Cowpox virus inhibits human dendritic cell immune function by nonlethal, nonproductive infection
- Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM (United States)
- Center for Infectious Disease and Immunity, University of New Mexico School of Medicine, Albuquerque, NM (United States)
- Dept. of Molecular Genetics and Microbiology, Duke University, Durham, NC (United States)
Orthopoxviruses encode multiple proteins that modulate host immune responses. We determined whether cowpox virus (CPXV), a representative orthopoxvirus, modulated innate and acquired immune functions of human primary myeloid DCs and plasmacytoid DCs and monocyte-derived DCs (MDDCs). A CPXV infection of DCs at a multiplicity of infection of 10 was nonproductive, altered cellular morphology, and failed to reduce cell viability. A CPXV infection of DCs did not stimulate cytokine or chemokine secretion directly, but suppressed toll-like receptor (TLR) agonist-induced cytokine secretion and a DC-stimulated mixed leukocyte reaction (MLR). LPS-stimulated NF-{kappa}B nuclear translocation and host cytokine gene transcription were suppressed in CPXV-infected MDDCs. Early viral immunomodulatory genes were upregulated in MDDCs, consistent with early DC immunosuppression via synthesis of intracellular viral proteins. We conclude that a nonproductive CPXV infection suppressed DC immune function by synthesizing early intracellular viral proteins that suppressed DC signaling pathways.
- OSTI ID:
- 21486929
- Journal Information:
- Virology, Vol. 412, Issue 2; Other Information: DOI: 10.1016/j.virol.2011.01.024; PII: S0042-6822(11)00038-9; Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; ISSN 0042-6822
- Country of Publication:
- United States
- Language:
- English
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