S-layer proteins of Lactobacillus acidophilus inhibits JUNV infection

It has been previously described that S-layer binds to the C-type lectin DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN, CD209). It was also shown that DC-SIGN is a cell-surface adhesion factor that enhances viral entry of several virus families. Among those, Junin virus (JUNV) entry is enhanced i...

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Detalles Bibliográficos
Autores principales: Martínez, María Guadalupe, Prado Acosta, Mariano, Candurra, Nélida Alicia, Ruzal, Sandra Mónica
Publicado: 2012
Materias:
Antiviral
Lactobacillus
Surface layer
antivirus agent
calcium ion
CD209 antigen
intercellular adhesion molecule 3
probiotic agent
protein slpa
unclassified drug
animal cell
Argentine hemorrhagic fever
article
cell strain 3T3
computer model
disease course
evaluation
human
Lactobacillus acidophilus
nonhuman
priority journal
virus entry
3T3 Cells
Amino Acid Sequence
Animals
Antiviral Agents
Arenaviridae Infections
Bacterial Proteins
Cell Adhesion Molecules
Cercopithecus aethiops
Consensus Sequence
Junin virus
Lectins, C-Type
Membrane Glycoproteins
Mice
Molecular Sequence Data
Receptors, Cell Surface
Vero Cells
Virus Internalization
Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0006291X_v422_n4_p590_Martinez
http://hdl.handle.net/20.500.12110/paper_0006291X_v422_n4_p590_Martinez
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:It has been previously described that S-layer binds to the C-type lectin DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN, CD209). It was also shown that DC-SIGN is a cell-surface adhesion factor that enhances viral entry of several virus families. Among those, Junin virus (JUNV) entry is enhanced in cells expressing DC-SIGN and for that reason surface-layer protein (S-layer) of Lactobacillus acidophilus ATCC 4365 was evaluated as a possible JUNV inhibitor. Experiments using 3T3 cells stably expressing DC-SIGN, showed an almost complete inhibition of JUNV infection when they were treated with S-layer in a similar extend as the inhibition shown by mannan. However no inhibition effect was observed in 3T3 wild type cells or in 3T3 cells expressing liver/lymph node-specific ICAM-3 grabbing nonintegrin (L-SIGN or DC-SIGNR or CD209L).Treatments with S-layer during different times in the infection demonstrated that inhibition was only observed when S-layer was presented in early stages of the viral infection. This inhibition does not involve the classic recognition of mannose by this C-type lectin as the S-layer showed no evidence to be glycosylated. In fact, the highly basic nature of the S-layer (pI>9.5) seems to be involved in electrostatic interactions between DC-SIGN and S-layer, since high pH abolished the inhibitory effect on infection cause by the S-layer. In silico analysis predicts a Ca 2+-dependant carbohydrate recognition domain in the SlpA protein.This novel characteristic of the S-layer, a GRAS status protein, contribute to the pathogen exclusion reported for this probiotic strain and may be applied as an antiviral agent to inhibit several kinds of viruses. © 2012 Elsevier Inc..

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