU - Glass, Mandy S
AU  - Glass MS
AD  - 3MRC University of Glasgow Centre for Virus Research, University of Glasgow,
      Garscube Campus, Glasgow, Scotland, UK 2Institute of Biomedical and Environmental
      Health Research, University of the West of Scotland, High Street, Paisley,
      Scotland, UK.
FAU - Abendroth, Allison
AU  - Abendroth A
AD  - 1Discipline of Infectious Diseases and Immunology, Sydney Medical School, Charles
      Perkins Centre, University of Sydney, Camperdown, New South Wales 2050,
      Australia.
FAU - McSharry, Brian P
AU  - McSharry BP
AD  - 1Discipline of Infectious Diseases and Immunology, Sydney Medical School, Charles
      Perkins Centre, University of Sydney, Camperdown, New South Wales 2050,
      Australia.
FAU - Slobedman, Barry
AU  - Slobedman B
AD  - 1Discipline of Infectious Diseases and Immunology, Sydney Medical School, Charles
      Perkins Centre, University of Sydney, Camperdown, New South Wales 2050,
      Australia.
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Gen Virol
JT  - The Journal of general virology
JID - 0077340
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Antigens, Nuclear)
RN  - 0 (Autoantigens)
RN  - 0 (DAXX protein, human)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Promyelocytic Leukemia Protein)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (nuclear dot protein 52, human)
RN  - 135844-47-2 (Sp100 protein, human)
RN  - 143220-95-5 (PML protein, human)
RN  - 77238-31-4 (Interferon-beta)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/*biosynthesis/genetics/immunology
MH  - Antigens, Nuclear/*biosynthesis/genetics/immunology
MH  - Autoantigens/*biosynthesis/genetics/immunology
MH  - Cell Line
MH  - Cytomegalovirus/*immunology
MH  - Cytomegalovirus Infections/*immunology/virology
MH  - Gene Expression Regulation, Viral/immunology
MH  - HEK293 Cells
MH  - Humans
MH  - Immunity, Innate/immunology
MH  - Interferon-beta/genetics/*immunology
MH  - Nuclear Proteins/*biosynthesis/genetics/immunology
MH  - Promyelocytic Leukemia Protein/*biosynthesis/genetics/immunology
MH  - RNA Interference
MH  - RNA, Small Interfering/genetics
MH  - Up-Regulation/immunology
EDAT- 2017/07/27 06:00
MHDA- 2017/08/05 06:00
CRDT- 2017/07/27 06:00
AID - 10.1099/jgv.0.000858 [doi]
PST - ppublish
SO  - J Gen Virol. 2017 Jul;98(7):1795-1805. doi: 10.1099/jgv.0.000858.