Cellular Control of Dengue Virus Replication: Role of Interferon-Inducible Genes

Takahashi, Hirotaka; Suzuki, Youichi

doi:10.5772/67984

Cited by 5 publications

(5 citation statements)

References 109 publications

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“…It is therefore possible that C19ORF66, by interacting with PABPC, slows down PABPC relocalization to the nucleus and restricts expression of viral genes. By interacting with PABPC and LARP, C19ORF66 was also hypothesized to regulate the decay of dengue RNA by possibly influencing either translation or localization to P bodies and stress granules (54). Determining whether C19ORF66 influences the PABPC shuttling pattern is an important future goal, as well as deciphering C19ORF66 interaction pattern upon KSHV infection and lytic reactivation.…”

Section: Discussionmentioning

confidence: 99%

C19ORF66 Broadly Escapes Virus-Induced Endonuclease Cleavage and Restricts Kaposi’s Sarcoma-Associated Herpesvirus

Rodríguez

Srivastav

Muller

2019

J Virol

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One striking characteristic of certain herpesviruses is their ability to induce rapid and widespread RNA decay in order to gain access to host resources. This phenotype is induced by viral endoribonucleases, including SOX in Kaposi's sarcoma-associated herpesvirus (KSHV), muSOX in murine gammaherpesvirus 68 (MHV68), BGLF5 in Epstein-Barr virus (EBV), and vhs in herpes simplex virus 1 (HSV-1). Here, we performed comparative transcriptome sequencing (RNA-seq) upon expression of these herpesviral endonucleases in order to characterize their effect on the host transcriptome. Consistent with previous reports, we found that approximately two-thirds of transcripts were downregulated in cells expressing any of these viral endonucleases. Among the transcripts spared from degradation, we uncovered a cluster of transcripts that systematically escaped degradation from all tested endonucleases. Among these escapees, we identified C19ORF66 and reveal that this transcript is protected from degradation by its 3= untranslated region (UTR). We then show that C19ORF66 is a potent KSHV restriction factor by impeding early viral gene expression, suggesting that its ability to escape viral cleavage may be an important component of the host response to viral infection. Collectively, our comparative approach is a powerful tool to pinpoint key regulators of the viral-host interplay and led us to uncover a novel KSHV regulator. IMPORTANCE Viruses are master regulators of the host gene expression machinery. This is crucial to promote viral infection and to dampen host immune responses. Many viruses, including herpesviruses, express RNases that reduce host gene expression through widespread mRNA decay. However, it emerged that some mRNAs escape this fate, although it has been difficult to determine whether these escaping transcripts benefit viral infection or instead participate in an antiviral mechanism. To tackle this question, we compared the effect of the herpesviral RNases on the human transcriptome and identified a cluster of transcripts consistently escaping degradation from all tested endonucleases. Among the protected mRNAs, we identified the transcript C19ORF66 and showed that it restricts Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Collectively, these results provide a framework to explore how the control of RNA fate in the context of viral-induced widespread mRNA degradation may influence the outcome of viral infection.

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Section: Discussionmentioning

confidence: 99%

C19ORF66 Broadly Escapes Virus-Induced Endonuclease Cleavage and Restricts Kaposi’s Sarcoma-Associated Herpesvirus

Rodríguez

Srivastav

Muller

2019

J Virol

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“…It is therefore possible that C19ORF66, by interacting with PABPC, slows down PABPC relocalization to nucleus and restricts expression of viral genes. By Interacting with PABPC and LARP, C19ORF66 was also hypothesized to regulate decay of Dengue RNA by possibly influencing either translation or localization to p-bodies and stress granules (53) Determining whether C19ORF66 influences the PABPC shuttling pattern is an important future goal, as well as deciphering C19ORF66 interaction pattern upon KSHV infection and lytic reactivation.…”

Section: Discussionmentioning

confidence: 99%

C19ORF66 broadly escapes viral-induced endonuclease cleavage and restricts Kaposi’s Sarcoma Associated Herpesvirus (KSHV)

