This work, including the efforts of Richard E Randall, was funded by Wellcome Trust (101788/Z/13/Z). This work, including the efforts of Steve Goodbourn, was funded by Wellcome Trust (101792/Z/13/Z).We have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line without causing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsy material or from laboratory contamination during generation of the cell line.Publisher PDFPeer reviewe

Davison, Andrew J.

Goodburn, Steve

Randall, Richard Edward

Wignall-Fleming, Elizabeth

Young, Dan Frushard

Genome Announcements

PubMed

This work, including the efforts of Richard E Randall, was funded by Wellcome Trust (101788/Z/13/Z). This work, including the efforts of Steve Goodbourn, was funded by Wellcome Trust (101792/Z/13/Z).We have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line without causing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsy material or from laboratory contamination during generation of the cell line.Peer reviewe

St Andrews Research Repository

Genome Sequence of the Parainfluenza Virus 5 Strain ThatPersistently Infects AGS CellsElizabeth Wignall-Fleming,a,b Dan F. Young,b Steve Goodbourn,c Andrew J. Davison,a Richard E. RandallbMRC – University of Glasgow Centre for Virus Research, Glasgow, United Kingdoma; Centre for Biomolecular Sciences, School of Biology, University of St. Andrews, St.Andrews, United Kingdomb; Division of Basic Medical Sciences, St. George’s, University of London, London, United KingdomcWe have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line withoutcausing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsymaterial or from laboratory contamination during generation of the cell line.Received 17 May 2016 Accepted 25 May 2016 Published 21 July 2016CitationWignall-Fleming E, Young DF, Goodbourn S, Davison AJ, Randall RE. 2016. Genome sequence of the parainfluenza virus 5 strain that persistently infects AGS cells.Genome Announc 4(4):e00653-16. doi:10.1128/genomeA.00653-16.Copyright © 2016 Wignall-Fleming et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.Address correspondence to Richard E. Randall, rer@st-and.ac.uk.Parainfluenza virus 5 (PIV5; genus Rubulavirus, subfamilyParamyxovirinae, family Paramyxoviridae [1]) possesses asingle-stranded, negative-sense RNA genome containing sevengenes that encode eight proteins (2). This virus has been isolatedfrom numerous species, including humans, monkeys, pigs, cattle,and dogs (3). PIV5 is not known to cause acute disease in humansbut has been associated with kennel cough in dogs and acute re-spiratory symptoms in pigs and calves. It can also cause unrecog-nized persistent infections of tissue culture cells and is likely toestablish persistent infections in vivo (4).The AGS cell line was derived from a human gastric adenocar-cinoma (5) and has been used commonly in biomedical research,but it is persistently infected with a strain of PIV5 (4). To deter-mine the genetic characteristics of this strain (PIV5-AGS), RNAwas isolated by TRIzol (Invitrogen) extraction of AGS cells(ATCC CRL-1739) and of A549 cells (ATCC CCL-185) infectedwith the strain isolated from AGS cells. Libraries were preparedusing a TruSeq stranded mRNA kit (Illumina) and sequenced us-ing a MiSeq platform (Illumina). The data, which consisted of2,973,486 and 2,874,556 paired-end reads (301 nucleotides [nt])for virus from AGS cells and PIV5-AGS-infected A549 cells, re-spectively, were aligned initially to the PIV5-W3genome sequence(accession no. JQ743318) (6) using Bowtie2 version 2.2.8 (7), andthe alignmentswere visualized usingTablet version 1.13.08.05 (8).Final corrections to the consensus sequences were then made onthe basis of fresh alignments. In each case, examination of theRNA strands from which reads were generated revealed thatgenomic RNA had copurified with viral mRNA, presumably as aresult of intermolecular hybridization, and thus it was possible todetermine the genome sequences (15,346 nt). The percentages ofthe aligned reads were 3.11 and 1.94 for virus from AGS cells andPIV5-AGS-infected A549 cells, respectively. The consensus se-quences were almost identical, differing only in the nucleotides atpositions 6910 and 7445, which were polymorphic, consisting ofmixtures of G and A residues in both genomes. This observationdemonstrated that the virus in persistently infected