Human norovirus (HuNoV) is the leading causative virus of non-bacterial food poisoning. Norovirus infections cause acute gastroenteritis in all age groups, from infants to the elderly. They can occur many times as long-term immunity is not established. Norovirus, the causative virus, grows only in the human intestine. Still, it is resistant to dryness and heat and can survive long, even in the natural environment. HuNoV infection is transmitted by eating contaminated food or coming into contact with contaminated food, and even a small number of 10 to 1000 viruses is enough to cause the infection. Norovirus (MNoV) is classified into ten gene clusters (GI-GX) and 49 genotypes, and GII.4 and GII.7. They have been known to be the leading cause of norovirus food poisoning in the past 20 years. Norovirus has no effective antiviral agents and is only treated symptomatically. Especially when infants and the elderly with weak resistance are infected, they are prone to “dehydration,” so caution is required.
On the other hand, brown algae such as kelp (LJ), wakame seaweed (UP), and wakame sporophyll (UPS) contain fucoidan. Fucoidan is a sulfated polysaccharide mainly composed of fucose. It has various beneficial actions, such as antioxidant, antiviral, and anticancer, but no effect on HuNoV has been reported. Hence, I would like to share the research content with you that investigated the antiviral effect of fucoidan on HuNoV and norovirus (MNoV) in this blog.
According to a study “Inhibitory Effects of Laminaria japonica Fucoidans Against Noroviruses” by Hyojin Kim et al., first, in order to investigate the survival of MNoV to fucoidan, and then treated with MNoV using 10 to 1000 µg/ml 3 kinds fucoidan (LJ, UP, UPS) for 3 hours and performing them by a plaque assay using RAW cells.
As a result, the survival rate of MNoV gradually decreased in a dose-dependent manner of fucoidan, demonstrating the inhibitory effect of fucoidan on MNoV growth. In addition, the GII4 domain of HuNoV is known to be involved in virus attachment to human tissues using tissue blood group antigen (HBGA) as a scaffold. So, after treating the GII4P domain with 250 to 1000 µg / mL of fucoidan derived from three types of brown algae, researchers calculated the binding inhibition rate of HBGA and fucoidan-treated P domain contained in saliva samples collected from volunteers. As a result, the binding between the P domain of HuNoV and HBGA was inhibited in a dose-dependent manner of fucoidan. A high binding inhibition rate of 54 to 72% was shown, especially in 1000 µg / mL LJ-derived fucoidan (Fig. 1). Therefore, it was confirmed that LJ-derived fucoidan might prevent HuNoV infection by inhibiting the binding of the P domain to HBGA.
Furthermore, to investigate the antiviral effect of LJ-derived fucoidan, STAT1-deficient mice were orally infected with MNoV of 3×104 PFU. Then 40 mg/kg/day of LJ-derived fucoidan was orally administered until four days after infection, resulting in weight change and virus in feces. They also evaluated the potency and so on. Mice in the control group exhibited significant weight loss with marked loss of appetite three days after infection, with signs of physical discomfort or malaise such as crouching, curling, and disordered fur.
In contrast, LJ fucoidan-treated mice lost little weight three days after infection and recovered rapidly five days after infection. When the virus titer in feces was measured by the plaque assay, the fucoidan-administered mice had significantly lower MNoV titers three days after infection than the control group (Fig. 2). As a result, it is proven that fucoidan derived from LJ may suppress NoV infection.
