A microRNA encoded by HSV-1 inhibits a cellular transcriptional repressor of viral immediate early and early genes

Wu, Wenjuan; Guo, ZhongPing; Zhang, Xuemei; Guo, Lei; Liu, Long-ding; Liao, Yun; Wang, Jingjing; Wang, Lichun; Li, Qihan

doi:10.1007/s11427-013-4458-4

Cited by 26 publications

(23 citation statements)

References 28 publications

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“…Although most identified targets of the 27 mature HSV-1 miRNAs are viral transcripts, recent research has described roles for these viral miRNAs in targeting cellular transcripts to promote immune evasion, viral replication, cell proliferation, and pathogenesis [ 82 , 83 ]. One such example is the targeting of PIGT by miR-H8.…”

Section: Herpesvirusesmentioning

confidence: 99%

The Diverse Roles of microRNAs at the Host–Virus Interface

Bernier

Sagan

2018

Viruses

107

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MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Through this activity, they are implicated in almost every cellular process investigated to date. Hence, it is not surprising that miRNAs play diverse roles in regulation of viral infections and antiviral responses. Diverse families of DNA and RNA viruses have been shown to take advantage of cellular miRNAs or produce virally encoded miRNAs that alter host or viral gene expression. MiRNA-mediated changes in gene expression have been demonstrated to modulate viral replication, antiviral immune responses, viral latency, and pathogenesis. Interestingly, viruses mediate both canonical and non-canonical interactions with miRNAs to downregulate specific targets or to promote viral genome stability, translation, and/or RNA accumulation. In this review, we focus on recent findings elucidating several key mechanisms employed by diverse virus families, with a focus on miRNAs at the host–virus interface during herpesvirus, polyomavirus, retroviruses, pestivirus, and hepacivirus infections.

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Section: Herpesvirusesmentioning

confidence: 99%

The Diverse Roles of microRNAs at the Host–Virus Interface

Bernier

Sagan

2018

Viruses

107

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“…HSV-1 encodes 18 stem-loops that result in 27 mature miRNA sequences [ 61 , 63 , 64 , 66 , 67 , 68 , 69 ], while HSV-2 also encodes for 18 stem-loops but only produce 24 mature miRNAs [ 62 , 65 , 66 ] ( Figure 1 ). The first report of a HSV-1 miRNA was in 2006 [ 61 ]; since then, several studies have attempted to unravel the functions of HSV-1 miRNAs [ 62 , 63 , 67 , 70 , 71 ].…”

Section: Alphaherpesvirus (Hsv-1 and Hsv-2) And Micrornasmentioning

confidence: 99%

“…Despite the fact that most identified targets of HSV-1 miRNAs are virus-encoded, hsv1-miR-H27 targets cellular transcriptional repressor Kelch-like 24 (KLHL24), which inhibits transcriptional efficiency of viral immediate early and early genes. Thus, opposite to other viral miRNAs, hsv1-miR-H27 seems to have an important role in immune evasion, viral replication, and proliferation [ 68 ]. Interestingly, HSV-2 and HSV-1 share a great homology between mRNA sequences [ 32 , 66 ].…”

Section: Alphaherpesvirus (Hsv-1 and Hsv-2) And Micrornasmentioning

confidence: 99%

The Role of microRNAs in the Pathogenesis of Herpesvirus Infection

Piedade

Azevedo‐Pereira

2016

Viruses

140

134

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MicroRNAs (miRNAs) are small non-coding RNAs important in gene regulation. They are able to regulate mRNA translation through base-pair complementarity. Cellular miRNAs have been involved in the regulation of nearly all cellular pathways, and their deregulation has been associated with several diseases such as cancer. Given the importance of microRNAs to cell homeostasis, it is no surprise that viruses have evolved to take advantage of this cellular pathway. Viruses have been reported to be able to encode and express functional viral microRNAs that target both viral and cellular transcripts. Moreover, viral inhibition of key proteins from the microRNA pathway and important changes in cellular microRNA pool have been reported upon viral infection. In addition, viruses have developed multiple mechanisms to avoid being targeted by cellular microRNAs. This complex interaction between host and viruses to control the microRNA pathway usually favors viral infection and persistence by either reducing immune detection, avoiding apoptosis, promoting cell growth, or promoting lytic or latent infection. One of the best examples of this virus-host-microRNA interplay emanates from members of the Herperviridae family, namely the herpes simplex virus type 1 and type 2 (HSV-1 and HSV-2), human cytomegalovirus (HCMV), human herpesvirus 8 (HHV-8), and the Epstein–Barr virus (EBV). In this review, we will focus on the general functions of microRNAs and the interactions between herpesviruses, human hosts, and microRNAs and will delve into the related mechanisms that contribute to infection and pathogenesis.

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“…First, immediate early genes (alpha) are transcribed, many of which encode for proteins contributing to immune evasion and work as factors controlling cell translation [ 67 ]. Then, follows the transcription of early genes (beta) that are required for DNA replication [ 68 ]. Finally, early late and late genes (gamma-1 and gamma-2) are transcribed, which mainly encode for structural components of virions, such as capsid, tegument, and surface proteins [ 69 , 70 ].…”

Section: Hsv Infectious Cyclementioning

confidence: 99%

Evasion of Early Antiviral Responses by Herpes Simplex Viruses

Suazo

Ibáñez

Retamal-Díaz

et al. 2015

Mediators of Inflammation

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Besides overcoming physical constraints, such as extreme temperatures, reduced humidity, elevated pressure, and natural predators, human pathogens further need to overcome an arsenal of antimicrobial components evolved by the host to limit infection, replication and optimally, reinfection. Herpes simplex virus-1 (HSV-1) and herpes simplex virus-2 (HSV-2) infect humans at a high frequency and persist within the host for life by establishing latency in neurons. To gain access to these cells, herpes simplex viruses (HSVs) must replicate and block immediate host antiviral responses elicited by epithelial cells and innate immune components early after infection. During these processes, infected and noninfected neighboring cells, as well as tissue-resident and patrolling immune cells, will sense viral components and cell-associated danger signals and secrete soluble mediators. While type-I interferons aim at limiting virus spread, cytokines and chemokines will modulate resident and incoming immune cells. In this paper, we discuss recent findings relative to the early steps taking place during HSV infection and replication. Further, we discuss how HSVs evade detection by host cells and the molecular mechanisms evolved by these viruses to circumvent early antiviral mechanisms, ultimately leading to neuron infection and the establishment of latency.

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A microRNA encoded by HSV-1 inhibits a cellular transcriptional repressor of viral immediate early and early genes

Cited by 26 publications

References 28 publications

The Diverse Roles of microRNAs at the Host–Virus Interface

The Diverse Roles of microRNAs at the Host–Virus Interface

The Role of microRNAs in the Pathogenesis of Herpesvirus Infection

Evasion of Early Antiviral Responses by Herpes Simplex Viruses

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