Host Immune Responses Against Type A Influenza Viruses

Hyosun Cho; Hyojeung Kang

doi:10.4167/jbv.2014.44.2.133

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

Review Article

J Bacteriol Virol 2014;44(2):133-139.

Published online: 9 February 2014

DOI: https://doi.org/10.4167/jbv.2014.44.2.133

Host Immune Responses Against Type A Influenza Viruses

Hyosun Cho¹, Hyojeung Kang^2,^*

¹Department of Pharmacy, College of Pharmacy, Duksung Women's University, Seoul, Korea

²Department of Pharmacy, College of Pharmacy, Kyungpook National University, Daegu, Korea

^*Corresponding author: Hyojeung Kang, Ph.D. Department of Pharmacy, College of Pharmacy, Kyungpook National University, Daegu, 702-701, Korea. Phone: +82-53-950-8569, Fax: +82-53-950-8557, e-mail: hkang72@knu.ac.kr

^** This work was supported by the Duksung Women's University Research Grants 3000001902.

Received 21 February 201420 March 2014 Accepted 31 March 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.

Keywords: Adaptive immunity, Hemagglutinin, Innate immunity, Neuraminidase, Type A influenza viruses

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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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