KRISHI
ICAR RESEARCH DATA REPOSITORY FOR KNOWLEDGE MANAGEMENT
(An Institutional Publication and Data Inventory Repository)
"Not Available": Please do not remove the default option "Not Available" for the fields where metadata information is not available
"1001-01-01": Date not available or not applicable for filling metadata infromation
"1001-01-01": Date not available or not applicable for filling metadata infromation
Please use this identifier to cite or link to this item:
http://krishi.icar.gov.in/jspui/handle/123456789/51458
Title: | Role of a single amino acid substitution of VP3 H142D for increased acid resistance of foot-and-mouth disease virus serotype A |
Authors: | Jitendra K Biswal Biswajit Das Gaurav K Sharma Sagar A Khulape Bramhadev Pattnaik |
ICAR Data Use Licennce: | http://krishi.icar.gov.in/PDF/ICAR_Data_Use_Licence.pdf |
Author's Affiliated institute: | ICAR::Project Directorate on Foot and Mouth Disease |
Published/ Complete Date: | 2016-04-01 |
Keywords: | Acid resistance; FMD virus; Mutant; Reverse genetics; Virus fitness. |
Publisher: | Springer |
Citation: | Not Available |
Series/Report no.: | Not Available; |
Abstract/Description: | Foot-and-mouth disease virus (FMDV) particles lose infectivity due to their dissociation into pentamers at pH value below 6.5. After the uptake of FMDV by receptor-mediated endocytosis, the acid-dependent dissociation process is required for the release of FMDV genome inside endosomes. Nevertheless, dissociation of FMDV particles in mildly acidic conditions renders the inactivated FMD vaccine less effective. To improve the acid stability of inactivated FMD vaccine during the manufacturing process, a serotype A IND 40/2000 (in-use vaccine strain) mutant with increased resistance to acid inactivation was generated through reverse genetics approach. Based upon the earlier reports, the crucial amino acid residue, H142 of VP3 capsid protein was substituted separately to various amino acid residues Arg (R), Phe (F), Ala (A), and Asp (D) on the full-genome length cDNA clone. While the H142 → R or H142 → F or H142 → A substitutions resulted in non-infectious FMDV, H142 → D mutation on VP3 protein (H3142D) resulted in the generation of mutant virus with enhanced resistance to acid-induced inactivation. In addition, H3142D substitution did not alter the replication ability and antigenicity of mutant as compared to the parental virus. However, the virus competition experiments revealed that the H3142D substitution conferred a loss of fitness for the mutant virus. Results from this study demonstrate that the H3142D substitution is the molecular determinant of acid-resistant phenotype in FMDV serotype A. |
ISSN: | Not Available |
Type(s) of content: | Journal |
Language: | English |
Name of Journal: | Virus Genes |
Journal Type: | Research |
NAAS Rating: | 7.99 |
Volume No.: | 52(2) |
Page Number: | 235-43 |
Source, DOI or any other URL: | 10.1007/s11262-016-1294-1 |
URI: | http://krishi.icar.gov.in/jspui/handle/123456789/51458 |
Appears in Collections: | AS-PDFMD-Publication |
Files in This Item:
There are no files associated with this item.
Items in KRISHI are protected by copyright, with all rights reserved, unless otherwise indicated.