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Review
. 2020 Dec 1:164:331-343.
doi: 10.1016/j.ijbiomac.2020.07.106. Epub 2020 Jul 14.

Application prospect of polysaccharides in the development of anti-novel coronavirus drugs and vaccines

Xiangyan Chen  1 , Wenwei Han  1 , Guixiang Wang  2 , Xia Zhao  3
Affiliations
Review

Application prospect of polysaccharides in the development of anti-novel coronavirus drugs and vaccines

Xiangyan Chen et al. Int J Biol Macromol. .

Abstract

Since the outbreak of the novel coronavirus disease COVID-19, caused by the SARS-CoV-2 virus, it has spread rapidly worldwide and poses a great threat to public health. This is the third serious coronavirus outbreak in <20 years, following SARS in 2002-2003 and MERS in 2012. So far, there are almost no specific clinically effective drugs and vaccines available for COVID-19. Polysaccharides with good safety, immune regulation and antiviral activity have broad application prospects in anti-virus, especially in anti-coronavirus applications. Here, we reviewed the antiviral mechanisms of some polysaccharides, such as glycosaminoglycans, marine polysaccharides, traditional Chinese medicine polysaccharides, and their application progress in anti-coronavirus. In particular, the application prospects of polysaccharide-based vaccine adjuvants, nanomaterials and drug delivery systems in the fight against novel coronavirus were also analyzed and summarized. Additionally, we speculate the possible mechanisms of polysaccharides anti-SARS-CoV-2, and propose the strategy of loading S or N protein from coronavirus onto polysaccharide capped gold nanoparticles vaccine for COVID-19 treatment. This review may provide a new approach for the development of COVID-19 therapeutic agents and vaccines.

Keywords: Antiviral activity; COVID-19; Coronavirus; Mechanism; Polysaccharides; SARS-CoV-2.

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Conflict of interest statement

Declaration of competing interest The authors have declared no conflict of interest.

Figures

Fig. 1
Fig. 1
The virus types and symptoms of 7 important pathogenic human coronaviruses.
Fig. 2
Fig. 2
The structure of CoV virion and S protein, (A) Depiction of the CoV virion; (B) Depiction of S protein. A single S protein is depicted as a rectangle, and relevant structural features are highlighted as follows: N-terminal receptor binding domain (N-RBD) in dark blue; C-RBD in brown; cleavage sites (CS) 1 and 2, fusion peptide (FP) in red, heptad repeat (HR) regions 1 and 2 in green; transmembrane span (TM) depicted as membrane bilayer; cytoplasmic tail (CT) in light blue.; (C) Structure of the MHV N-RBD in complex with its CEACAM receptor.; (D) Structure of the SARS C-RBD in complex with its ACE2 receptor.; (E) Structure of the post-fusion HR1-HR2 bundle [7].
Fig. 3
Fig. 3
The structures of several polysaccharides (GAGs, marine polysaccharides, and terrestrial plant polysaccharides).
Fig. 4
Fig. 4
Life cycle of highly pathogenic human CoVs. These CoVs enter host cells by first binding to their respective cellular receptors via the surface S protein. Viral genomic RNA is released and translated into viral polymerase proteins. Viral RNA and nucleocapsid (N) structural protein are replicated, transcribed, or synthesized in the cytoplasm, whereas other viral structural proteins, including S, membrane (M), and envelope (E), are transcribed then translated in the endoplasmic reticulum (ER) and transported to the Golgi. The viral RNA–N complex and S, M, and E proteins are further assembled in the ER–Golgi intermediate compartment (ERGIC) to form a mature virion, then released from host cells [62].
Fig. 5
Fig. 5
The illustration about potential role of EGFR in lung fibrosis. Physical injury or a pathogen ① initiates the wound healing response by damaging healthy tissue, releasing EGFR ligands ② and activating the EGFR pathway. This results in an exaggerated wound healing response leading to a fibrotic lung ③. The early use of inhibitors like tyrosine kinase ④ could prevent the normal progress of wound healing and fibrosis [72].
Fig. 6
Fig. 6
The mechanism of 3,6-O-sulfated chitosan inhibiting HBV [95].
Fig. 7
Fig. 7
The molecular mechanisms of PGS inhibits HBV replication. Cellular NF-κB and Raf/MEK/ERK signaling pathways are associated with the activation of innate immune system such as interferon system. PGS can bind and enter into HepG2.2.15 cells to activate the NF-κB and Raf/MEK/ERK pathways to enhance the interferon system, and indirectly suppress HBV transcription [42].
Fig. 8
Fig. 8
COV immunosensor array chip (a). The immunosensor fabrication steps (b), the detection process of the competitive immunosensor for the virus (c) [131].
Fig. 9
Fig. 9
The proposed schematics illustrating the S or N protein from coronavirus loaded onto polysaccharides capped AuNPs.
Fig. 10
Fig. 10
The proposed mechanisms of polysaccharides anti-SARS-CoV-2.
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