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Effect of human milk oligosaccharides on rotavirus infectivity in MA104 cells
Author(s) -
Chen Xin,
Li Min,
Kuhlenschmidt Theresa B.,
Kuhlenschmidt Mark S.,
Donovan Sharon M.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.584.18
Human milk is rich in oligosaccharides (HMO) that exert prebiotic and antiinfective activities. Human milk feeding reduces the incidence of rotavirus (RV) infection in infants. Herein, the anti‐RV activity of oligosaccharides was tested in established in vitro systems for assessing cellular RV binding and RV infectivity/replication. HMO isolated from human milk, pure neutral and acidic HMO (lacto‐N‐neotetraose, LNnT; 3′‐sialyllactose, 3′‐SL; 6′‐SL; 2′‐fucosyllactose, 2′‐FL; 3′‐FL), and a 1:1 mixture of galactooligosaccharide (GOS) and polydextrose (PDX) were tested against human Wa strain RV and Group A porcine RV strain OSU. Wa strain RV was not inhibited by any oligosaccharide. Infectivity by OSU strain RV was dose‐dependently inhibited by HMO, 3′‐SL and 6′‐SL, but not by LNnT, 2′‐FL, 3′‐FL or PDX/GOS. 3′‐SL and 6′‐SL inhibited OSU strain RV at a dose of 2 mg/ml, whereas 8 mg/ml HMO was needed to inhibit RV infectivity. There was a concordance between inhibition of 125 I‐RV cellular binding and infectivity/replication for 3′‐SL and 6′‐SL, whereas HMO reduced replication (53% inhibition) to a greater extent than binding (30% inhibition), suggesting that HMO could also exert postbinding effects, which could include blocking entry into the cell or viral replication (Supported by the China Scholarship Council and R01 HD061929).

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