Association of sulphatide with influenza A virus (IAV) haemagglutinin (HA) delivered to the cell surface promotes progeny virus production. However, it is not known whether there is direct binding of HA to sulphatide. In this study, we found that recombinant HA, which was produced by a baculovirus protein expression system from the HA gene of A/duck/HK/313/4/78 (H5N3), bound to sulphatide in a dose-dependent manner and that the binding was inhibited by a specific antibody. Our results indicate that the recombinant HA is useful for elucidation of the binding domain of HA with sulphatide and for the development of new anti-IAV agents.
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http://dx.doi.org/10.1093/jb/mvq013 | DOI Listing |
Front Mol Biosci
October 2024
Department of Dravyaguna, Faculty of Ayurveda, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India.
(CST) is a key enzyme in sulfatide biosynthesis and regulation of the myelin sheath in the nervous system. To counter sulfatide accumulation with the deficiency of aryl sulfatase A, CST is considered a target protein in substrate reduction therapy in metachromatic leukodystrophy. In this study, 461 phytoconstituents from four herbs of Medhya Rasayana were screened using multi-pronged virtual screening methods including molecular docking, molecular dynamics (MD) simulation, and reverse pharmacophore analysis.
View Article and Find Full Text PDFJ Biochem
September 2024
Department of Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka 422-8526, Japan.
Noroviruses are a prevalent cause of human viral gastroenteritis, yet the precise mechanisms underlying their infection cycle, particularly their interactions with and entry into cells, remain poorly understood. Human norovirus (HuNoV) primarily targets human small intestinal epithelial cells, within which 3-O-sulfogalactosylceramide (sulfatide) ranks among the most abundant glycosphingolipids (GSLs). While sulfatide involvement in the binding and infection mechanism of several viruses has been documented, its interaction with noroviruses remains underexplored.
View Article and Find Full Text PDFFront Immunol
May 2024
Division of Human Immunology, International Vaccine Design Center, The Institute of Medical Science, The University of Tokyo (IMSUT), Tokyo, Japan.
Inhibitory natural killer (NK) cell receptors recognize MHC class I (MHC-I) in on target cells and suppress cytotoxicity. Some NK cell receptors recognize MHC-I in , but the role of this interaction is uncertain. Ly49Q, an atypical Ly49 receptor expressed in non-NK cells, binds MHC-I in and mediates chemotaxis of neutrophils and type I interferon production by plasmacytoid dendritic cells.
View Article and Find Full Text PDFACS Omega
March 2024
Department of Dravyaguna, Faculty of Ayurveda, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, Uttar Pradesh, India.
Cerebroside sulfotransferase (CST) is emerging as an important therapeutic target to develop substrate reduction therapy (SRT) for metachromatic leukodystrophy (MLD), a rare neurodegenerative lysosomal storage disorder. MLD develops with progressive impairment and destruction of the myelin sheath as a result of accumulation of sulfatide around the nerve cells in the absence of its recycling mechanism with deficiency of arylsulfatase A (ARSA). Sulfatide is the product of the catalytic action of cerebroside sulfotransferase (CST), which needs to be regulated under pathophysiological conditions by inhibitor development.
View Article and Find Full Text PDFInt J Biol Macromol
February 2024
Department of Dravyaguna, Faculty of Ayurveda, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, Uttar Pradesh, India.
This review is an effort towards the development of substrate reduction therapy using cerebroside sulfotransferase (CST) as a target protein for the development of inhibitors intended to treat pathophysiological condition resulting from the accumulation of sulfatide, a product from the catalytic action of CST. Accumulation of sulfatides leads to progressive impairment and destruction of the myelin structure, disruption of normal physiological transmission of electrical impulse between nerve cells, axonal loss in the central and peripheral nervous system and cumulatively gives a clinical manifestation of metachromatic leukodystrophy. Thus, there is a need to develop specific and potent CST inhibitors to positively control sulfatide accumulation.
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