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Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons

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Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons. / Osterlund, Pamela; Pirhonen, Jaana; Ikonen, Niina; Rönkkö, Esa; Strengell, Mari; Mäkelä, Sanna M; Broman, Mia; Hamming, Ole J; Hartmann, Rune; Ziegler, Thedi; Julkunen, Ilkka.

In: Journal of Virology, Vol. 84, No. 3, 01.02.2010, p. 1414-1422.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Osterlund, P, Pirhonen, J, Ikonen, N, Rönkkö, E, Strengell, M, Mäkelä, SM, Broman, M, Hamming, OJ, Hartmann, R, Ziegler, T & Julkunen, I 2010, 'Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons', Journal of Virology, vol. 84, no. 3, pp. 1414-1422. https://doi.org/10.1128/JVI.01619-09

APA

Osterlund, P., Pirhonen, J., Ikonen, N., Rönkkö, E., Strengell, M., Mäkelä, S. M., Broman, M., Hamming, O. J., Hartmann, R., Ziegler, T., & Julkunen, I. (2010). Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons. Journal of Virology, 84(3), 1414-1422. https://doi.org/10.1128/JVI.01619-09

CBE

Osterlund P, Pirhonen J, Ikonen N, Rönkkö E, Strengell M, Mäkelä SM, Broman M, Hamming OJ, Hartmann R, Ziegler T, Julkunen I. 2010. Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons. Journal of Virology. 84(3):1414-1422. https://doi.org/10.1128/JVI.01619-09

MLA

Vancouver

Author

Osterlund, Pamela ; Pirhonen, Jaana ; Ikonen, Niina ; Rönkkö, Esa ; Strengell, Mari ; Mäkelä, Sanna M ; Broman, Mia ; Hamming, Ole J ; Hartmann, Rune ; Ziegler, Thedi ; Julkunen, Ilkka. / Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons. In: Journal of Virology. 2010 ; Vol. 84, No. 3. pp. 1414-1422.

Bibtex

@article{a3bf0d00ff5a11de9c17000ea68e967b,
title = "Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons",
abstract = "In less than three months after the first cases of swine-origin 2009 influenza A (H1N1) virus infections were reported from Mexico, WHO declared a pandemic. The pandemic virus is antigenically distinct from seasonal influenza viruses and the majority of human population lacks immunity against this virus. We have studied the activation of innate immune responses in pandemic virus-infected human monocyte-derived dendritic cells (DC) and macrophages. Pandemic A/Finland/553/2009 virus, representing a typical North American/European lineage virus, replicated very well in these cells. The pandemic virus, as well as the seasonal A/Brisbane/59/07 (H1N1) and A/New Caledonia/20/99 (H1N1) viruses, induced type I (IFN-alpha/beta) and type III (IFN-lambda1-3) IFN, CXCL10 and TNF-alpha gene expression weakly in DCs. Mouse adapted A/WSN/33 (H1N1) and human A/Udorn/72 (H3N2) viruses, instead, induced efficiently the expression of antiviral and proinflammatory genes. Both IFN-alpha and IFN-beta inhibited the replication of the pandemic (H1N1) virus. The potential of IFN-lambda3 to inhibit the viral replication was lower than that of type I IFNs. However, the pandemic virus was more sensitive to the antiviral IFN-lambda3 than the seasonal A/Brisbane/59/07 (H1N1) virus. The present study demonstrates that the novel pandemic (H1N1) influenza A virus can readily replicate in human primary DCs and macrophages and efficiently avoid the activation of innate antiviral responses. It is, however, highly sensitive to the antiviral actions of IFNs, which may provide us an additional means to treat severe cases of infection especially if a significant drug resistance will emerge.",
author = "Pamela Osterlund and Jaana Pirhonen and Niina Ikonen and Esa R{\"o}nkk{\"o} and Mari Strengell and M{\"a}kel{\"a}, {Sanna M} and Mia Broman and Hamming, {Ole J} and Rune Hartmann and Thedi Ziegler and Ilkka Julkunen",
year = "2010",
month = feb,
day = "1",
doi = "10.1128/JVI.01619-09",
language = "English",
volume = "84",
pages = "1414--1422",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "3",

