Abstract

Influenza A viruses (IAVs) are highly contagious pathogens infecting human and numerous animals. The viruses cause millions of infection cases and thousands of deaths every year, thus making IAVs a continual threat to global health. Upon IAV infection, host innate immune system is triggered and activated to restrict virus replication and clear pathogens. Subsequently, host adaptive immunity is involved in specific virus clearance. On the other hand, to achieve a successful infection, IAVs also apply multiple strategies to avoid be detected and eliminated by the host immunity. In the current review, we present a general description on recent work regarding different host cells and molecules facilitating antiviral defenses against IAV infection and how IAVs antagonize host immune responses.

Highlights

  • Influenza A virus (IAV) can infect a wide range of warm-blooded animals, including birds, pigs, horses, and humans

  • T cells differentiate into cytotoxic T lymphocytes (CTLs) and defend IAV infection via producing cytokines and effector molecules, and cytotoxic effects of infected cells mediated by MHC

  • For NOD-like receptor family, pyrin domain containing 3 (NLRP3) and NLR apoptosis inhibitory protein 5 were activated after IAV infection [140]

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Summary

Introduction

Influenza A virus (IAV) can infect a wide range of warm-blooded animals, including birds, pigs, horses, and humans. The viruses cause respiratory disease and be transmitted by inhalation of virus-containing dust particles or aerosols [1]. Severe IAV infection can cause lung inflammation and acute respiratory distress syndrome (ARDS), which may lead to mortality. The eight viral gene segments encode as many as 18 proteins. Besides polymerase basic 1 (PB1), PB1-N40, PB1-F2, PB2, polymerase acid (PA), hemagglutinin (HA), nucleoprotein (NP), neuraminidase (NA), matrix 1 (M1), matrix 2 (M2), nonstructural protein 1 (NS1) and NS2 ( known as nuclear export protein, NEP), new viral proteins were recently uncovered, such as PB2-S1 [3], PA-X (product of ribosomal frameshifting) [4], PA-related proteins PA-N155 and PA-N182 [5], M42 [6], and NS3 [7]. According to the genetic and antigenic diversity of the HA and NA proteins, IAVs were divided into 18 HA and 11 NA subtypes. H17N10 and H18N11 subtypes were recently identified in bats [8,9]

IAV Viral Proteins
Antigenic Shift and Antigenic Drift
Influenza A Virus Host Switch Events
Life Cycle of Influenza A Virus
Host Immune Responses Against IAV Infection
Immune Cells Involved in IAV Infection
Activation of Innate Immunity in IAV Infection
Schematic
Autophagy
Adaptive Immunity against IAV Infection
Apoptosis against IAV Infection
The Intrinsic and Extrinsic Apoptosis Pathway
Apoptosis after IAV Infection
Findings
Perspectives

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