Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.

Ariel Rodriguez; Alicia Pérez-González; M Jaber Hossain; Li-Mei Chen; Thierry Rolling; Pilar Pérez-Breña; Ruben Donis; Georg Kochs; Amelia Nieto

Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.

Standard

Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II. / Rodriguez, Ariel; Pérez-González, Alicia; Hossain, M Jaber; Chen, Li-Mei; Rolling, Thierry; Pérez-Breña, Pilar; Donis, Ruben; Kochs, Georg; Nieto, Amelia.

In: J VIROL, Vol. 83, No. 21, 21, 2009, p. 11166-11174.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Rodriguez, A, Pérez-González, A, Hossain, MJ, Chen, L-M, Rolling, T, Pérez-Breña, P, Donis, R, Kochs, G & Nieto, A 2009, 'Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.', J VIROL, vol. 83, no. 21, 21, pp. 11166-11174. <http://www.ncbi.nlm.nih.gov/pubmed/19692472?dopt=Citation>

APA

Rodriguez, A., Pérez-González, A., Hossain, M. J., Chen, L-M., Rolling, T., Pérez-Breña, P., Donis, R., Kochs, G., & Nieto, A. (2009). Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II. J VIROL, 83(21), 11166-11174. [21]. http://www.ncbi.nlm.nih.gov/pubmed/19692472?dopt=Citation

Vancouver

Rodriguez A, Pérez-González A, Hossain MJ, Chen L-M, Rolling T, Pérez-Breña P et al. Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II. J VIROL. 2009;83(21):11166-11174. 21.

Bibtex

@article{c6b65f462a0b4a72abaede030fc9941d,

title = "Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.",

abstract = "We have previously shown that infection with laboratory-passaged strains of influenza virus causes both specific degradation of the largest subunit of the RNA polymerase II complex (RNAP II) and inhibition of host cell transcription. When infection with natural human and avian isolates belonging to different antigenic subtypes was examined, we observed that all of these viruses efficiently induce the proteolytic process. To evaluate whether this process is a general feature of nonattenuated viruses, we studied the behavior of the influenza virus strains A/PR8/8/34 (PR8) and the cold-adapted A/Ann Arbor/6/60 (AA), which are currently used as the donor strains for vaccine seeds due to their attenuated phenotype. We have observed that upon infection with these strains, degradation of the RNAP II does not occur. Moreover, by runoff experiments we observe that PR8 has a reduced ability to inhibit cellular mRNA transcription. In addition, a hypervirulent PR8 (hvPR8) variant that multiplies much faster than standard PR8 (lvPR8) in infected cells and is more virulent in mice than the parental PR8 virus, efficiently induces RNAP II degradation. Studies with reassortant viruses containing defined genome segments of both hvPR8 and lvPR8 indicate that PA and PB2 subunits individually contribute to the ability of influenza virus to degrade the RNAP II. In addition, recently it has been reported that the inclusion of PA or PB2 from hvPR8 in lvPR8 recombinant viruses, highly increases their pathogenicity. Together, the data indicate that the capacity of the influenza virus to degrade RNAP II and inhibit the host cell transcription machinery is a feature of influenza A viruses that might contribute to their virulence.",

keywords = "Animals, Humans, Mice, Transcription, Genetic, Cell Line, RNA, Messenger/genetics/metabolism, Influenza A virus/genetics/*metabolism, Protein Subunits/genetics/*metabolism, RNA Polymerase II/genetics/*metabolism, RNA, Viral, Animals, Humans, Mice, Transcription, Genetic, Cell Line, RNA, Messenger/genetics/metabolism, Influenza A virus/genetics/*metabolism, Protein Subunits/genetics/*metabolism, RNA Polymerase II/genetics/*metabolism, RNA, Viral",

author = "Ariel Rodriguez and Alicia P{\'e}rez-Gonz{\'a}lez and Hossain, {M Jaber} and Li-Mei Chen and Thierry Rolling and Pilar P{\'e}rez-Bre{\~n}a and Ruben Donis and Georg Kochs and Amelia Nieto",

year = "2009",

language = "English",

volume = "83",

pages = "11166--11174",

journal = "J VIROL",

issn = "0022-538X",

publisher = "American Society for Microbiology",

number = "21",

}

RIS

TY - JOUR

T1 - Attenuated strains of influenza A viruses do not induce degradation of RNA polymerase II.