cells is notdefective; the possibility of defectiveness had been suggested pre-viously from the observation that AGS cells do not exhibit viralcytopathology (4).As in several other PIV5 strains (6), the SH gene is unlikely tobe functional in PIV5-AGS, because it contains a 1-nt deletion.This deletion is compensated by a 1-nt insertion in the noncodingregion between the HN and L genes, the genome thereby con-forming to the rule of six (9). Phylogenetic analysis of thePIV5-AGS sequence in comparison with the sequences of 17other strains available fromGenBank showed that PIV5-AGS ismost closely related to human strains. Although this findingdoes not explain the origin of PIV5 in the AGS cell line, itsuggests that infection from a human was involved, either be-cause virus was present in the biopsy material or because thecell line was contaminated in the laboratory during its genera-tion.Nucleotide sequence accession number. The PIV5-AGS ge-nome sequence present in persistently infected AGS cells has beendeposited in GenBank under the accession no. KX060176.ACKNOWLEDGMENTSThe University of St. Andrews and the University of Glasgow are charitiesregistered in Scotland (SC013532 and SC004401, respectively). This studywas funded by grants from theWellcome Trust (101788/Z/13/Z) to Rich-ard E. Randall, theWellcomeTrust (101792/Z/13/Z) to SteveGoodbourn,and the Medical Research Council (MRC) (G0801822) to the MRC –University of Glasgow Centre for Virus Research.FUNDING INFORMATIONThis work, including the efforts of Richard E Randall, was funded byWellcome Trust (101788/Z/13/Z). This work, including the efforts ofSteve Goodbourn, was funded by Wellcome Trust (101792/Z/13/Z).REFERENCES1. Wang L-F, Collins PL, Fouchier RAM, Kurath G, Lamb RA, Randall RE,RimaBK. 2012. Family Paramyxoviridae, p 672–685. In KingAMQ,AdamsMJ, Carstens EB, Lefkowitz EJ (ed), Virus taxonomy, ninth report of theInternational Committee on Taxonomy of Viruses. Elsevier Academic,London, United Kingdom.2. Parks GD, Manuse MJ, Johnson JB. 2011. The parainfluenza virus simiancrossmarkGenome AnnouncementsJuly/August 2016 Volume 4 Issue 4 e00653-16 genomea.asm.org 1 on July 26, 2016 by ST ANDREWS UNIVhttp://genomea.asm.org/Downloaded from virus. In Samal SK (ed), The biology of paramyxoviruses, vol 5. CaisterAcademic Press, Norfolk, United Kingdom.3. Chatziandreou N, Stock N, Young D, Andrejeva J, Hagmaier K,McGeoch DJ, Randall RE. 2004. Relationships and host range of human,canine, simian and porcine isolates of simian virus, 5 (parainfluenza virus5). J Gen Virol 85:3007–3016.4. Young DF, Carlos TS, Hagmaier K, Fan L, Randall RE. 2007. AGS andother tissue culture cells can unknowingly be persistently infected withPIV5; a virus that blocks interferon signalling by degrading STAT1. Virol-ogy 365:238–240. http://dx.doi.org/10.1016/j.virol.2007.03.061.5. Barranco SC, Townsend CM, Jr, Casartelli C, Macik BG, Burger NL,Boerwinkle WR, Gourley WK. 1983. Establishment and characterizationof an in vitro model system for human adenocarcinoma of the stomach.Cancer Res 43:1703–1709.6. Rima BK, Gatherer D, Young DF, Norsted H, Randall RE, DavisonAJ. 2014. Stability of the parainfluenza virus 5 genome revealed by deepsequencing of strains isolated from different hosts and following passagein cell culture. J Virol 88:3826 –3836. http://dx.doi.org/10.1128/JVI.03351-13.7. Langmead B, Salzberg SL. 2012. Fast gapped-read alignment with Bowtie2. Nat Methods 9:357–359. http://dx.doi.org/10.1038/nmeth.1923.8. Milne I, Bayer M, Cardle L, Shaw P, Stephen G, Wright F, MarshallD. 2010. Tablet—next generation sequence assembly visualization.Bioinformatics 26:401– 402. http://dx.doi.org/10.1093/bioinformatics/btp666.9. Calain P, Roux L. 1993. The rule of six, a basic feature for efficientreplication of Sendai virus defective interfering RNA. J Virol 67:4822–4830.Wignall-Fleming et al.Genome Announcements2 genomea.asm.org July/August 2016 Volume 4 Issue 4 e00653-16 on July 26, 2016 by ST ANDREWS UNIVhttp://genomea.asm.org/Downloaded from 

Genome sequence of the parainfluenza virus 5 strain that persistently infects AGS cells

We have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line without causing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsy material or from laboratory contamination during generation of the cell line

Wingnall-Fleming, Elizabeth

Young, Dan F.

