The Role of VP16 in the Life Cycle of Alphaherpesviruses

Fan, Dengjian; Wang, Mingshu; Cheng, Anchun; Jia, Renyong; Yang, Qiao; Wu, Ying; Zhu, Dekang; Zhao, Xinxin; Chen, Shun; Liu, Mafeng; Zhang, Shaqiu; Ou, Xumin; Mao, Sai; Gao, Qun; Sun, Di; Wen, Xingjian; Liu, Yunya; Yu, Yanling; Zhang, Ling; Tian, Bin; Pan, Leichang; Chen, Xiaoyue

doi:10.3389/fmicb.2020.01910

Cited by 29 publications

(23 citation statements)

References 154 publications

(242 reference statements)

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“…Specific protein-1 (Sp1) was called proponent-specific binding factor needed for SV40 immediate early (IE) gene transcription [ 23 ]. Sp1 was once thought to be the general transcript factor used to transcribe many “housekeeping genes,” also known as maintenance genes [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

The Current Status of SSRP1 in Cancer: Tribulation and Road Ahead

Jia

Guo

Wang

et al. 2022

Journal of Healthcare Engineering

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Background and Objectives. Owing to the complexity and heterogeneity of tumors, cancer’s early diagnoses and treatment have become a provocation. Structure-specific recognition protein-1 (SSRP1) is a histone (H3-H4 or H2A-H2B) chaperone in chromatin-related processes such as transcription, cell cycle control, and DNA replication, reported in various tumor tissues. It may also be used as a biomarker. This study aimed to highlight the role of SSRP1 in cancer with a focus on the current progress and future perspective. Methods. We search PubMed and Web of Sciences with keywords “SSRP1” and “Cancer.” Only English literature was included, and conference papers and abstract were all excluded. Results. Transcription factors are classified into three groups based on their DNA binding motifs: simple helix-loop-helix (bHLH), classical zinc fingers (ZF-TFs), and homeodomains. The tumor-suppressive miR-497 (microRNA-497) acted as an undesirable regulator of SSRP1 upregulation, which led to tumor growth. The siRNA (small interfering RNA) knockdown of SSRP1 hindered cell proliferation along with incursion and glioma cell migration. Through the AKT (also known as protein kinase B) signaling pathway, SSRP1 silencing affected cancer apoptosis and cell proliferation. Conclusion. The MAPK (mitogen-activated protein kinase) signaling pathway’s phosphorylation was suppressed when SSRP1 was depleted. The effect of curaxins on p53 and NF-B (nuclear factor-κB), and their toxicity to cancer cells, is attributable to the FACT (facilitates chromatin transcription) complex’s chromatin trapping.

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Section: Introductionmentioning

confidence: 99%

The Current Status of SSRP1 in Cancer: Tribulation and Road Ahead

Jia

Guo

Wang

et al. 2022

Journal of Healthcare Engineering

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“…α/IE genes, which include infected cell polypeptides (ICP), ICP0, ICP4, ICP22, and ICP27, regulate early gene expression of viral replication. The transcription of α/IE genes, requiring the presence of viral trans-activator VP16 in vivo, can also occur in the absence of prior or de-novo viral protein synthesis [ 6 , 7 , 8 , 9 ]. The primary function of α/IE gene-encoded proteins is the activation of β/E gene expression.…”

Section: Introductionmentioning

confidence: 99%

“…Reactivation of virus can lead to asymptomatic or symptomatic shedding of HSV. Asymptomatic shedding is often defined as detection of HSV in the absence of lesions, or if symptoms are present, they are not recognized by the patient or clinician as related to HSV [ 7 ]. Symptomatic shedding often results in recurrent disease at the initial infection site, resulting in gingivostomatitis, orolabial herpes, herpes stromal keratitis and fatal herpes sporadic encephalitis (HSE) [ 2 , 3 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Ginkgolic Acid Inhibits Herpes Simplex Virus Type 1 Skin Infection and Prevents Zosteriform Spread in Mice