Rodríguez

Srivastav

Muller

2018

Preprint

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9One striking characteristic of certain herpesviruses is their ability to induce rapid and 10 widespread RNA decay in order to gain access to host resources. This phenotype is induced by 11 viral endoribonucleases, including SOX in KSHV, muSOX in MHV68, BGLF5 in EBV and vhs in 12 HSV-1. Here, we performed comparative RNA-seq upon expression of these herpesviral 13 endonucleases in order to characterize their effect on the host transcriptome. Consistent with 14 previous reports, we found that approximately two thirds of transcripts are downregulated in 15 cells expressing any of these viral endonucleases. Among transcripts spared from degradation, 16we uncovered a cluster of transcripts that systematically escape degradation from all tested 17 endonucleases. Among these escapees, we identified C19ORF66 and reveal that like the 18 previously identified escapees, this transcript is protected from degradation by its 3'UTR. We 19 then show that C19ORF66, a known anti-viral protein, is a potent KSHV restriction factor, 20suggesting that its ability to escape viral cleavage may be an important component of the host 21 response to viral infection. Collectively, our comparative approach is a powerful tool to pinpoint 22 key regulators of the viral-host interplay and led us to uncover a novel KSHV regulator. 23 24 25 26 All rights reserved. No reuse allowed without permission.The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/506410 doi: bioRxiv preprint characterized by a defined sequence motif (19) rendering it difficult to identify new escaping 48 transcripts by traditional sequence search. Consequently, the host vs. viral endonuclease 49 dichotomy to only defining characteristic of this novel type of RNA element. 50 All rights reserved. No reuse allowed without permission.

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“…8.Immature virus particles pass through the Golgi body where they undergo modifications. 9.Virions are released by endocytosis [27][28][29][30][31][32].…”

Section: Entry Of Virus Inside Cell and Replicationmentioning

confidence: 99%

Dengue Epidemic Is a Global Recurrent Crisis: Review of the Literature

Araf¹,

Ullah²,

Faruqui³

et al. 2020

Preprint

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Purpose: This review highlights the global scenario of dengue outbreaks, dengue pathogenesis, symptoms, immune response, diagnosis methods and preventive measures which facilitates the better understanding of the global expansion and concerns relating to the disease. Recent Findings: A recent study showed that natural killer cells of the infected person become activated soon after the infection which may help in treatment and vaccine development. A research team has also produced synthetically engineered mosquitoes that can prevent the transmission and dissemination of the dengue virus by the activation of an antibody. Furthermore, a mutation in the protein envelope of the dengue virus leads to variation in shapes, developing resistance towards the vaccine. Summary: The mosquito vectors marked their worldwide distribution through an increasing number of reported cases which was further facilitated by the growth in the shipping and commerce industries. The immune system, through activation of the innate and adaptive immune responses, facilitates the recruitment of an array of leukocytes which help neutralize the virus. Apart from the laboratory standard PRNT method, several other dengue detection methods such as ELISA, RT-LAMP and several optical, microfluidic and electrochemical methods have been developed. The existence of the 4 different viral serotypes makes the secondary infection life-threatening and also leads to difficulties in vaccine development. Since Dengvaxia® (CYD-TDV) has its own set of drawbacks and limitations, several companies have been investing for the production of more potential vaccines that are currently in trial.

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Cellular Control of Dengue Virus Replication: Role of Interferon-Inducible Genes

Cited by 5 publications

References 109 publications

C19ORF66 Broadly Escapes Virus-Induced Endonuclease Cleavage and Restricts Kaposi’s Sarcoma-Associated Herpesvirus

C19ORF66 Broadly Escapes Virus-Induced Endonuclease Cleavage and Restricts Kaposi’s Sarcoma-Associated Herpesvirus

C19ORF66 broadly escapes viral-induced endonuclease cleavage and restricts Kaposi’s Sarcoma Associated Herpesvirus (KSHV)

Dengue Epidemic Is a Global Recurrent Crisis: Review of the Literature

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