Relation of depressive symptoms to C-reactive protein and pathogen burden (cytomegalovirus, herpes simplex virus, Epstein-Barr virus) in patients with earlier acute coronary syndromes

2005 ◽  
Vol 95 (3) ◽  
pp. 317-321 ◽  
Author(s):  
Gregory E. Miller ◽  
Kenneth E. Freedland ◽  
Stephen Duntley ◽  
Robert M. Carney
2016 ◽  
Vol 90 (11) ◽  
pp. 5353-5367 ◽  
Author(s):  
Jayaraju Dheekollu ◽  
Andreas Wiedmer ◽  
Daniel Sentana-Lledo ◽  
Joel Cassel ◽  
Troy Messick ◽  
...  

ABSTRACTEpstein-Barr virus (EBV) establishes latent infections as multicopy episomes with complex patterns of viral gene transcription and chromatin structure. The EBV origin of plasmid replication (OriP) has been implicated as a critical control element for viral transcription, as well as viral DNA replication and episome maintenance. Here, we examine cellular factors that bind OriP and regulate histone modification, transcription regulation, and episome maintenance. We found that OriP is enriched for histone H3 lysine 4 (H3K4) methylation in multiple cell types and latency types. Host cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase complex, and transcription factor OCT2 (octamer-binding transcription factor 2) bound cooperatively with EBNA1 (Epstein-Barr virus nuclear antigen 1) at OriP. Depletion of OCT2 or HCF1 deregulated latency transcription and histone modifications at OriP, as well as the OriP-regulated latency type-dependent C promoter (Cp) and Q promoter (Qp). HCF1 depletion led to a loss of histone H3K4me3 (trimethylation of histone H3 at lysine 4) and H3 acetylation at Cp in type III latency and Qp in type I latency, as well as an increase in heterochromatic H3K9me3 at these sites. HCF1 depletion resulted in the loss of EBV episomes from Burkitt's lymphoma cells with type I latency and reactivation from lymphoblastoid cells (LCLs) with type III latency. These findings indicate that HCF1 and OCT2 function at OriP to regulate viral transcription, histone modifications, and episome maintenance. As HCF1 is best known for its function in herpes simplex virus 1 (HSV-1) immediate early gene transcription, our findings suggest that EBV latency transcription shares unexpected features with HSV gene regulation.IMPORTANCEEBV latency is associated with several human cancers. Viral latent cycle gene expression is regulated by the epigenetic control of the OriP enhancer region. Here, we show that cellular factors OCT2 and HCF1 bind OriP in association with EBNA1 to maintain elevated histone H3K4me3 and transcriptional enhancer function. HCF1 is known as a transcriptional coactivator of herpes simplex virus (HSV) immediate early (IE) transcription, suggesting that OriP enhancer shares aspects of HSV IE transcription control.


2002 ◽  
Vol 76 (18) ◽  
pp. 9420-9433 ◽  
Author(s):  
Julie L. Boyer ◽  
Sankar Swaminathan ◽  
Saul J. Silverstein

ABSTRACT The herpes simplex virus type 1 (HSV-1) ICP27 protein is an essential RNA-binding protein that shuttles between the nucleus and cytoplasm to increase the cytoplasmic accumulation of viral late mRNAs. ICP27 homologs have been identified in each of the herpesvirus subfamilies, and accumulating evidence indicates that homologs from the gammaherpesvirus subfamily function similarly to ICP27. In particular, the Epstein-Barr virus (EBV) SM protein posttranscriptionally regulates gene expression, binds RNA in vitro and in vivo, and shuttles between the nucleus and cytoplasm. To determine if these two proteins function through a common mechanism, the ability of EBV SM to complement the growth defect of an HSV-1 ICP27-null virus was examined in a transient-expression assay. ICP27 stimulated the growth of the null mutant more efficiently than did SM, but the ability of SM to compensate for the ICP27 defects suggests conservation of common functions. To assay for complementation in the context of a viral infection, the growth properties of an HSV recombinant expressing SM in an ICP27-null background were analyzed. SM stimulated growth of the recombinant, although this growth was reduced by comparison to that of an ICP27-expressing virus. By contrast, an HSV recombinant expressing an SM mutant allele defective for transactivation activity and nucleocytoplasmic shuttling did not grow at all. These results suggest that SM and ICP27 may regulate gene expression through a common pathway that is evolutionarily conserved in herpesviruses.


PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222607 ◽  
Author(s):  
Jakub Dworzański ◽  
Bartłomiej Drop ◽  
Ewa Kliszczewska ◽  
Małgorzata Strycharz-Dudziak ◽  
Małgorzata Polz-Dacewicz

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 18506-18506
Author(s):  
W. P. Witt ◽  
S. Pickard ◽  
T. Kuzel ◽  
T. McDade ◽  
S. Perry ◽  
...  

18506 Background: Informal caregivers of prostate cancer patients often experience chronic psychological stress that may adversely impact their physical and mental health, and their ability to care for their families and the patient. This study aims to determine the association between perceived and biological stress among informal caregivers of prostate cancer patients. Methods: A total of 24 informal caregivers of prostate cancer patients were recruited from both the Jesse Brown VA Center (Lakeside and Westside, Chicago) and the Robert H. Lurie Comprehensive Cancer Center at Northwestern University. Caregivers completed self-reported measures of stress, somatization, life events, burden, health status (SF-36) and mental health. Capillary blood spot samples from caregivers were used to examine two measures of biological stress, Epstein-Barr virus antibody titer and C-reactive protein. Results: Informal caregivers had a mean age of 63 years and were mostly female and spouses of patients with prostate cancer. Many had preexisting co-morbidities, including 45.8% with hypertension, 45.8% with arthritis, and 33.3% with diabetes. Nearly 30% had been hospitalized in the last 12 months. 33.3% of caregivers experienced at least one major life event in the last year and 62.5% had symptoms of somatization illness. Caregivers with symptoms of somatization illness had higher mean Epstein-Barr antibody titers as compared with those without symptoms (Mean EBV antibody titer: 198.3 versus 141.8, respectively (p < 0.05)). Caregiver-reported measures were not correlated with C-reactive protein levels. Caregivers with higher levels of strain perceived more stress in their lives (p < 0.05), but showed relatively high self-esteem (mean = 30.6, SD = 2.8, on a 7–35 scale). Conclusions: These preliminary findings suggest that informal caregivers who report symptoms of somatization illness exhibit signs of relative suppression of the cell-mediated immune processes as a result of the reactivation of the Epstein-Barr virus. Final analyses will be conducted that control for potential confounders and will further elucidate if caregiver stress is associated with suppression of the immune system. No significant financial relationships to disclose.


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