Absence of CD28-CTLA4-PD-L1 Costimulatory Molecules Reduces Herpes Simplex Virus 1 Reactivation

Matundan, Harry H.; Jaggi, Ujjaldeep; Yu, Jack; Akbari, Omid; Ghiasi, Homayon

doi:10.1128/mbio.01176-21

Cited by 2 publications

(1 citation statement)

References 66 publications

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“…Mutant viruses lacking ICP22 replicate poorly in murine ocular models and are sensitive to interferon [60]. At the same time, recombinant expression of CD80 or deletion of the aforementioned ligands can directly influence the degree of reactivation from latency and corneal pathology [59,[61][62][63][64]. Interestingly, the region of ICP22 responsible for reduced CD80 promoter activity is within amino acids 305-345 [65], well outside of the region binding CDK9, indicating multiple mechanisms by which ICP22 inhibits the transcription of cellular genes.…”

Section: Ctd Phosphorylationmentioning

confidence: 99%

A Review of the Multipronged Attack of Herpes Simplex Virus 1 on the Host Transcriptional Machinery

Hennig

Djaković

Dölken

et al. 2021

Viruses

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During lytic infection, herpes simplex virus (HSV) 1 induces a rapid shutoff of host RNA synthesis while redirecting transcriptional machinery to viral genes. In addition to being a major human pathogen, there is burgeoning clinical interest in HSV as a vector in gene delivery and oncolytic therapies, necessitating research into transcriptional control. This review summarizes the array of impacts that HSV has on RNA Polymerase (Pol) II, which transcribes all mRNA in infected cells. We discuss alterations in Pol II holoenzymes, post-translational modifications, and how viral proteins regulate specific activities such as promoter-proximal pausing, splicing, histone repositioning, and termination with respect to host genes. Recent technological innovations that have reshaped our understanding of previous observations are summarized in detail, along with specific research directions and technical considerations for future studies.

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Section: Ctd Phosphorylationmentioning

confidence: 99%

A Review of the Multipronged Attack of Herpes Simplex Virus 1 on the Host Transcriptional Machinery

Hennig

Djaković

Dölken

et al. 2021

Viruses

View full text Add to dashboard Cite

show abstract

Small Noncoding RNA (sncRNA1) within the Latency-Associated Transcript Modulates Herpes Simplex Virus 1 Virulence and the Host Immune Response during Acute but Not Latent Infection

Tormanen

Matundan

Wang

et al. 2022

J Virol

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HSV-1 latency-associated transcript (LAT) plays a major role in establishing latency and reactivation; however, the mechanism by which LAT controls these processes is largely unknown. In this study, we sought to establish the role of the small noncoding RNA1 (sncRNA1) encoded within LAT during HSV-1 ocular infection. Our results suggest that sncRNA1 has a protective role during acute ocular infection by modulating the innate immune response to infection.

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Absence of CD28-CTLA4-PD-L1 Costimulatory Molecules Reduces Herpes Simplex Virus 1 Reactivation

Abstract: Costimulatory molecules play an important role in activation of T cell responses, and T cells contribute to HSV-1-induced eye disease in the host. Similar to HSV-1 ICP22, the cellular costimulatory molecules CD28, CTLA4, and PD-L1 also bind to CD80.

Cited by 2 publications

References 66 publications

A Review of the Multipronged Attack of Herpes Simplex Virus 1 on the Host Transcriptional Machinery

A Review of the Multipronged Attack of Herpes Simplex Virus 1 on the Host Transcriptional Machinery

Small Noncoding RNA (sncRNA1) within the Latency-Associated Transcript Modulates Herpes Simplex Virus 1 Virulence and the Host Immune Response during Acute but Not Latent Infection

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