}

RIS

TY - JOUR

T1 - Pandemic H1N1 2009 Influenza A Virus Induces Weak Cytokine Response in Human Macrophages and Dendritic Cells and Is Highly Sensitive to Antiviral Actions of Interferons

AU - Osterlund, Pamela

AU - Pirhonen, Jaana

AU - Ikonen, Niina

AU - Rönkkö, Esa

AU - Strengell, Mari

AU - Mäkelä, Sanna M

AU - Broman, Mia

AU - Hamming, Ole J

AU - Hartmann, Rune

AU - Ziegler, Thedi

AU - Julkunen, Ilkka

PY - 2010/2/1

Y1 - 2010/2/1

N2 - In less than three months after the first cases of swine-origin 2009 influenza A (H1N1) virus infections were reported from Mexico, WHO declared a pandemic. The pandemic virus is antigenically distinct from seasonal influenza viruses and the majority of human population lacks immunity against this virus. We have studied the activation of innate immune responses in pandemic virus-infected human monocyte-derived dendritic cells (DC) and macrophages. Pandemic A/Finland/553/2009 virus, representing a typical North American/European lineage virus, replicated very well in these cells. The pandemic virus, as well as the seasonal A/Brisbane/59/07 (H1N1) and A/New Caledonia/20/99 (H1N1) viruses, induced type I (IFN-alpha/beta) and type III (IFN-lambda1-3) IFN, CXCL10 and TNF-alpha gene expression weakly in DCs. Mouse adapted A/WSN/33 (H1N1) and human A/Udorn/72 (H3N2) viruses, instead, induced efficiently the expression of antiviral and proinflammatory genes. Both IFN-alpha and IFN-beta inhibited the replication of the pandemic (H1N1) virus. The potential of IFN-lambda3 to inhibit the viral replication was lower than that of type I IFNs. However, the pandemic virus was more sensitive to the antiviral IFN-lambda3 than the seasonal A/Brisbane/59/07 (H1N1) virus. The present study demonstrates that the novel pandemic (H1N1) influenza A virus can readily replicate in human primary DCs and macrophages and efficiently avoid the activation of innate antiviral responses. It is, however, highly sensitive to the antiviral actions of IFNs, which may provide us an additional means to treat severe cases of infection especially if a significant drug resistance will emerge.

AB - In less than three months after the first cases of swine-origin 2009 influenza A (H1N1) virus infections were reported from Mexico, WHO declared a pandemic. The pandemic virus is antigenically distinct from seasonal influenza viruses and the majority of human population lacks immunity against this virus. We have studied the activation of innate immune responses in pandemic virus-infected human monocyte-derived dendritic cells (DC) and macrophages. Pandemic A/Finland/553/2009 virus, representing a typical North American/European lineage virus, replicated very well in these cells. The pandemic virus, as well as the seasonal A/Brisbane/59/07 (H1N1) and A/New Caledonia/20/99 (H1N1) viruses, induced type I (IFN-alpha/beta) and type III (IFN-lambda1-3) IFN, CXCL10 and TNF-alpha gene expression weakly in DCs. Mouse adapted A/WSN/33 (H1N1) and human A/Udorn/72 (H3N2) viruses, instead, induced efficiently the expression of antiviral and proinflammatory genes. Both IFN-alpha and IFN-beta inhibited the replication of the pandemic (H1N1) virus. The potential of IFN-lambda3 to inhibit the viral replication was lower than that of type I IFNs. However, the pandemic virus was more sensitive to the antiviral IFN-lambda3 than the seasonal A/Brisbane/59/07 (H1N1) virus. The present study demonstrates that the novel pandemic (H1N1) influenza A virus can readily replicate in human primary DCs and macrophages and efficiently avoid the activation of innate antiviral responses. It is, however, highly sensitive to the antiviral actions of IFNs, which may provide us an additional means to treat severe cases of infection especially if a significant drug resistance will emerge.

U2 - 10.1128/JVI.01619-09

DO - 10.1128/JVI.01619-09

M3 - Journal article

C2 - 19939920

VL - 84

SP - 1414

EP - 1422

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 3

ER -