MicroRNA Regulation of Human Herpesvirus Latency

Chen, Siyu; Deng, Yue; Pan, Dongli

doi:10.3390/v14061215

Cited by 16 publications

(11 citation statements)

References 120 publications

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“…Understanding of this mechanism is the first step in identifying potential interventions in at-risk individuals. Known mechanisms of EBV reactivation in non-COVID settings include host/viral miRNAs ( Chen et al, 2022 ), other viral genes, histone modifications, reactive oxygen species, the cellular stress response, and cell transcription factors binding to viral promoters ( Sausen et al, 2021 ). Other potential mechanisms include cytokine-mediated reactivation or loss of immune control.…”

Section: Reactivation Of Latent Pathogensmentioning

confidence: 99%

Viral persistence, reactivation, and mechanisms of long COVID

Chen

Jülg

Mohandas

et al. 2023

eLife

119

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The COVID-19 global pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has infected hundreds of millions of individuals. Following COVID-19 infection, a subset can develop a wide range of chronic symptoms affecting diverse organ systems referred to as post-acute sequelae of SARS-CoV-2 infection (PASC), also known as long COVID. A National Institutes of Health-sponsored initiative, RECOVER: Researching COVID to Enhance Recovery, has sought to understand the basis of long COVID in a large cohort. Given the range of symptoms that occur in long COVID, the mechanisms that may underlie these diverse symptoms may also be diverse. In this review, we focus on the emerging literature supporting the role(s) that viral persistence or reactivation of viruses may play in PASC. Persistence of SARS-CoV-2 RNA or antigens is reported in some organs, yet the mechanism by which they do so and how they may be associated with pathogenic immune responses is unclear. Understanding the mechanisms of persistence of RNA, antigen or other reactivated viruses and how they may relate to specific inflammatory responses that drive symptoms of PASC may provide a rationale for treatment.

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Section: Reactivation Of Latent Pathogensmentioning

confidence: 99%

Viral persistence, reactivation, and mechanisms of long COVID

Chen

Jülg

Mohandas

et al. 2023

eLife

119

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“…HCMV, HHV-6, and HHV-7 are master regulators of cells, controlling cellular signaling, responses, and fate through a variety of mechanisms that are temporally regulated to match the viral lifecycle and the cell type and differentiation stage. In HCMV, multiple viral proteins ( Collins-McMillen et al., 2018 ), miRNAs ( Chen et al., 2022 ; Diggins and Hancock, 2022 ), and cellular pathways ( Smith et al., 2021 ) regulate viral and host cell signaling ( Figure 2 ). This regulation varies depending on the cell type or model system hosting the virus ( Crawford et al., 2022 ) and is specific to cell fate and viral lifecycle stage, setting up precisely tuned regulatory mechanisms by the virus.…”

Section: Discussion and Perspectivesmentioning

confidence: 99%

Hematopoietic stem cells and betaherpesvirus latency

Crawford

2023

Front. Cell. Infect. Microbiol.

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The human betaherpesviruses including human cytomegalovirus (HCMV), human herpesvirus (HHV)-6a and HHV-6b, and HHV-7 infect and establish latency in CD34+ hematopoietic stem and progenitor cells (HPCs). The diverse repertoire of HPCs in humans and the complex interactions between these viruses and host HPCs regulate the viral lifecycle, including latency. Precise manipulation of host and viral factors contribute to preferential maintenance of the viral genome, increased host cell survival, and specific manipulation of the cellular environment including suppression of neighboring cells and immune control. The dynamic control of these processes by the virus regulate inter- and intra-host signals critical to the establishment of chronic infection. Regulation occurs through direct viral protein interactions and cellular signaling, miRNA regulation, and viral mimics of cellular receptors and ligands, all leading to control of cell proliferation, survival, and differentiation. Hematopoietic stem cells have unique biological properties and the tandem control of virus and host make this a unique environment for chronic herpesvirus infection in the bone marrow. This review highlights the elegant complexities of the betaherpesvirus latency and HPC virus-host interactions.

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“…LAT may regulate latency via antisense RNA binding and the destruction of ICP0 transcripts [57]. Additionally, cellular and viral microRNAs suppress the expression of IE genes involved in the onset of lytic replication [61]. Viral microRNAs are transcribed by the LAT promoter and may target either viral lytic genes or host genes involved in transcriptional regulation and chromatin silencing, as depicted in Figure 2A [61,62].…”

Section: Hsv-1 Lifecycle: Latent Infectionmentioning

confidence: 99%

“…Additionally, cellular and viral microRNAs suppress the expression of IE genes involved in the onset of lytic replication [61]. Viral microRNAs are transcribed by the LAT promoter and may target either viral lytic genes or host genes involved in transcriptional regulation and chromatin silencing, as depicted in Figure 2A [61,62]. The viral microRNA miR-H2-3p suppresses ICP0 expression though antisense pairing to the coding region of ICP0 (akin to LAT) [63].…”

Section: Hsv-1 Lifecycle: Latent Infectionmentioning

confidence: 99%

Models of Herpes Simplex Virus Latency

Canova,

Charron,

Leib

2024

Viruses

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Our current understanding of HSV latency is based on a variety of clinical observations, and in vivo, ex vivo, and in vitro model systems, each with unique advantages and drawbacks. The criteria for authentically modeling HSV latency include the ability to easily manipulate host genetics and biological pathways, as well as mimicking the immune response and viral pathogenesis in human infections. Although realistically modeling HSV latency is necessary when choosing a model, the cost, time requirement, ethical constraints, and reagent availability are also equally important. Presently, there remains a pressing need for in vivo models that more closely recapitulate human HSV infection. While the current in vivo, ex vivo, and in vitro models used to study HSV latency have limitations, they provide further insights that add to our understanding of latency. In vivo models have shed light on natural infection routes and the interplay between the host immune response and the virus during latency, while in vitro models have been invaluable in elucidating molecular pathways involved in latency. Below, we review the relative advantages and disadvantages of current HSV models and highlight insights gained through each.

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MicroRNA Regulation of Human Herpesvirus Latency

Cited by 16 publications

References 120 publications

Viral persistence, reactivation, and mechanisms of long COVID

Viral persistence, reactivation, and mechanisms of long COVID

Hematopoietic stem cells and betaherpesvirus latency

Models of Herpes Simplex Virus Latency

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