Goodbourn, Steve

Randall, Richard E.

Enlighten: Publications

Enlighten

Genome Sequence of the Parainfluenza Virus 5 Strain ThatPersistently Infects AGS CellsElizabeth Wignall-Fleming,a,b Dan F. Young,b Steve Goodbourn,c Andrew J. Davison,a Richard E. RandallbMRC – University of Glasgow Centre for Virus Research, Glasgow, United Kingdoma; Centre for Biomolecular Sciences, School of Biology, University of St. Andrews, St.Andrews, United Kingdomb; Division of Basic Medical Sciences, St. George’s, University of London, London, United KingdomcWe have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line withoutcausing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsymaterial or from laboratory contamination during generation of the cell line.Received 17 May 2016 Accepted 25 May 2016 Published 21 July 2016CitationWignall-Fleming E, Young DF, Goodbourn S, Davison AJ, Randall RE. 2016. Genome sequence of the parainfluenza virus 5 strain that persistently infects AGS cells.Genome Announc 4(4):e00653-16. doi:10.1128/genomeA.00653-16.Copyright © 2016 Wignall-Fleming et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.Address correspondence to Richard E. Randall, rer@st-and.ac.uk.Parainfluenza virus 5 (PIV5; genus Rubulavirus, subfamilyParamyxovirinae, family Paramyxoviridae [1]) possesses asingle-stranded, negative-sense RNA genome containing sevengenes that encode eight proteins (2). This virus has been isolatedfrom numerous species, including humans, monkeys, pigs, cattle,and dogs (3). PIV5 is not known to cause acute disease in humansbut has been associated with kennel cough in dogs and acute re-spiratory symptoms in pigs and calves. It can also cause unrecog-nized persistent infections of tissue culture cells and is likely toestablish persistent infections in vivo (4).The AGS cell line was derived from a human gastric adenocar-cinoma (5) and has been used commonly in biomedical research,but it is persistently infected with a strain of PIV5 (4). To deter-mine the genetic characteristics of this strain (PIV5-AGS), RNAwas isolated by TRIzol (Invitrogen) extraction of AGS cells(ATCC CRL-1739) and of A549 cells (ATCC CCL-185) infectedwith the strain isolated from AGS cells. Libraries were preparedusing a TruSeq stranded mRNA kit (Illumina) and sequenced us-ing a MiSeq platform (Illumina). The data, which consisted of2,973,486 and 2,874,556 paired-end reads (301 nucleotides [nt])for virus from AGS cells and PIV5-AGS-infected A549 cells, re-spectively, were aligned initially to the PIV5-W3genome sequence(accession no. JQ743318) (6) using Bowtie2 version 2.2.8 (7), andthe alignmentswere visualized usingTablet version 1.13.08.05 (8).Final corrections to the consensus sequences were then made onthe basis of fresh alignments. In each case, examination of theRNA strands from which reads were generated revealed thatgenomic RNA had copurified with viral mRNA, presumably as aresult of intermolecular hybridization, and thus it was possible todetermine the genome sequences (15,346 nt). The percentages ofthe aligned reads were 3.11 and 1.94 for virus from AGS cells andPIV5-AGS-infected A549 cells, respectively. The consensus se-quences were almost identical, differing only in the nucleotides atpositions 6910 and 7445, which were polymorphic, consisting ofmixtures of G and A residues in both genomes. This observationdemonstrated that the virus in persistently infected cells is notdefective; the possibility of defectiveness had been suggested pre-viously from the observation that AGS cells do not exhibit viralcytopathology (4).As in several other PIV5 strains (6), the SH gene is unlikely tobe functional in PIV5-AGS, because it contains a 1-nt deletion.This deletion is compensated by