Lactobacillus crispatus Strain KT-11 S-Layer Protein can inhibit Rotavirus Infection: Sialic acid would be deeply involved

A group from Shinshu University, Nagano, Japan, etc. has reported that Lactobacillus crispatus Strain KT-11 S-Layer Protein can inhibit Rotavirus Infection and sialic acid could be involved in initiation of virus infection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8902352/

Lactic acid bacteria, including the genus Lactobacillus play a crucial role in the production of fermented dairy products such as cheese, yoghurt, and fermented milk. In recent years, there has been considerable focus on the action of the S-layer protein (SLP) of lactic acid bacteria as an antiviral component.

The effect of Lactobacillus crispatus KT-11 SLP on the infection of Rotavirus DS-1 strain in Caco-2 cells is shown below. DS-1 infection was significantly suppressed by pre-infection treatment with KT-11 SLP in a concentration-dependent manner. Conversely, KT-11 SLP did not suppress the infection of the Rotavirus Wa strain even after pre-infection treatment at 100 μg/mL.

The entry of rotavirus into cells is a complex multistep process, in which different domains of rotavirus surface proteins interact with cell-surface molecules that function as receptors for adhesion and entry. Among them, several carbohydrates, such as terminal sialic acids and histo-blood group antigens, have been reported to be involved in rotavirus attachment to target cells. As shown above, KT-11 SLP significantly inhibited the infection of the DS-1 strain in Caco-2 cells in a dose-dependent manner. The initial interactions of human rotavirus strains with host cells is dependent on the VP4 genotype. According to the classification based on the molecular properties of VP4 (P-types), the DS-1 strain is classified as the P[4] genotype. Increasing evidence indicates that the P[4] genotype rotaviruses, including the DS-1 strain, use H-type 1 and Lewis-b antigens for infection. Actually, H-type 1 and Lewis-b antigens have been reported in Caco-2 cells. This result suggests that the possibility of that DS-1 infection is inhibited by competitive binding of KT-11 SLP to these antigens. However, contrary to the expectations, infection of the Wa strain, another dominant P[8] subtype reported using the same H-type antigen and Lewis-b for infection, was not inhibited in the presence of KT-11 SLP.

Recently, it was reported that DS-1 strain infection was significantly inhibited by 3′-sialyl lactose and 6′-sialyl lactose, whereas the Wa strain was inhibited by 2′-fucosyl lactose. Therefore, compounds containing sialic acid could be deeply involved in the infection of DS-1 strain.