Understanding the role of galectins toward influenza A virus infection

ABSTRACT

Introduction

Influenza A virus (IAV) is highly contagious and causes respiratory diseases in birds, mammals, and humans. Some strains of IAV, whether from human or avian sources, have developed resistance to existing antiviral drugs. Therefore, the discovery of new influenza antiviral drugs and therapeutic approaches is crucial. Recent studies have shown that galectins (Gal), a group of β-galactose-binding lectins, play a role in regulating various viral infections, including IAVs.

Areas covered

This review provides an overview of the roles of different galectins in IAV infection. We discuss the characteristics of galectins, their impact on IAV infection and spread, and highlight their positive or negative regulatory functions and potential mechanisms during IAV infection. Furthermore, we explore the potential application of galectins in IAV therapy.

Expert opinion

Galectins were first identified in the mid-1970s, and currently, 15 mammalian galectins have been identified. While all galectin members possess the carbohydrate recognition domain (CRD) that interacts with β-galactoside, their regulatory functions vary in different DNA or RNA virus infections. Certain galectin members have been found to regulate IAV infection through diverse mechanisms. Therefore, a comprehensive understanding of their roles in IAV infection is essential, as it may pave the way for novel therapeutic strategies.

KEYWORDS:

• Influenza A virus
• galectins
• antiviral drug
• therapeutic strategy
• Review

Article highlights

• Galectin-1, galectin-3, and galectin-9 are found to be the most predominant galectins reported to participate in virus infection.

• Both endogenous and exogenous roles of galectins are known to play similar or even opposite roles in the regulation of IAV replication.

• Galectin-1 and galectin-9 exert inhibitory capabilities, whereas galectin-3 displays various roles toward IAV infection.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Author contributions

ZS Yang and CY Lin prepared and revised the manuscript. MB Khan and MC Hsu helped to analyze the data. W Assavalapsakul and A Thitithanyanont revised and edited the manuscript. SF Wang conceived the study and revised the draft.

Acknowledgments

The authors would like to express their gratitude to the staff at Kaohsiung Medical University Hospital and Center for Tropical Medicine and Infectious Disease, Kaohsiung Medical University for their technical assistance, as well as to Professor Fu-Tong Liu from the Institute of Biomedical Sciences, Academia Sinica, Taiwan for his invaluable assistance.

Additional information

Funding

This work was supported by grants from the National Science and Technology Council, R.O.C. (112-2918-I-037 -002 & 112-2320-B-037 -032 -MY3) and Kaohsiung Medical University Research Center Grant (KMU-TC112B01), and a grant from the Kaohsiung Medical University Research Foundation (KMU-M108006 & KMU-M112007) as well as a grant from Academia and Industry Collaboration Project of Kaohsiung Medical University(#KMU-S111019 & S112002).