a 1-nt insertion in the noncodingregion between the HN and L genes, the genome thereby con-forming to the rule of six (9). Phylogenetic analysis of thePIV5-AGS sequence in comparison with the sequences of 17other strains available fromGenBank showed that PIV5-AGS ismost closely related to human strains. Although this findingdoes not explain the origin of PIV5 in the AGS cell line, itsuggests that infection from a human was involved, either be-cause virus was present in the biopsy material or because thecell line was contaminated in the laboratory during its genera-tion.Nucleotide sequence accession number. The PIV5-AGS ge-nome sequence present in persistently infected AGS cells has beendeposited in GenBank under the accession no. KX060176.ACKNOWLEDGMENTSThe University of St. Andrews and the University of Glasgow are charitiesregistered in Scotland (SC013532 and SC004401, respectively). This studywas funded by grants from theWellcome Trust (101788/Z/13/Z) to Rich-ard E. Randall, theWellcomeTrust (101792/Z/13/Z) to SteveGoodbourn,and the Medical Research Council (MRC) (G0801822) to the MRC –University of Glasgow Centre for Virus Research.FUNDING INFORMATIONThis work, including the efforts of Richard E Randall, was funded byWellcome Trust (101788/Z/13/Z). This work, including the efforts ofSteve Goodbourn, was funded by Wellcome Trust (101792/Z/13/Z).REFERENCES1. Wang L-F, Collins PL, Fouchier RAM, Kurath G, Lamb RA, Randall RE,RimaBK. 2012. Family Paramyxoviridae, p 672–685. In KingAMQ,AdamsMJ, Carstens EB, Lefkowitz EJ (ed), Virus taxonomy, ninth report of theInternational Committee on Taxonomy of Viruses. Elsevier Academic,London, United Kingdom.2. Parks GD, Manuse MJ, Johnson JB. 2011. The parainfluenza virus simiancrossmarkGenome AnnouncementsJuly/August 2016 Volume 4 Issue 4 e00653-16 genomea.asm.org 1 on August 9, 2016 by SWETS SUBSCRIPTION SERVICEhttp://genomea.asm.org/Downloaded from virus. In Samal SK (ed), The biology of paramyxoviruses, vol 5. CaisterAcademic Press, Norfolk, United Kingdom.3. Chatziandreou N, Stock N, Young D, Andrejeva J, Hagmaier K,McGeoch DJ, Randall RE. 2004. Relationships and host range of human,canine, simian and porcine isolates of simian virus, 5 (parainfluenza virus5). J Gen Virol 85:3007–3016.4. Young DF, Carlos TS, Hagmaier K, Fan L, Randall RE. 2007. AGS andother tissue culture cells can unknowingly be persistently infected withPIV5; a virus that blocks interferon signalling by degrading STAT1. Virol-ogy 365:238–240. http://dx.doi.org/10.1016/j.virol.2007.03.061.5. Barranco SC, Townsend CM, Jr, Casartelli C, Macik BG, Burger NL,Boerwinkle WR, Gourley WK. 1983. Establishment and characterizationof an in vitro model system for human adenocarcinoma of the stomach.Cancer Res 43:1703–1709.6. Rima BK, Gatherer D, Young DF, Norsted H, Randall RE, DavisonAJ. 2014. Stability of the parainfluenza virus 5 genome revealed by deepsequencing of strains isolated from different hosts and following passagein cell culture. J Virol 88:3826 –3836. http://dx.doi.org/10.1128/JVI.03351-13.7. Langmead B, Salzberg SL. 2012. Fast gapped-read alignment with Bowtie2. Nat Methods 9:357–359. http://dx.doi.org/10.1038/nmeth.1923.8. Milne I, Bayer M, Cardle L, Shaw P, Stephen G, Wright F, MarshallD. 2010. Tablet—next generation sequence assembly visualization.Bioinformatics 26:401– 402. http://dx.doi.org/10.1093/bioinformatics/btp666.9. Calain P, Roux L. 1993. The rule of six, a basic feature for efficientreplication of Sendai virus defective interfering RNA. J Virol 67:4822–4830.Wignall-Fleming et al.Genome Announcements2 genomea.asm.org July/August 2016 Volume 4 Issue 4 e00653-16 on August 9, 2016 by SWETS SUBSCRIPTION SERVICEhttp://genomea.asm.org/Downloaded from 

