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. 2025 Feb 17;17(2):278.
doi: 10.3390/v17020278.

Significant Association Between Increased Abundance of Selected Bacterial Lipopolysaccharides and Norovirus Diarrhea Among South African Infants

Lerato P Kgosana  1 , Mapaseka L Seheri  1 , Cliff A Magwira  1
Affiliations

Significant Association Between Increased Abundance of Selected Bacterial Lipopolysaccharides and Norovirus Diarrhea Among South African Infants

Lerato P Kgosana et al. Viruses. .

Abstract

Bacterial lipopolysaccharides (LPS) have been shown to promote enteric viral infections. This study assessed whether possessing elevated levels of LPS was associated with norovirus infection. Fecal samples from diarrheic norovirus-positive (DNP) (n = 26), non-diarrheal norovirus-negative (NDNN) (n = 26), asymptomatic norovirus-positive (ANP) (n = 15), and diarrheic norovirus-negative (DNN) (n =15) infants were assayed for selected bacterial LPS by quantitative PCR. The mean levels of selected LPS gene targets were significantly high in DNP infants (6.17 ± 2.14 CFU/g) versus NDNN infants (4.13 ± 2.25 CFU/g), p = 0.003. So too was the abundance between DNP and DNN infants (p = 0.0023). The levels of selected LPS gene targets were high regardless of whether the infection was symptomatic or asymptomatic, p = 0.3808. The average expression of genes coding for selected LPS and their signalling molecule, Toll-like receptor 4 (TLR4), increased 7- and 2.5-fold, respectively, in DNP versus NDNN children. Infants possessing elevated levels of selected LPS-rich bacteria were 1.51 times more likely to develop norovirus diarrhea (95% CI: 1.14-2.01, p = 0.004). In conclusion, norovirus infection was associated with abundance of selected bacterial LPS, suggesting a possible role of bacterial LPS in norovirus infection.

Keywords: TLR4; abundance; bacterial lipopolysaccharide; gene expression; norovirus diarrhea.

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Conflict of interest statement

The authors declare no potential conflicts of interest.

Figures

Figure 1
Figure 1
Average abundance of all selected LPS-rich bacteria in (a) DNP vs. NDNN (b) DNP vs. ANP (c) DNP vs. DNN (d) DNP vs. NDNN at 3.5 months of age, (e) DNP vs. NDNN at 9 months of age. — denotes the mean.
Figure 2
Figure 2
Abundance of each of the selected LPS-rich bacteria in (a) DNP vs. NDNN (K. pneumonia), (b) DNP vs. ANP (K. pneumonia), (c) DNP vs. DNN (K. pneumonia), (d) DNP vs. NDNN (K. pneumonia) at 3.5 months old (e) DNP vs. NDNN (S. marcescens), (f) DNP vs. ANP (S. marcescens), (g) DNP vs. DNN (S. marcescens), (h) DNP9 vs. NDNN9 (S. marcescens), (i) DNP vs. NDNN (P. aeruginosa).
Figure 2
Figure 2
Abundance of each of the selected LPS-rich bacteria in (a) DNP vs. NDNN (K. pneumonia), (b) DNP vs. ANP (K. pneumonia), (c) DNP vs. DNN (K. pneumonia), (d) DNP vs. NDNN (K. pneumonia) at 3.5 months old (e) DNP vs. NDNN (S. marcescens), (f) DNP vs. ANP (S. marcescens), (g) DNP vs. DNN (S. marcescens), (h) DNP9 vs. NDNN9 (S. marcescens), (i) DNP vs. NDNN (P. aeruginosa).
Figure 3
Figure 3
Abundance of N-acetylglucosamine in all selected bacteria (a) DNP vs. NDNN (b) DNP vs. ANP (c) DNP vs. DNN (d) DNP vs. NDNN at 9 months of age.
Figure 4
Figure 4
Expression of LPS genes of selected LPS-rich bacteria, N-acetylglucosamine and TLR4 between DNP and NDNN study groups: (a) mean of all selected LPS genes, (b) S. marcescens, (c) K. pneumoniae, (d) N-acetylglucosamine, and (e) TLR4.
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