Bhutta

Shechter

Gallo³

et al. 2021

Viruses

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Herpes simplex virus type 1 (HSV-1) causes a lifelong latent infection with an estimated global prevalence of 66%. Primary and recurrent HSV infections are characterized by a tingling sensation, followed by an eruption of vesicles, which can cause painful erosions. Commonly used antiviral drugs against HSV infection are nucleoside analogues including acyclovir (ACV), famciclovir, and valacyclovir. Although these nucleoside analogues reduce morbidity and mortality in immunocompetent individuals, ACV-resistant HSV strains (ACVR-HSV) have been isolated from immunocompromised patients. Thus, ACVR-HSV infection poses a critical emerging public health concern. Recently, we reported that ginkgolic acid (GA) inhibits HSV-1 by disrupting viral structure, blocking fusion, and inhibiting viral protein synthesis. Additionally, we showed GA affords a broad spectrum of fusion inhibition of all three classes of fusion proteins, including those of HIV, Ebola, influenza A and Epstein Barr viruses. Here we report GA’s antiviral activity against HSV-1 skin infection in BALB/cJ mice. GA-treated mice demonstrated a significantly reduced mortality rate and decreased infection scores compared to controls treated with dimethylsulfoxide (DMSO)-vehicle. Furthermore, GA efficiently inhibited ACVR-HSV-1 strain 17+ in vitro and in vivo. Since GA’s mechanism of action includes virucidal activity and fusion inhibition, it is expected to work alone or synergistically with other anti-viral drugs, and we anticipate it to be effective against additional cutaneous and potentially systemic viral infections.

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“…VP16 and host cell factor 1 (HCF-1) bind together and are recruited to VP16-responsive enhancer elements in the immediate early (IE) viral promoters through cellular factor POU homeodomain protein Oct-1 (39). Together, this VP16-induced complex recruits additional factors involved in transcriptional activation, including general transcription factors, ATP-dependent chromatin remodelers, and histone modifying enzymes (32,(40)(41)(42)(43)(44). Synthesis of the IE proteins is required for early (E) mRNA transcription.…”

Section: Introductionmentioning

confidence: 99%

DLK-dependent biphasic reactivation of herpes simplex virus latency established in the absence of antivirals

Dochnal

Merchant

Schinlever

et al. 2022

Preprint

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An understanding of the molecular events that regulate entry of herpes simplex virus type 1 (HSV-1) into a latent infection of neurons and subsequent reactivation requires model systems. However, establishing a latent-like infection in cultured neurons is problematic as the release of any infectious virus can potentially superinfect the cultures. Here, we describe a new reporter virus, HSV-1 Stayput-GFP, that is defective for cell-to-cell spread. Use of this virus permits the establishment of a quiescent infection of neurons without the need for a viral DNA replication inhibitor. As such, Stayput-GFP provides a new model to study latency establishment and reactivation at the single neuron level. We demonstrate that reactivation involves an initial wave of viral gene expression consistent with the Phase I previously observed in primary neuron models where a viral DNA replication inhibitor is used during latency establishment. Phase I gene expression was dependent on the cell stress protein DLK but independent of histone demethylase activity and viral DNA replication. Progression into the later, Phase II wave of reactivation, characterized by detectable late viral protein synthesis and a requirement for histone demethylase activity, is also observed in the Stayput-GFP model system. These data demonstrate that the two waves of viral gene expression following HSV-1 reactivation are independent of secondary infection and occur when latent infections are established in the absence of a viral DNA replication inhibitor.

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The Role of VP16 in the Life Cycle of Alphaherpesviruses

Cited by 29 publications

References 154 publications

The Current Status of SSRP1 in Cancer: Tribulation and Road Ahead

The Current Status of SSRP1 in Cancer: Tribulation and Road Ahead

Ginkgolic Acid Inhibits Herpes Simplex Virus Type 1 Skin Infection and Prevents Zosteriform Spread in Mice

DLK-dependent biphasic reactivation of herpes simplex virus latency established in the absence of antivirals

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