Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells

Both hepatitis B virus (HBV), an hepadnavirus with a DNA genome, and hepatitis A virus (HAV), a picornavirus, require the TRAMP-like host ZCCHC14-TENT4 complex for efficient replication. However, whereas HBV requires the nucleotidyltransferase activity of TENT4 to extend and stabilize the 3′ poly(A)...

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Main Authors: You Li, Ankit Gupta, Brian N. Papas, David Aponte-Diaz, Jayden M. Harris, Ichiro Misumi, Jason K. Whitmire, Craig E. Cameron, Marcos Morgan, Stanley M. Lemon
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Viruses
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Online Access:https://www.mdpi.com/1999-4915/17/5/665
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author You Li
Ankit Gupta
Brian N. Papas
David Aponte-Diaz
Jayden M. Harris
Ichiro Misumi
Jason K. Whitmire
Craig E. Cameron
Marcos Morgan
Stanley M. Lemon
author_facet You Li
Ankit Gupta
Brian N. Papas
David Aponte-Diaz
Jayden M. Harris
Ichiro Misumi
Jason K. Whitmire
Craig E. Cameron
Marcos Morgan
Stanley M. Lemon
author_sort You Li
collection DOAJ
description Both hepatitis B virus (HBV), an hepadnavirus with a DNA genome, and hepatitis A virus (HAV), a picornavirus, require the TRAMP-like host ZCCHC14-TENT4 complex for efficient replication. However, whereas HBV requires the nucleotidyltransferase activity of TENT4 to extend and stabilize the 3′ poly(A) tails of mRNA transcribed from its genome, the role played by TENT4 in HAV replication is uncertain. HAV proteins are synthesized directly from its genomic RNA, which possesses a 3′ poly(A) tail, with its length and composition presumably maintained by 3D<sup>pol</sup>-catalyzed RNA transcription during its replicative cycle. Using nanopore long-read sequencing of RNA from infected cells, we confirm here that the length of the HAV 3′ poly(A) tail is not altered by treating infected cells with RG7834, a small molecule TENT4 inhibitor with potent anti-HAV activity. Despite this, TENT4 catalytic activity is essential for HAV replication. Surprisingly, nanopore sequencing revealed a low abundance of HAV subgenomic RNAs (hsRNAs) that extend from the 5′ end of the genome to a site within the 5′ untranslated RNA (5′UTR) immediately downstream of a stem-loop to which the ZCCHC14-TENT4 complex is recruited. These hsRNAs are polyadenylated, and their abundance is sharply reduced by RG7834 treatment, implying they are likely products of TENT4. Similar subgenomic RNAs were not identified in poliovirus-infected cells. hsRNAs are present not only in HAV-infected cell culture but also in the liver of HAV-infected mice, where they represent 1–3% of all HAV transcripts, suggesting their physiological relevance. However, transfecting exogenous hsRNA into TENT4-depleted cells failed to rescue HAV replication, leaving the functional role of hsRNA unresolved. These findings reveal a novel picornaviral subgenomic RNA species while highlighting mechanistic differences in the manner in which HAV and HBV exploit the host ZCCHC4-TENT4 complex for their replication.
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spelling doaj-art-e9a061bcb03c43ba85cfb76b4316bcac2025-08-20T03:47:58ZengMDPI AGViruses1999-49152025-05-0117566510.3390/v17050665Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected CellsYou Li0Ankit Gupta1Brian N. Papas2David Aponte-Diaz3Jayden M. Harris4Ichiro Misumi5Jason K. Whitmire6Craig E. Cameron7Marcos Morgan8Stanley M. Lemon9Department of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USAReproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC 27709, USAIntegrative Bioinformatics, Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC 27709, USADepartment of Microbiology & Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USADepartment of Microbiology & Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USADepartment of Genetics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USADepartment of Genetics, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USADepartment of Microbiology & Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USAReproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, NC 27709, USADepartment of Microbiology & Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USABoth hepatitis B virus (HBV), an hepadnavirus with a DNA genome, and hepatitis A virus (HAV), a picornavirus, require the TRAMP-like host ZCCHC14-TENT4 complex for efficient replication. However, whereas HBV requires the nucleotidyltransferase activity of TENT4 to extend and stabilize the 3′ poly(A) tails of mRNA transcribed from its genome, the role played by TENT4 in HAV replication is uncertain. HAV proteins are synthesized directly from its genomic RNA, which possesses a 3′ poly(A) tail, with its length and composition presumably maintained by 3D<sup>pol</sup>-catalyzed RNA transcription during its replicative cycle. Using nanopore long-read sequencing of RNA from infected cells, we confirm here that the length of the HAV 3′ poly(A) tail is not altered by treating infected cells with RG7834, a small molecule TENT4 inhibitor with potent anti-HAV activity. Despite this, TENT4 catalytic activity is essential for HAV replication. Surprisingly, nanopore sequencing revealed a low abundance of HAV subgenomic RNAs (hsRNAs) that extend from the 5′ end of the genome to a site within the 5′ untranslated RNA (5′UTR) immediately downstream of a stem-loop to which the ZCCHC14-TENT4 complex is recruited. These hsRNAs are polyadenylated, and their abundance is sharply reduced by RG7834 treatment, implying they are likely products of TENT4. Similar subgenomic RNAs were not identified in poliovirus-infected cells. hsRNAs are present not only in HAV-infected cell culture but also in the liver of HAV-infected mice, where they represent 1–3% of all HAV transcripts, suggesting their physiological relevance. However, transfecting exogenous hsRNA into TENT4-depleted cells failed to rescue HAV replication, leaving the functional role of hsRNA unresolved. These findings reveal a novel picornaviral subgenomic RNA species while highlighting mechanistic differences in the manner in which HAV and HBV exploit the host ZCCHC4-TENT4 complex for their replication.https://www.mdpi.com/1999-4915/17/5/665nanopore sequencinghepatoviruspicornavirusterminal nucleotidyltransferaseZCCHC14PAPD5/7
spellingShingle You Li
Ankit Gupta
Brian N. Papas
David Aponte-Diaz
Jayden M. Harris
Ichiro Misumi
Jason K. Whitmire
Craig E. Cameron
Marcos Morgan
Stanley M. Lemon
Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
Viruses
nanopore sequencing
hepatovirus
picornavirus
terminal nucleotidyltransferase
ZCCHC14
PAPD5/7
title Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
title_full Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
title_fullStr Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
title_full_unstemmed Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
title_short Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
title_sort noncanonical poly a polymerase tent4 drives expression of subgenomic hepatitis a virus rnas in infected cells
topic nanopore sequencing
hepatovirus
picornavirus
terminal nucleotidyltransferase
ZCCHC14
PAPD5/7
url https://www.mdpi.com/1999-4915/17/5/665
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