Affiliation:
1. Plum
Island Animal Disease Center, North Atlantic Area, Agricultural
Research Service, U.S. Department of Agriculture, Greenport,
New York 11944
Abstract
ABSTRACT
The
genome of foot-and-mouth disease virus (FMDV) differs from that of
other picornaviruses in that it encodes a larger 3A protein
(>50% longer than poliovirus 3A), as well as three
copies of protein 3B (also known as VPg). Previous studies have shown
that a deletion of amino acids 93 to 102 of the 153-codon 3A protein is
associated with an inability of a Taiwanese strain of FMDV (O/TAW/97)
to cause disease in bovines. Recently, an Asian virus with a second 3A
deletion (amino acids 133 to 143) has also been detected (N.
J. Knowles et al., J. Virol.
75:
1551-1556, 2001).
Genetically engineered viruses harboring the amino acids 93 to 102 or
133 to 143 grew well in porcine cells but replicated poorly in bovine
cells, whereas a genetically engineered derivative of the O/TAW/97
virus expressing a full-length 3A (strain A12) grew well in both cell
types. Interestingly, a virus with a deletion spanning amino acid 93 to
144 also grew well in porcine cells and caused disease in swine.
Further, genetically engineered viruses containing only a single copy
of VPg were readily recovered with the full-length 3A, the deleted 3A
(amino acids 93 to 102), or the “super” deleted forms
of 3A (missing amino acids 93 to 144). All of the single-VPg viruses
were attenuated in porcine cells and replicated poorly in bovine cells.
The single-VPg viruses produced a mild disease in swine, indicating
that the VPg copy number is an important determinant of host range and
virulence. The association of VPg copy number with increased virulence
in vivo may help to explain why all naturally occurring FMDVs have
retained three copies of
VPg.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Cited by
105 articles.
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