Journal article
Reduction of natural killer but not effector CD8 T lymphocytes in three consecutive cases of severe/lethal H1N1/09 influenza A virus infection.
- Abstract:
- BACKGROUND: The cause of severe disease in some patients infected with pandemic influenza A virus is unclear. METHODOLOGY/PRINCIPAL FINDINGS: We present the cellular immunology profile in the blood, and detailed clinical (and post-mortem) findings of three patients with rapidly progressive infection, including a pregnant patient who died. The striking finding is of reduction in natural killer (NK) cells but preservation of activated effector CD8 T lymphocytes; with viraemia in the patient who had no NK cells. Comparison with control groups suggests that the reduction of NK cells is unique to these severely ill patients. CONCLUSION/SIGNIFICANCE: Our report shows markedly reduced NK cells in the three patients that we sampled and raises the hypothesis that NK may have a more significant role than T lymphocytes in controlling viral burden when the host is confronted with a new influenza A virus subtype.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 693.3KB, Terms of use)
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- Publisher copy:
- 10.1371/journal.pone.0010675
Authors
- Publisher:
- Public Library of Science
- Journal:
- PloS one More from this journal
- Volume:
- 5
- Issue:
- 5
- Pages:
- e10675
- Publication date:
- 2010-01-01
- DOI:
- EISSN:
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1932-6203
- ISSN:
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1932-6203
- Language:
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English
- Keywords:
- Pubs id:
-
58615
- UUID:
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uuid:d505ecc2-cd9e-47d6-8ebb-2e9a852ffef4
- Local pid:
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pubs:58615
- Source identifiers:
-
58615
- Deposit date:
-
2012-12-19
- ARK identifier:
Terms of use
- Copyright holder:
- Denney et al
- Copyright date:
- 2010
- Notes:
- Copyright 2010 Denney et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
- Licence:
- CC Attribution (CC BY)
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