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Article: Natural infection of a homozygous Δ24 CCR5 red-capped mangabey with an R2b-tropic simian immunodeficiency virus

TitleNatural infection of a homozygous Δ24 CCR5 red-capped mangabey with an R2b-tropic simian immunodeficiency virus
Authors
Issue Date1998
PublisherRockefeller University Press. The Journal's web site is located at http://www.jem.org
Citation
Journal Of Experimental Medicine, 1998, v. 188 n. 11, p. 2057-2065 How to Cite?
AbstractA homozygous 24-bp deletion (Δ24) was found in the CC chemokine receptor 5 (CCR5) of 11 out of 15 red-capped mangabeys (RCMs), Cercocebus torquatus torquatus, both in Africa and in an American zoo. The CCR5 Δ24 defect encompassed eight amino acids in frame in the fourth transmembrane region. Unexpectedly, RCM-009, one of 11 homozygotes (Δ24CCR5/Δ24CCR5), was found to be naturally infected with a divergent simian immunodeficiency virus (SIV) strain, which was not R5-tropic, but used CCR2b (R2b) as its major coreceptor. SIVrcmGab1 was the only R2b-tropic SIV among other divergent SIVs tested. Cells transfected with the Δ24 CCR5 did not support entry of R5- tropic SIVmac, SIVcpz, SIVmne, HIV-2, or HIV-1, and were also inactive in signal transduction mediated by β-chemokines. At 86.6%, the Δ24 allelic frequency was significantly higher than that of the 32-bp deletion found in humans. The Δ24 frequency was 4.1% in 34 sooty mangabeys (SMs), a geographically isolated subspecies that was naturally infected with RS- tropic SIV. Finding identical deletions in two mangabey subspecies separated for 10,000 years or more dates the Δ24 CCR5 deletion as ancient. However, the source of the selective pressure for the high rate of CCR5 deletion in RCMs remains to be determined. The high allelic frequency of the Δ24 CCR5 in RCMs, in comparison to that of SMs, suggests that R2b-tropism may have been acquired by SIVrcm, as an adaptation to CCR5 genetic defects appeared in its host.
Persistent Identifierhttp://hdl.handle.net/10722/157285
ISSN
2015 Impact Factor: 11.24
2015 SCImago Journal Rankings: 10.762
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Zen_US
dc.contributor.authorKwon, Den_US
dc.contributor.authorJin, Zen_US
dc.contributor.authorMonard, Sen_US
dc.contributor.authorTelfer, Pen_US
dc.contributor.authorJones, MSen_US
dc.contributor.authorLu, CYen_US
dc.contributor.authorAguilar, RFen_US
dc.contributor.authorHo, DDen_US
dc.contributor.authorMarx, PAen_US
dc.date.accessioned2012-08-08T08:48:40Z-
dc.date.available2012-08-08T08:48:40Z-
dc.date.issued1998en_US
dc.identifier.citationJournal Of Experimental Medicine, 1998, v. 188 n. 11, p. 2057-2065en_US
dc.identifier.issn0022-1007en_US
dc.identifier.urihttp://hdl.handle.net/10722/157285-
dc.description.abstractA homozygous 24-bp deletion (Δ24) was found in the CC chemokine receptor 5 (CCR5) of 11 out of 15 red-capped mangabeys (RCMs), Cercocebus torquatus torquatus, both in Africa and in an American zoo. The CCR5 Δ24 defect encompassed eight amino acids in frame in the fourth transmembrane region. Unexpectedly, RCM-009, one of 11 homozygotes (Δ24CCR5/Δ24CCR5), was found to be naturally infected with a divergent simian immunodeficiency virus (SIV) strain, which was not R5-tropic, but used CCR2b (R2b) as its major coreceptor. SIVrcmGab1 was the only R2b-tropic SIV among other divergent SIVs tested. Cells transfected with the Δ24 CCR5 did not support entry of R5- tropic SIVmac, SIVcpz, SIVmne, HIV-2, or HIV-1, and were also inactive in signal transduction mediated by β-chemokines. At 86.6%, the Δ24 allelic frequency was significantly higher than that of the 32-bp deletion found in humans. The Δ24 frequency was 4.1% in 34 sooty mangabeys (SMs), a geographically isolated subspecies that was naturally infected with RS- tropic SIV. Finding identical deletions in two mangabey subspecies separated for 10,000 years or more dates the Δ24 CCR5 deletion as ancient. However, the source of the selective pressure for the high rate of CCR5 deletion in RCMs remains to be determined. The high allelic frequency of the Δ24 CCR5 in RCMs, in comparison to that of SMs, suggests that R2b-tropism may have been acquired by SIVrcm, as an adaptation to CCR5 genetic defects appeared in its host.en_US
dc.languageengen_US
dc.publisherRockefeller University Press. The Journal's web site is located at http://www.jem.orgen_US
dc.relation.ispartofJournal of Experimental Medicineen_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCercocebusen_US
dc.subject.meshGenetic Predisposition To Diseaseen_US
dc.subject.meshHomozygoteen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshReceptors, Ccr5 - Genetics - Immunologyen_US
dc.subject.meshSequence Alignmenten_US
dc.subject.meshSimian Acquired Immunodeficiency Syndrome - Genetics - Immunologyen_US
dc.subject.meshSimian Immunodeficiency Virusen_US
dc.titleNatural infection of a homozygous Δ24 CCR5 red-capped mangabey with an R2b-tropic simian immunodeficiency virusen_US
dc.typeArticleen_US
dc.identifier.emailChen, Z:zchenai@hkucc.hku.hken_US
dc.identifier.authorityChen, Z=rp00243en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1084/jem.188.11.2057en_US
dc.identifier.pmid9841919-
dc.identifier.scopuseid_2-s2.0-0031775146en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031775146&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume188en_US
dc.identifier.issue11en_US
dc.identifier.spage2057en_US
dc.identifier.epage2065en_US
dc.identifier.isiWOS:000077484700009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChen, Z=35271180800en_US
dc.identifier.scopusauthoridKwon, D=7103159876en_US
dc.identifier.scopusauthoridJin, Z=7403625656en_US
dc.identifier.scopusauthoridMonard, S=6603617420en_US
dc.identifier.scopusauthoridTelfer, P=36907430100en_US
dc.identifier.scopusauthoridJones, MS=13104613100en_US
dc.identifier.scopusauthoridLu, CY=16448264900en_US
dc.identifier.scopusauthoridAguilar, RF=35972444300en_US
dc.identifier.scopusauthoridHo, DD=7402971998en_US
dc.identifier.scopusauthoridMarx, PA=7102894750en_US

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