| pubmed-article:19917610 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C0035253 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C0961954 | lld:lifeskim |
| pubmed-article:19917610 | lifeskim:mentions | umls-concept:C1100939 | lld:lifeskim |
| pubmed-article:19917610 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19917610 | pubmed:dateCreated | 2010-1-11 | lld:pubmed |
| pubmed-article:19917610 | pubmed:abstractText | CXCR4-using human immunodeficiency virus, type 1 (HIV-1) variants emerge late in the course of infection in >40% of individuals infected with clade B HIV-1 but are described less commonly with clade C isolates. Tat is secreted by HIV-1-infected cells where it acts on both uninfected bystander cells and infected cells. In this study, we show that clade B Tat, but not clade C Tat, increases CXCR4 surface expression on resting CD4+ T cells through a CCR2b-dependent mechanism that does not involve de novo protein synthesis. The expression of plectin, a cytolinker protein that plays an important role as a scaffolding platform for proteins involved in cellular signaling including CXCR4 signaling and trafficking, was found to be significantly increased following B Tat but not C Tat treatment. Knockdown of plectin using RNA interference showed that plectin is essential for the B Tat-induced translocation of CXCR4 to the surface of resting CD4+ T cells. The increased surface CXCR4 expression following B Tat treatment led to increased function of CXCR4 including increased chemoattraction toward CXCR4-using-gp120. Moreover, increased CXCR4 surface expression rendered resting CD4+ T cells more permissive to X4 but not R5 HIV-1 infection. However, neither B Tat nor C Tat was able to up-regulate surface expression of CXCR4 on activated CD4+ T cells, and both proteins inhibited the infection of activated CD4+ T cells with X4 but not R5 HIV-1. Thus, B Tat, but not C Tat, has the capacity to render resting, but not activated, CD4+ T cells more susceptible to X4 HIV-1 infection. | lld:pubmed |
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| pubmed-article:19917610 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19917610 | pubmed:citationSubset | IM | lld:pubmed |
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