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29300007
Sooty mangabey genome sequence provides insight into AIDS resistance in a natural SIV host.

Nature, 2018/01/03;553(7686):77-81.

Palesch D[1], Bosinger SE[1, 2], Tharp GK[1], Vanderford TH[1], Paiardini M[1, 2], Chahroudi A[1, 3], Johnson ZP[1], Kirchhoff F[4], Hahn BH[5], Norgren RB[6], Patel NB[1], Sodora DL[7], Dawoud RA[1], Stewart CB[8], Seepo SM[8], Harris RA[9, 10], Liu Y[9], Raveendran M[9, 10], Han Y[9], English A[9], Thomas GWC[11], Hahn MW[11], Pipes L[12], Mason CE[12], Muzny DM[9, 10], Gibbs RA[9, 10], Sauter D[4], Worley K[9, 10], Rogers J[9, 10], Silvestri G[1, 2]

Affiliations

PMID: 29300007DOI: 10.1038/nature25140

Impact factor: 69.504

Abstract
In contrast to infections with human immunodeficiency virus (HIV) in humans and simian immunodeficiency virus (SIV) in macaques, SIV infection of a natural host, sooty mangabeys (Cercocebus atys), is non-pathogenic despite high viraemia. Here we sequenced and assembled the genome of a captive sooty mangabey. We conducted genome-wide comparative analyses of transcript assemblies from C. atys and AIDS-susceptible species, such as humans and macaques, to identify candidates for host genetic factors that influence susceptibility. We identified several immune-related genes in the genome of C. atys that show substantial sequence divergence from macaques or humans. One of these sequence divergences, a C-terminal frameshift in the toll-like receptor-4 (TLR4) gene of C. atys, is associated with a blunted in vitro response to TLR-4 ligands. In addition, we found a major structural change in exons 3-4 of the immune-regulatory protein intercellular adhesion molecule 2 (ICAM-2); expression of this variant leads to reduced cell surface expression of ICAM-2. These data provide a resource for comparative genomic studies of HIV and/or SIV pathogenesis and may help to elucidate the mechanisms by which SIV-infected sooty mangabeys avoid AIDS.
MeSH terms
Acquired Immunodeficiency Syndrome; Amino Acid Sequence; Animals; Cell Adhesion Molecules; Cercocebus atys; Exons; Female; Frameshift Mutation; Genetic Predisposition to Disease; Genetic Variation; Genome; Genomics; HIV; Host Specificity; Humans; Macaca; Sequence Deletion; Simian Acquired Immunodeficiency Syndrome; Simian Immunodeficiency Virus; Species Specificity; Toll-Like Receptor 4; Transcriptome; Whole Genome Sequencing
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