Abstract
Small ruminant lentivirus (SRLV) infections of sheep are influenced by genetics on both the host and pathogen sides. Genetic variation in the ovine transmembrane 154 (TMEM154) gene associates with infection susceptibility, and distinct SRLV genetic subgroups infect sheep in association with their TMEM154 diplotypes. In this study, a novel SRLV subgroup was identified that naturally infected sheep with various TMEM154 diplotypes, including those homozygous for a rare frameshift mutation (A4 delta53), which is predicted to abolish TMEM154 protein function. Thus, these SRLVs may infect sheep that lack functional TMEM154, and may not be restricted by TMEM154 diplotypes in establishing infections.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-015-0162-7) contains supplementary material, which is available to authorized users.
Highlights
Small ruminant lentivirus (SRLV) infections of sheep are influenced by genetics on both the host and pathogen sides
Sequence representatives of SRLV subgroups 1 and 2 were included in the analyses, as were those of what we describe as subgroup 3, which infected a flock of sheep in the Western United States [29], and has not been tested for an association with transmembrane 154 (TMEM154) genotypes
Subgroup 4 SRLVs can infect sheep with TMEM154 “4,4” diplotypes that are homozygous for the TMEM154 A4Δ53 mutation, as well as sheep that do not have haplotype 4
Summary
Small ruminant lentivirus (SRLV) infections of sheep are influenced by genetics on both the host and pathogen sides. Sheep with a copy of either haplotype 2 or 3, both of which encode a glutamate amino acid residue at position 35 (E35) of the extracellular portion of TMEM154, have an increased risk of SRLV infection.
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