Severe Infection With Avian Influenza A Virus is Associated With Delayed Immune Recovery in Survivors

Human infection with avian influenza A virus (H7N9) is a concern because of the mortality rate. Previously, we characterized immunological responses during active infection with it and reported evidence of impaired antigen-presenting capability, particularly in severely affected individuals. Here we...

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Published inMedicine (Baltimore) Vol. 95; no. 5; p. e2606
Main Authors Chen, Jianing, Cui, Guangying, Lu, Chong, Ding, Yulong, Gao, Hainv, Zhu, Yixin, Wei, Yingfeng, Wang, Lin, Uede, Toshimitsu, Li, Lanjuan, Diao, Hongyan
Format Journal Article
LanguageEnglish
Published United States Wolters Kluwer Health 01.02.2016
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Summary:Human infection with avian influenza A virus (H7N9) is a concern because of the mortality rate. Previously, we characterized immunological responses during active infection with it and reported evidence of impaired antigen-presenting capability, particularly in severely affected individuals. Here we describe an investigation of immunological responses during a 1-year follow-up of survivors of H7N9 infection. Survivors of H7N9 infection were classified as having had mild (n = 42) or severe infection (n = 26). Their immune status, including human leukocyte antigen-DR expression on monocytes, and their ability to mount cytokine responses were assessed at 1, 3, and 12 months postinfection.The total lymphocyte count and the percentages of different types of lymphocytes had normalized by 1 month postinfection. However, there was evidence of ongoing impairment of immune responses in those who had had severe infection. This included reduced human leukocyte antigen-DR expression on CD14 monocytes, reduced interferon-γ production by T cells, and higher plasma levels of the matrix metalloproteinases 2, 3, and 9. By 3 months postinfection, these had all normalized.After severe H7N9 infection, recovery of the antigen-presenting capability of monocytes and T-cell responses are delayed. This may lead to an increased vulnerability to secondary bacterial infections.
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ISSN:0025-7974
1536-5964
DOI:10.1097/MD.0000000000002606