Abstract
The direct effect of the rotavirus NSP4114-135 and Norovirus NV464-483 peptides on 36Cl uptake was studied by using villus cell brush border membrane (BBM) isolated from young rabbits. Both peptides inhibited the Cl-/H+ symport activity about equally and partially. The interaction involved one peptide-binding site per carrier unit. Whereas in vitro NSP4114-135 caused nonspecific inhibition of the Cl-/H+ symporter, the situation in vivo is different. Because rotavirus infection in young rabbits accelerated both Cl- influx and Cl- efflux rates across villi BBM without stimulating Cl- transport in crypt BBM, we conclude that the NSP4114-135 peptide, which causes diarrhea in young rodents, did not have any direct, specific effect on either intestinal absorption or secretion of chloride. The lack of direct effect of NSP4 on chloride transport strengthens the hypothesis that NSP4 would trigger signal transduction pathways to enhance net chloride secretion at the onset of rotavirus diarrhea.
Highlights
Rotavirus is the major cause of infantile gastroenteritis and each year causes 611000 deaths worldwide
The rotavirus NSP4114-135 peptide has been shown to interact with small unilamellar phospholipid vesicles characterized by highly curved membrane regions [4]
It is unknown whether such interaction of NSP4 with a putative membrane receptor may be important for its biological activity
Summary
Rotavirus is the major cause of infantile gastroenteritis and each year causes 611000 deaths worldwide. The rotavirus NSP4114-135 peptide has been shown to interact with small unilamellar phospholipid vesicles characterized by highly curved membrane regions [4].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
