Journal List > J Bacteriol Virol > v.44(2) > 1034124

Cho and Kang: Host Immune Responses Against Type A Influenza Viruses

Abstract

The influenza viruses are divided into 3 different types, A, B and C, all of them are known as human pathogens. However, only type A influenza viruses cause both epidemic and pandemic influenza. Typically, influenza virus infects a respiratory tract, targets a lung and causes an acute infectious disease. Influenza infection can be identified by a high fever, headache, body ache and extreme fatigue. Host immune system against Influenza infection consists of innate immune response and adaptive immune response. Innate immune responses include recognition of influenza viruses by alveolar macrophages and natural killer cells. Adaptive immune responses contain influenza virus specific antibody production by B cells and killing infected cells by cytotoxic T cells. Initially, influenza viruses are recognized by pattern recognition receptors (PRRs) on respiratory epithelial cells and alveolar macrophages, which can induce efficient anti-viral immune responses. Host immune responses play crucial roles in defense against influenza virus infection but sometimes these may contribute to immuno-pathology, which results in serious tissue damage. In this review, we went over the understanding of current literature on subtypes of influenza A viruses, important viral antigens and anti-viral immune mechanisms.

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Table 1.
Host immune recognition of influenza infection
Immune system Immune components Virus recognition
Innate immunity Alveolar macrophage
Dendritic cell
Natural killer cell
TLR7, TLR3, RIG-1, NLRP3 (13)
NCR e.g., NKp46 (21)
Adaptive immunity B cell (antibody)
CD8+ T cell (CTL)
CD4+ T cell (Th1, Th2, Treg)
Viral antigen e.g., H, N (23)
Viral peptide on MHC I (27)
Viral peptide on MHC II (32, 34)

TLR7, toll like receptor 7; TLR3, toll like receptor 3; RIG-1, retinoic acid inducible gene-I; NLRP3, nucleotide-binding oligomerization domain like receptor family pyrin domain containing 3; NCR, natural cytotoxicity receptor; NKp46, Natural killer cell p46-related protein; CTL, cytotoxicity T lymphocyte; Th, helper T cell; Treg, regulatory T cell; H, hemagglutinin; N, neuraminidase; MHC, major histocompatibility complex.

Table 2.
Link between influenza infection and production of cytokine/chemokine*
Cytokine/chemokine Function
IFN-γ Inhibits viral replication
Stimulates CTL mediated killing
Increases MHC I expression
Activates macrophage and neutrophil
Promotes T cell proliferation
TNF-α Stimulates macrophage phagocytosis
Increases vascular permeability
IL-1 Increases vascular permeability
Stimulates IL-6 production
IL-6 Activates T cell
MIP-1β (CCL4), MIG (CXCL9), IP-10 (CXCL10) Monocyte, T cell chemoattractant
RANTES (CCL5) Monocyte, T cell, dendritic cell chemoattractant, Activate T cell
IL-8 (CXCL8) Neutrophil, T cell chemoattractatnt
Activate T cell

* Table 2 is modified from La Gruta et al (36).

IFN-γ, interferon-gamma; TNF-α, Tumor necrosis factor-alpha; IL-1, 6, 8, interleukin-1, 6, 8; MP-1β, macrophage inflammatory protein-1 beta; CCL4, 5, chemokine (C-C motif) ligand 4,5; MG monokine induced by gamma interferon; CXCL8, 9, 10, C-X-C motif chemokine ligand 8, 9, 10; IP-10, Interferon gamma-induced protein-10; RANTES, regulated on activation normal T cell expressed and secreted.

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