Abstract
Innate and adaptive immune responses play critical roles in the body’s defense against viruses. We investigated the host immune response against the 2009 pandemic H1N1 influenza virus [A(H1N1)pdm09] in patients before and after anti-influenza therapy and found that the numbers of dendritic cells and T cells were significantly reduced compared with those of a healthy control group. In contrast, the frequency of natural killer, γδT and T regulatory (Treg) cells increased, and the concentrations of plasma interferon (IFN)-α/γ and interleukin (IL-15) were significantly higher than those of the control. Following therapy the frequency of γδT and Treg cells returned to normal; the counts of myeloid dendritic and plasmacytoid dendritic cells were still lower than the control, while the concentrations of IFN-α/γ and IL-15 remained high. We show that infection with A (H1N1)pdm09 was accompanied by changes in peripheral blood lymphocyte subgroups and cytokine profiles, leading to deleterious imbalances in innate and adaptive immunity.
Highlights
The novel swine-origin pandemic 2009 influenza virus [A(H1N1)pdm09] was first identified in April 2009
A(H1N1)pdm09 has gene segments from Eurasian swine H1N1 viruses and a North American triple-reassortant virus [3, 15]. Sequence analysis of this new pandemic virus revealed that in the triple-reassortant virus, the haemagglutinin (HA), nucleoprotein (NP), and nonstructural (NS) gene segments were derived from the classical swine viruses, the polymerase basic 1 (PB1) segment was from human H3N2 virus, and the polymerase basic 2 (PB2) and polymerase acidic (PA) segments were from avian viruses [3]
We found that A(H1N1)pdm09 infection was associated with a severe impairment of the innate immune responses characterized by a profound weakening of myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) subsets, which persisted for a certain period after recovery from infection
Summary
The novel swine-origin pandemic 2009 influenza virus [A(H1N1)pdm09] was first identified in April 2009. This novel virus spread worldwide and had already caused about 17,000 deaths by the start of 2010 [14]. A(H1N1)pdm has gene segments from Eurasian swine H1N1 viruses and a North American triple-reassortant virus [3, 15]. Sequence analysis of this new pandemic virus revealed that in the triple-reassortant virus, the haemagglutinin (HA), nucleoprotein (NP), and nonstructural (NS) gene segments were derived from the classical swine viruses, the polymerase basic 1 (PB1) segment was from human H3N2 virus, and the polymerase basic 2 (PB2) and polymerase acidic (PA) segments were from avian viruses [3]. A(H1N1)pdm is genetically and antigenically distinct from previous seasonal human influenza A viruses, and the majority of the human population does not have pre-existing immunity to it
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