Effect of latent human immunodeficiency virus infection on cell surface phenotype
Journal of Virology, ISSN: 0022-538X, Vol: 76, Issue: 4, Page: 1673-1681
2002
- 26Citations
- 28Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations26
- Citation Indexes26
- 26
- CrossRef24
- Captures28
- Readers28
- 28
Article Description
Highly active antiretroviral therapy has succeeded in many cases in suppressing virus production in patients infected with human immunodeficiency virus (HIV); however, once treatment is discontinued, virus replication is rekindled. One reservoir capable of harboring HIV in a latent state and igniting renewed infection once therapy is terminated is a resting T cell. Due to the sparsity of T cells latently infected with HIV in vivo, it has been difficult to study viral and cellular interactions during latency. The SCID-hu (Thy/Liv) mouse model of HIV latency, however, provides high percentages of latently infected cells, allowing a detailed analysis of phenotype. Herein we show that latently infected cells appear phenotypically normal. Following cellular stimulation, the virus completes its life cycle and induces phenotypic changes, such as CD4 and major histocompatibility complex class I down-regulation, in the infected cell. In addition, HIV expression following activation did not correlate with expression of the cellular activation marker CD25. The apparently normal phenotype and lack of HIV expression in latently infected cells could prevent recognition by the immune response and contribute to the long-lived nature of this reservoir.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036147830&origin=inward; http://dx.doi.org/10.1128/jvi.76.4.1673-1681.2002; http://www.ncbi.nlm.nih.gov/pubmed/11799162; https://journals.asm.org/doi/10.1128/JVI.76.4.1673-1681.2002; http://jvi.asm.org/cgi/doi/10.1128/JVI.76.4.1673-1681.2002; https://syndication.highwire.org/content/doi/10.1128/JVI.76.4.1673-1681.2002; https://dx.doi.org/10.1128/jvi.76.4.1673-1681.2002; https://jvi.asm.org/content/76/4/1673
American Society for Microbiology
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