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Who Has herpes And Why Should You Care?Herpes is in the virus family called herpesviruses which includes the Epstein–Barr virus, However, either type of herpes can cause oral or genital infections. Treating Herpes Naturally With Larrea TridentataGenital herpes, Shingles, Chickenpox, Epstein–Barr, and other herpes outbreaks. Herpes Viruses70% of adults have Herpes simplex, and primary lesions just cause inflammation and sores, although may cause temporal lobe encephalitis. EMDR And Immunics Related – YouTubeherpes simplex, rosacea, HSV-1 (oral herpes) and HSV-2 (genital herpes), acid reflux, acne, allergies, amenorrhea, anxiety, arthritis, asthma, autoimmune disease, chronic fatigue syndrome (CFS), Epstein–Barr, cold sores, oral herpes, COPD What Might Cause ME? Your browser JavaScript is turned off causing certain features of the NIAID Institute of Allergy and Infectious Diseases web site to work incorrectly. Research in the Molecular Genetics Section focuses on the mechanisms involved in gene expression of the alpha-herpesviruses: herpes simplex (HSV) and varicella zoster (VZV). For herpes simplex virus, infection results in establishment of latency specifically in neurons of sensory ganglia, and reactivation produces disease that can range from mild oral or genital lesions to keratoconjunctivitis, blindness, neurological issues, and encephalitis. As with its cellular hosts, viral gene expression is tightly regulated, and expression is dictated by a complex series of cellular and viral regulatory proteins that promote the expression of several classes of genes in a sequential manner (Immediate Early – Early – DNA replication – Late).
A critical component of this reguatory network is the cellular transcriptional activator HCF-1. In addition to these direct factors, the virus is also regulated by an overlay of regulation that is determined by the host cell’s chromatin modulation machinery.
In addition to its role in regulation of the viral IE gene expression upon initial infection, HCF-1 also plays a significant role in replication of the viral genome, presumably via required chromatin modulation of DNA replication. While HCF-1 is a critical component of the viral lytic replication cycle, it is also hypothesized to be a determinant of the latency-reactivation cycles. These studies have also led to the development of novel chromatin modulation inhibitors that block viral gene expression and provide proof of principle for the development of epigenetic inhibitors as novel antivirals. Daou S, Mashtalir N, Hammond-Martel I, Pak H, Yu H, Sui G, Vogel JL, Kristie TM, Affar el B. As with all classes of herpesviruses, infection with HSV or VZV results in a primary infection followed by the establishment of a lifelong latent infection. The expression of Immediate Early (IE) genes is induced rapidly upon initial lytic infection.
While multiple DNA binding transcription factors regulate IE genes, this coactivator HCF-1 interacts with and modulates the transcriptional potential.


Recent data have demonstrated that HCF-1 interacts with or is a component of numerous cellular chromatin modulation complexes, and it is in this capacity that it plays a significant role in modulating viral IE gene expression.
The protein interacts with histone chaperones and localizes to foci of viral DNA synthesis at later times in infection.
The MGS has demonstrated that HCF-1 is uniquely sequestered in the cytoplasm of sensory neurons where the virus establishes latency and is rapidly transported to the nucleus upon stimulation that results in viral reactivation.
HCF-1 is sequestered in the cytoplasm of sensory neurons and is rapidly relocalized to the nucleus upon stimuli that results in viral reactivation from latency. Inhibition of HCF-1-associated chromatin modulation enzymes blocks viral reactivation from latency. Crosstalk between O-GlcNAcylation and proteolytic cleavage regulates the host cell factor-1 maturation pathway.
Control of alpha-herpesvirus IE gene expression by HCF-1 coupled chromatin modification activities.
Transcriptional coactivator HCF-1 couples the histone chaperone Asf1b to HSV-1 DNA replication components.
Inhibition of the histone demethylase LSD1 blocks alpha-herpesvirus lytic replication and reactivation from latency. Recruitment of the transcriptional coactivator HCF-1 to viral immediate-early promoters during initiation of reactivation from latency of herpes simplex virus type 1. The coactivator host cell factor-1 mediates Set1 and MLL1 H3K4 trimethylation at herpesvirus immediate early promoters for initiation of infection.
Periodically, these latent viruses can reactivate or re-enter the lytic replication state, resulting in recurrent disease. Upon primary infection with herpes simplex virus, the viral genome is injected into the nucleus, and viral genes are expressed in a regulated, sequential manner beginning with IE. Multiple cellular and viral DNA binding transcription factors of distinct families bind regulatory sites in the viral IE promoter-enhancer domains.
Studies in the MGS are focused on the role of HCF-1-mediated chromatin control of HSV and other herpesvirus infection.
Continuing projects investigate the HCF-1 role and complexes in both viral and cellular DNA replication.
Later in infection, viral replication foci coalesce into replication factories (characterized by staining with the viral-encoded, single-stranded DNA binding protein UL29).


The MGS continues to investigate the role of HCF-1, its associated factors, and chromatin modulation components in the control of latency-reactivation. Immunohistochemical staining of unstimulated sensory ganglia (trigeminal ganglia) shows punctate cytoplasmic localization of HCF-1. TCP (tranylcypromine), a Mono-Amine Oxidase Inhibitor (MAOI) inhibits the activity of the histone H3K9 demethylase LSD1. The primary means of regulation is via the assembly of enhancer complexes that include the cellular coactivator HCF-1.
Reactivation of HSV-1 from latently infected sensory ganglia is blocked by MAOIs and other LSD1 inhibitors, resulting in suppression of viral progeny production. Progeny virus may then infect local sensory neurons where the virus becomes quiescent and lytic genes are not expressed. This protein also interacts and mediates the transcriptional potential of many factors that contribute to IE transcription. Immunofluorescent staining of stimulated ganglia shows neurons undergoing viral reactivation (Control) as determined by expression of the viral single strand binding protein UL29. Various stress stimuli result in re-entry into the lytic replication cycle and production of virus that is released from the neurons and re-infects cells to produce recurrent disease.
Acyclovir (ACV), a DNA replication inhibitor, does not block the expression of viral proteins and the initiation of viral reactivation. In contrast, MAOIs prevent expression of viral IE genes and suppress reactivation at early stages. Kristie focused on the interaction of components involved in the formation of transcriptional enhancer complexes. Kristie joined the NIAID Laboratory of Viral Diseases in 1993, became a senior investigator in 2000, and became chief of the Molecular Genetics Section in 2001.



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