The Functional Role of the 3′ Untranslated Region and Poly(A) Tail of Duck Hepatitis A Virus Type 1 in Viral Replication and Regulation of IRES-Mediated Translation

Chen, Junhao; Zhang, Ruihua; Lin, Shaoli; Li, Pengfei; Lan, Jingjing; Song, Shasha; Gao, Jiming; Wang, Yu; Xie, Zhixun; Li, Fu-Chang; Shi-jin, Jiang

doi:10.3389/fmicb.2018.02250

Cited by 15 publications

(13 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Up until now, little information is known about the replication mechanism of DHAV-1. Recently, we demonstrated that the 3′ UTR and the poly(A) tail could function as individual elements to enhance the DHAV-1 IRES-mediated translation [25]. In this research, we found that IGF2BP1 strongly enhanced DHAV-1 IRES-mediated translation efficiency through interaction with 3′ UTR.…”

Section: Introductionmentioning

confidence: 63%

IGF2BP1 Significantly Enhances Translation Efficiency of Duck Hepatitis A Virus Type 1 without Affecting Viral Replication

et al. 2019

Self Cite

View full text Add to dashboard Cite

As a disease characterized by severe liver necrosis and hemorrhage, duck viral hepatitis (DVH) is mainly caused by duck hepatitis A virus (DHAV). The positive-strand RNA genome of DHAV type 1 (DHAV-1) contains an internal ribosome entry site (IRES) element within the 5′ untranslated region (UTR), structured sequence elements within the 3′ UTR, and a poly(A) tail at the 3′ terminus. In this study, we first examined that insulin-like growth factor-2 mRNA-binding protein-1 (IGF2BP1) specifically interacted with the DHAV-1 3′ UTR by RNA pull-down assay. The interaction between IGF2BP1 and DHAV-1 3′ UTR strongly enhanced IRES-mediated translation efficiency but failed to regulate DHAV-1 replication in a duck embryo epithelial (DEE) cell line. The viral propagation of DHAV-1 strongly enhanced IGF2BP1 expression level, and viral protein accumulation was identified as the key point to this increment. Collectively, our data demonstrated the positive role of IGF2BP1 in DHAV-1 viral proteins translation and provided data support for the replication mechanism of DHAV-1.

show abstract

Section: Introductionmentioning

confidence: 63%

IGF2BP1 Significantly Enhances Translation Efficiency of Duck Hepatitis A Virus Type 1 without Affecting Viral Replication

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…One of our constructs containing 19 adenine residues failed to express a detectable level of the green fluorescent signal. Previous studies have shown that 3 UTR and the length of poly A tail of RNA viruses are responsible for viral genome replication [14,16]. In the poliovirus, the 10-fold increase in negative-strand RNA synthesis occurred by increasing the numbers of adenine from 12 to 13 residues [48].…”

Section: Discussionmentioning

confidence: 98%

“…In the poliovirus, the 10-fold increase in negative-strand RNA synthesis occurred by increasing the numbers of adenine from 12 to 13 residues [48]. In addition, increasing the poly A tail length from 15 to 20 residues has been shown to improve the viral copy number of duck hepatitis A virus type 1 [14]. In the hepatitis C virus, the poly A tail with 50 adenine residues demonstrated enhanced translation efficiency, depending upon its IRES [49].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, the protein translation activity of each viral 5 UTR appeared to be enhanced by the cognate 3 UTR [17]. Additionally, the length of poly A tail drastically influenced translation efficiency in duck hepatitis A virus type 1 [14].…”

Section: Introductionmentioning

confidence: 98%

“…Moreover, FMDV 3 UTR specifically interacts with the 5 UTR cis-acting element to regulate viral replication [12]. Picornavirus 3 UTR contains two stable stemloops that are involved in the negative-strand synthesis of viral RNA [12,13] by serving as a template for uridylylated 3B to initiate viral RNA replication by 3D pol [14]. The downstream 3 UTR contains a poly A tail with variable lengths, which is crucial for the negative-strand synthesis.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A Novel Plasmid DNA-Based Foot and Mouth Disease Virus Minigenome for Intracytoplasmic mRNA Production

Semkum

Kaewborisuth

Thangthamniyom

et al. 2021

Viruses

View full text Add to dashboard Cite

Picornaviruses are non-enveloped, single-stranded RNA viruses that cause highly contagious diseases, such as polio and hand, foot-and-mouth disease (HFMD) in human, and foot-and-mouth disease (FMD) in animals. Reverse genetics and minigenome of picornaviruses mainly depend on in vitro transcription and RNA transfection; however, this approach is inefficient due to the rapid degradation of RNA template. Although DNA-based reverse genetics systems driven by mammalian RNA polymerase I and/or II promoters display the advantage of rescuing the engineered FMDV, the enzymatic functions are restricted in the nuclear compartment. To overcome these limitations, we successfully established a novel DNA-based vector, namely pKLS3, an FMDV minigenome containing the minimum cis-acting elements of FMDV essential for intracytoplasmic transcription and translation of a foreign gene. A combination of pKLS3 minigenome and the helper plasmids yielded the efficient production of uncapped-green florescent protein (GFP) mRNA visualized in the transfected cells. We have demonstrated the application of the pKLS3 for cell-based antiviral drug screening. Not only is the DNA-based FMDV minigenome system useful for the FMDV research and development but it could be implemented for generating other picornavirus minigenomes. Additionally, the prospective applications of this viral minigenome system as a vector for DNA and mRNA vaccines are also discussed.

show abstract

Modulation of various host cellular machinery during COVID‐19 infection

Malvankar,

Singh,

Ravi Kumar

et al. 2023

Reviews in Medical Virology

View full text Add to dashboard Cite

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV2) emerged in December 2019, causing a range of respiratory infections from mild to severe. This resulted in the ongoing global COVID‐19 pandemic, which has had a significant impact on public health. The World Health Organization declared COVID‐19 as a global pandemic in March 2020. Viruses are intracellular pathogens that rely on the host's machinery to establish a successful infection. They exploit the gene expression machinery of host cells to facilitate their own replication. Gaining a better understanding of gene expression modulation in SARS‐CoV2 is crucial for designing and developing effective antiviral strategies. Efforts are currently underway to understand the molecular‐level interaction between the host and the pathogen. In this review, we describe how SARS‐CoV2 infection modulates gene expression by interfering with cellular processes, including transcription, post‐transcription, translation, post‐translation, epigenetic modifications as well as processing and degradation pathways. Additionally, we emphasise the therapeutic implications of these findings in the development of new therapies to treat SARS‐CoV2 infection.

show abstract

The Functional Role of the 3′ Untranslated Region and Poly(A) Tail of Duck Hepatitis A Virus Type 1 in Viral Replication and Regulation of IRES-Mediated Translation

Cited by 15 publications

References 56 publications

IGF2BP1 Significantly Enhances Translation Efficiency of Duck Hepatitis A Virus Type 1 without Affecting Viral Replication

IGF2BP1 Significantly Enhances Translation Efficiency of Duck Hepatitis A Virus Type 1 without Affecting Viral Replication

A Novel Plasmid DNA-Based Foot and Mouth Disease Virus Minigenome for Intracytoplasmic mRNA Production

Modulation of various host cellular machinery during COVID‐19 infection

Contact Info

Product

Resources

About