AU - Rodriguez, Ariel

AU - Pérez-González, Alicia

AU - Hossain, M Jaber

AU - Chen, Li-Mei

AU - Rolling, Thierry

AU - Pérez-Breña, Pilar

AU - Donis, Ruben

AU - Kochs, Georg

AU - Nieto, Amelia

PY - 2009

Y1 - 2009

N2 - We have previously shown that infection with laboratory-passaged strains of influenza virus causes both specific degradation of the largest subunit of the RNA polymerase II complex (RNAP II) and inhibition of host cell transcription. When infection with natural human and avian isolates belonging to different antigenic subtypes was examined, we observed that all of these viruses efficiently induce the proteolytic process. To evaluate whether this process is a general feature of nonattenuated viruses, we studied the behavior of the influenza virus strains A/PR8/8/34 (PR8) and the cold-adapted A/Ann Arbor/6/60 (AA), which are currently used as the donor strains for vaccine seeds due to their attenuated phenotype. We have observed that upon infection with these strains, degradation of the RNAP II does not occur. Moreover, by runoff experiments we observe that PR8 has a reduced ability to inhibit cellular mRNA transcription. In addition, a hypervirulent PR8 (hvPR8) variant that multiplies much faster than standard PR8 (lvPR8) in infected cells and is more virulent in mice than the parental PR8 virus, efficiently induces RNAP II degradation. Studies with reassortant viruses containing defined genome segments of both hvPR8 and lvPR8 indicate that PA and PB2 subunits individually contribute to the ability of influenza virus to degrade the RNAP II. In addition, recently it has been reported that the inclusion of PA or PB2 from hvPR8 in lvPR8 recombinant viruses, highly increases their pathogenicity. Together, the data indicate that the capacity of the influenza virus to degrade RNAP II and inhibit the host cell transcription machinery is a feature of influenza A viruses that might contribute to their virulence.

AB - We have previously shown that infection with laboratory-passaged strains of influenza virus causes both specific degradation of the largest subunit of the RNA polymerase II complex (RNAP II) and inhibition of host cell transcription. When infection with natural human and avian isolates belonging to different antigenic subtypes was examined, we observed that all of these viruses efficiently induce the proteolytic process. To evaluate whether this process is a general feature of nonattenuated viruses, we studied the behavior of the influenza virus strains A/PR8/8/34 (PR8) and the cold-adapted A/Ann Arbor/6/60 (AA), which are currently used as the donor strains for vaccine seeds due to their attenuated phenotype. We have observed that upon infection with these strains, degradation of the RNAP II does not occur. Moreover, by runoff experiments we observe that PR8 has a reduced ability to inhibit cellular mRNA transcription. In addition, a hypervirulent PR8 (hvPR8) variant that multiplies much faster than standard PR8 (lvPR8) in infected cells and is more virulent in mice than the parental PR8 virus, efficiently induces RNAP II degradation. Studies with reassortant viruses containing defined genome segments of both hvPR8 and lvPR8 indicate that PA and PB2 subunits individually contribute to the ability of influenza virus to degrade the RNAP II. In addition, recently it has been reported that the inclusion of PA or PB2 from hvPR8 in lvPR8 recombinant viruses, highly increases their pathogenicity. Together, the data indicate that the capacity of the influenza virus to degrade RNAP II and inhibit the host cell transcription machinery is a feature of influenza A viruses that might contribute to their virulence.

KW - Animals

KW - Humans

KW - Mice

KW - Transcription, Genetic

KW - Cell Line

KW - RNA, Messenger/genetics/metabolism

KW - Influenza A virus/genetics/metabolism

KW - Protein Subunits/genetics/metabolism

KW - RNA Polymerase II/genetics/metabolism

KW - RNA, Viral

KW - Animals

KW - Humans

KW - Mice

KW - Transcription, Genetic

KW - Cell Line

KW - RNA, Messenger/genetics/metabolism

KW - Influenza A virus/genetics/metabolism

KW - Protein Subunits/genetics/metabolism

KW - RNA Polymerase II/genetics/metabolism

KW - RNA, Viral

M3 - SCORING: Journal article

VL - 83

SP - 11166

EP - 11174

JO - J VIROL

JF - J VIROL

SN - 0022-538X

IS - 21

M1 - 21

ER -