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TCR triggering transcriptionally downregulates CCR5 expression on rhesus macaque CD4(+) T-cells with no measurable effect on susceptibility to SIV infection.

Abstract：

:Studies using transformed human cell lines suggest that most SIV strains use CCR5 as co-receptor. Our analysis of primary rhesus macaque CD4(+) T-cell clones revealed marked differences in susceptibility to SIV(mac)239 infection. We investigated whether different levels of CCR5 expression account for clonal differences in SIV(mac)239 susceptibility. Macaque CD4(+) T-cells showed significant CCR5 downregulation 1-2days following CD3 mAb stimulation, which gradually recovered at resting state, 7-10days after activation. Exposure of clones to SIV(mac)239 during their CCR5(low) or CCR5(high) expression states revealed differences in SIV susceptibility independent of surface CCR5 levels. Furthermore, a CCR5 antagonist similarly reduced SIV(mac)239 infection of clones during their CCR5(low) or CCR5(high) expression states. Our data suggest a model where i) very low levels of CCR5 are sufficient for efficient SIV infection, ii) CCR5 levels above this threshold do not enhance infection, and iii) low level infection can occur in the absence of CCR5.

journal_name

Virology

journal_title

Virology

authors

Minang JT,Trivett MT,Barsov EV,Del Prete GQ,Trubey CM,Thomas JA,Gorelick RJ,Piatak M Jr,Ott DE,Ohlen C

doi

10.1016/j.virol.2010.10.005

subject

Has Abstract

pub_date

2011-01-05 00:00:00

pages

132-40

issue

1

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(10)00641-0

journal_volume

409

pub_type

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