English

University of St Andrews Research Portal

Wignall-Fleming, E

Young, DF

Goodbourn, S

Davison, AJ

Randall, RE

St George's Online Research Archive

Genome Sequence of the Parainfluenza Virus 5 Strain ThatPersistently Infects AGS CellsElizabeth Wignall-Fleming,a,b Dan F. Young,b Steve Goodbourn,c Andrew J. Davison,a Richard E. RandallbMRC – University of Glasgow Centre for Virus Research, Glasgow, United Kingdoma; Centre for Biomolecular Sciences, School of Biology, University of St. Andrews, St.Andrews, United Kingdomb; Division of Basic Medical Sciences, St. George’s, University of London, London, United KingdomcWe have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line withoutcausing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsymaterial or from laboratory contamination during generation of the cell line.Received 17 May 2016 Accepted 25 May 2016 Published 21 July 2016CitationWignall-Fleming E, Young DF, Goodbourn S, Davison AJ, Randall RE. 2016. Genome sequence of the parainfluenza virus 5 strain that persistently infects AGS cells.Genome Announc 4(4):e00653-16. doi:10.1128/genomeA.00653-16.Copyright © 2016 Wignall-Fleming et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.Address correspondence to Richard E. Randall, rer@st-and.ac.uk.Parainfluenza virus 5 (PIV5; genus Rubulavirus, subfamilyParamyxovirinae, family Paramyxoviridae [1]) possesses asingle-stranded, negative-sense RNA genome containing sevengenes that encode eight proteins (2). This virus has been isolatedfrom numerous species, including humans, monkeys, pigs, cattle,and dogs (3). PIV5 is not known to cause acute disease in humansbut has been associated with kennel cough in dogs and acute re-spiratory symptoms in pigs and calves. It can also cause unrecog-nized persistent infections of tissue culture cells and is likely toestablish persistent infections in vivo (4).The AGS cell line was derived from a human gastric adenocar-cinoma (5) and has been used commonly in biomedical research,but it is persistently infected with a strain of PIV5 (4). To deter-mine the genetic characteristics of this strain (PIV5-AGS), RNAwas isolated by TRIzol (Invitrogen) extraction of AGS cells(ATCC CRL-1739) and of A549 cells (ATCC CCL-185) infectedwith the strain isolated from AGS cells. Libraries were preparedusing a TruSeq stranded mRNA kit (Illumina) and sequenced us-ing a MiSeq platform (Illumina). The data, which consisted of2,973,486 and 2,874,556 paired-end reads (301 nucleotides [nt])for virus from AGS cells and PIV5-AGS-infected A549 cells, re-spectively, were aligned initially to the PIV5-W3genome sequence(accession no. JQ743318) (6) using Bowtie2 version 2.2.8 (7), andthe alignmentswere visualized usingTablet version 1.13.08.05 (8).Final corrections to the consensus sequences were then made onthe basis of fresh alignments. In each case, examination of theRNA strands from which reads were generated revealed thatgenomic RNA had copurified with viral mRNA, presumably as aresult of intermolecular hybridization, and thus it was possible todetermine the genome sequences (15,346 nt). The percentages ofthe aligned reads were 3.11 and 1.94 for virus from AGS cells andPIV5-AGS-infected A549 cells, respectively. The consensus se-quences were almost identical, differing only in the nucleotides atpositions 6910 and 7445, which were polymorphic, consisting ofmixtures of G and A residues in both genomes. This observationdemonstrated that the virus in persistently infected cells is notdefective; the possibility of defectiveness had been suggested pre-viously from the observation that AGS cells do not exhibit viralcytopathology (4).As in several other PIV5 strains (6), the SH gene is unlikely tobe functional in PIV5-AGS, because it contains a 1-nt deletion.This deletion is compensated by a 1-nt insertion in the noncodingregion between the HN and L genes, the genome thereby con-forming to the rule of six (9). Phylogenetic analysis of thePIV5-AGS sequence in comparison with the sequences of 17other strains available fromGenBank showed that PIV5-AGS ismost closely related to human strains. Although this findingdoes not explain the origin of PIV5 in the