Effect of antibody to HIV-1 Tat protein on viral replication in vitro and progression of HIV-1 disease in vivo

M. C. Re, G. Furlini, M. Vignoli, E. Ramazzotti, G. Roderigo, V. De Rosa, G. Zauli, S. Lolli, S. Capitani, M. La Placa

Research output: Contribution to journalArticlepeer-review


In HIV-1-infected cell cultures, a relatively low concentration (5 μg/ml) of monoclonal antibody (mAb) against HIV-1-transactivating Tat protein was an efficient inhibitor of HIV-1 replication both in HIV-1(IIIB)-infected Jurkat cell and peripheral blood mononuclear cell (PBMC) cultures and significantly reduced the expression of a Tat-responsive CAT-reporter construct in HIV- 1(IIIB)-infected Jurkat cells. Anti-Tat mAb also caused a significant reduction and a consistent delay in HIV-1 replication when added to PBMCs from HIV-1-infected patients cocultivated with phytohemagglutinin (PHA)stimulated normal PBMCs. These data indicate that an autocrine-paracrine loop sustained by extracellular Tat protein, which is actively released by HIV-1-infected cells, may affect HIV-1 replication in cell cultures in vitro. An inverse relationship between natural anti-Tat antibody levels and p24 antigenemia was demonstrated by retrospective analysis of serial serum samples obtained from 10 HIV-1-seropositive hemophiliac patients followed over a 7-9-year period. This datum points to a possible influence of anti- Tat antibody on the progression of HIV-1 disease in vivo. These findings have strong implications for Tat protein as a possible target for specific immunotherapy in HIV-1-infected patients.

Original languageEnglish
Pages (from-to)408-416
Number of pages9
JournalJournal of Acquired Immune Deficiency Syndromes and Human Retrovirology
Issue number4
Publication statusPublished - 1995


  • anti-Tat antibody
  • Hemophiliac patients
  • HIV-1
  • p24 Antigen
  • Tat protein

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Immunology and Allergy


Dive into the research topics of 'Effect of antibody to HIV-1 Tat protein on viral replication in vitro and progression of HIV-1 disease in vivo'. Together they form a unique fingerprint.

Cite this