Abstract

Influenza A virus (IAV) is an important zoonotic pathogen that can cause disease in animals such as poultry and pigs, and it can cause infection and even death in humans, posing a serious threat to public health. IAV is an enveloped virus that relies on host cell metabolic systems, especially lipid metabolism systems, to complete its life cycle in host cells. On the other side, host cells regulate their metabolic processes to prevent IAV replication and maintain their normal physiological functions. This review summarizes the roles of fatty acid, cholesterol, phospholipid and glycolipid metabolism in IAV infection, proposes future research challenges, and looks forward to the prospective application of lipid metabolism modification to limit IAV infection, which will provide new directions for the development of anti-influenza drugs.

Highlights

  • Influenza viruses are single-stranded, negative-sense RNA viruses that can be further classified into four types (A, B, C and D) based on the antigenic differences in the nucleoprotein (NP) and matrix protein (M)

  • Further studies showed that protectin D1 (PD1) inhibited the nuclear export of influenza A virus (IAV) mRNA and suppressed viral replication [24]. Another in vitro study showed that lipoxygenin B4 (LXB4), derived from omega-6 polyunsaturated fatty acids (PUFA) arachidonic acid (AA), promoted the expression of B lymphocyte-induced maturation protein 1 (Blimp1) and X-box binding protein 1 (XBP1), the key transcription factors involved in plasma cell differentiation, thereby increasing the number of effector B cells and production of IgG, which promoted host resistance to IAV [25]

  • Studies have shown that mice fed long-chain PUFA such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have enhanced susceptibility to IAV, leading to increased morbidity and mortality [27], and further analysis revealed that EPA and DHA suppressed splenic natural killer (NK) cell activity, significantly reduced the number of CD8+ T cells in the lungs, and inhibited macrophage inflammatory protein-1α (MIP-1α), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) mRNA expression [28], severely suppressing the host immune response to IAV

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Summary

Introduction

Influenza viruses are single-stranded, negative-sense RNA viruses that can be further classified into four types (A, B, C and D) based on the antigenic differences in the nucleoprotein (NP) and matrix protein (M). Among these types, influenza A virus (IAV) has the widest host range and is the most harmful. IAV does not have its own metabolic system and must depend on the host cell metabolic system to complete its life cycle. Series of changes occur in lipid metabolism, which play a positive or negative role in multiple stages of the IAV life cycle FFAA ((yyeellllooww)),, CChhooll ((ggrreeeenn)),, PPLL ((ddaarrkk ggrraayy)) aanndd GGLL ((bbrroowwnn)) aarree tthhee flfoiopuuirdr smm, aFaiiAnn elliixppiisiddt mccooamminpplyoonnineennthttsseppcrryeetssoeepnnlttasiinnmc,ceeClllhlsso,, lmmaoonssdtt oPofLf wwexhhiiisccthhinaarrtehececoocmemlplpomonneeemnntbtssraoonffetthhaenebdbiiocoyllotooggpiicclaaalslmmm,eeammnbdbrraGannLee.e. xAAismmt oomnnaggintthlhyeessinee ltihpeidesx,trFaAceelxluislat rmsapiancley. iAnftthereIcAyVtopinlfaescmts, hCohsotlcaenllds, PaLseerxieisstoifncthhaencgeelsl mocecmurbirnanliepiadndmceytatbooplliassmm,,wahnidchGpLlaeyxiastpmosaiitnivlye ionr tnheegeaxtitvraecreollleulianrmspualctiep.lAe fstteargIeAsVofinthfeecItAs Vholsiftececlylcs,lea. series of changes occur in lipid metabolism, which play a positive or negative role in multiple stages of the IAV life cycle

Positive and Negative Regulation of FA Metabolism in IAV Infection
Chol Plays a Major Role in Fusion and Release during the IAV Life Cycle
PL Metabolism Is Involved in Multiple Stages of IAV Infection
An Appropriate GL Concentration Is Important for IAV Infection
Conclusions and Perspective
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