AGS cell line, itsuggests that infection from a human was involved, either be-cause virus was present in the biopsy material or because thecell line was contaminated in the laboratory during its genera-tion.Nucleotide sequence accession number. The PIV5-AGS ge-nome sequence present in persistently infected AGS cells has beendeposited in GenBank under the accession no. KX060176.ACKNOWLEDGMENTSThe University of St. Andrews and the University of Glasgow are charitiesregistered in Scotland (SC013532 and SC004401, respectively). This studywas funded by grants from theWellcome Trust (101788/Z/13/Z) to Rich-ard E. Randall, theWellcomeTrust (101792/Z/13/Z) to SteveGoodbourn,and the Medical Research Council (MRC) (G0801822) to the MRC –University of Glasgow Centre for Virus Research.FUNDING INFORMATIONThis work, including the efforts of Richard E Randall, was funded byWellcome Trust (101788/Z/13/Z). This work, including the efforts ofSteve Goodbourn, was funded by Wellcome Trust (101792/Z/13/Z).REFERENCES1. Wang L-F, Collins PL, Fouchier RAM, Kurath G, Lamb RA, Randall RE,RimaBK. 2012. Family Paramyxoviridae, p 672–685. In KingAMQ,AdamsMJ, Carstens EB, Lefkowitz EJ (ed), Virus taxonomy, ninth report of theInternational Committee on Taxonomy of Viruses. Elsevier Academic,London, United Kingdom.2. Parks GD, Manuse MJ, Johnson JB. 2011. The parainfluenza virus simiancrossmarkGenome AnnouncementsJuly/August 2016 Volume 4 Issue 4 e00653-16 genomea.asm.org 1virus. In Samal SK (ed), The biology of paramyxoviruses, vol 5. CaisterAcademic Press, Norfolk, United Kingdom.3. Chatziandreou N, Stock N, Young D, Andrejeva J, Hagmaier K,McGeoch DJ, Randall RE. 2004. Relationships and host range of human,canine, simian and porcine isolates of simian virus, 5 (parainfluenza virus5). J Gen Virol 85:3007–3016.4. Young DF, Carlos TS, Hagmaier K, Fan L, Randall RE. 2007. AGS andother tissue culture cells can unknowingly be persistently infected withPIV5; a virus that blocks interferon signalling by degrading STAT1. Virol-ogy 365:238–240. http://dx.doi.org/10.1016/j.virol.2007.03.061.5. Barranco SC, Townsend CM, Jr, Casartelli C, Macik BG, Burger NL,Boerwinkle WR, Gourley WK. 1983. Establishment and characterizationof an in vitro model system for human adenocarcinoma of the stomach.Cancer Res 43:1703–1709.6. Rima BK, Gatherer D, Young DF, Norsted H, Randall RE, DavisonAJ. 2014. Stability of the parainfluenza virus 5 genome revealed by deepsequencing of strains isolated from different hosts and following passagein cell culture. J Virol 88:3826 –3836. http://dx.doi.org/10.1128/JVI.03351-13.7. Langmead B, Salzberg SL. 2012. Fast gapped-read alignment with Bowtie2. Nat Methods 9:357–359. http://dx.doi.org/10.1038/nmeth.1923.8. Milne I, Bayer M, Cardle L, Shaw P, Stephen G, Wright F, MarshallD. 2010. Tablet—next generation sequence assembly visualization.Bioinformatics 26:401– 402. http://dx.doi.org/10.1093/bioinformatics/btp666.9. Calain P, Roux L. 1993. The rule of six, a basic feature for efficientreplication of Sendai virus defective interfering RNA. J Virol 67:4822–4830.Wignall-Fleming et al.Genome Announcements2 genomea.asm.org July/August 2016 Volume 4 Issue 4 e00653-16

Genome Sequence of the Parainfluenza Virus 5 Strain That Persistently Infects AGS Cells.

University of St. Andrews - Pure

ABSTRACT
          We have sequenced the parainfluenza virus 5 strain that persistently infects the commonly used AGS human cell line without causing cytopathology. This virus is most closely related to human strains, indicating that it may have originated from biopsy material or from laboratory contamination during generation of the cell line.</jats:p

Elizabeth Wignall-Fleming

Dan F. Young

Steve Goodbourn

Andrew J. Davison

Richard E. Randall

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Genome Sequence of the Parainfluenza Virus 5 Strain That Persistently Infects AGS Cells

http://dx.doi.org/10.1128/genomeA.00653-16

Genome sequence of the parainfluenza virus 5 strain that persistently infects AGS cells

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University of St. Andrews - Pure

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