English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Induction of human immunodeficiency virus (HIV) replication in infected CD4+ T lymphocytes requires cellular activation. The ligation of CD28, a signal-transducing receptor with a natural ligand on activated B cells and antigen-presenting cells, provides a costimulating signal for interleukin 2 production and T-cell proliferation as well as coactivation of the transfected HIV long terminal repeat in Jurkat cells. The aim of the present study was to investigate the ability of CD28 ligation to activate HIV type 1 (HIV-1) replication in naturally infected CD4+ lymphocytes either alone or in combination with immobilized anti-CD3 monoclonal antibody. Our results show that HIV-1 was successfully isolated from 16 of 28 patients. For 5 of these 16, virus was isolated only when anti-CD28 was added in combination with the anti-CD3. Moreover, stimulation by anti-CD28 alone induced HIV-1 replication in 5 of 12 patients tested, in the absence of cell proliferation. We found no correlation between the level of CD3- or CD28-induced proliferative response and induction of HIV-1 replication. Therefore, CD28 ligation, a nonmitogenic CD4+ T-cell activation signal, is sufficient to induce transcription and replication of HIV-1 in naturally infected lymphocytes.

journal of virology

A novel mode of human immunodeficiency virus type 1 (HIV-1) activation: ligation of CD28 alone induces HIV-1 replication in naturally infected lymphocytes