Simultaneous Measurement of Antibodies to Epstein-Barr Virus, Human Herpesvirus 6, Herpes Simplex Virus Types 1 and 2, and 14 Enteroviruses in Chronic Fatigue Syndrome: Is There Evidence of Activation of a Nonspecific Polyclonal Immune Response?

HIV infection is commonly associated with activation and dissemination of several other viral pathogens, including herpes simplex virus 1/2, human cytomegalovirus, human herpesvirus 8, Epstein-Barr virus, Varicella Zoster virus, and human papillomavirus, which behave as opportunistic agents and cause various diseases in immunocompromised hosts. The increased frequency and severity of diseases caused by these viruses in HIV-infected individuals is due mainly to dysfunction of both the adaptive and innate immune responses to viral pathogens. In addition, molecular interactions between HIV and these opportunistic viruses are likely to play critical roles in the progression of disease, including neoplasia. This report reviews the critical aspects of HIV interaction with opportunistic viruses, including Epstein-Barr virus, human cytomegalovirus, herpes simplex virus, Varicella Zoster virus, human herpesvirus 8, and human papillomavirus.

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Acute Human Herpesvirus-7-associated Encephalitis in a Young Adult Coinfected with Herpes Simplex Virus -1/2 and Epstein-Barr Virus

International Neuropsychiatric Disease Journal ◽

10.9734/indj/2017/34258 ◽

2017 ◽

Vol 9 (3) ◽

pp. 1-5

Author(s):

Pavel Dyachenko

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Young Adult ◽

Epstein Barr Virus ◽

Human Herpesvirus ◽

Herpes Simplex Virus 1 ◽

Barr Virus ◽

Epstein Barr ◽

Simplex Virus

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HCF1 and OCT2 Cooperate with EBNA1 To Enhance OriP-Dependent Transcription and Episome Maintenance of Latent Epstein-Barr Virus

Journal of Virology ◽

10.1128/jvi.00239-16 ◽

2016 ◽

Vol 90 (11) ◽

pp. 5353-5367 ◽

Cited By ~ 9

Author(s):

Jayaraju Dheekollu ◽

Andreas Wiedmer ◽

Daniel Sentana-Lledo ◽

Joel Cassel ◽

Troy Messick ◽

...

Keyword(s):

Transcription Factor ◽

Herpes Simplex Virus ◽

Herpes Simplex ◽

Epstein Barr Virus ◽

Histone H3 ◽

Type I ◽

Barr Virus ◽

Cellular Factors ◽

Epstein Barr ◽

Simplex Virus

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.

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