Production of interferons and beta-chemokines by placental trophoblasts of HIV-1-infected women

Infect Dis Obstet Gynecol. 2001;9(2):95-104. doi: 10.1155/S1064744901000175.


Objective: The mechanism whereby the placental cells of a human immunodeficiency virus (HIV)-1-infected mother protect the fetus from HIV-1 infection is unclear. Interferons (IFNs) inhibit the replication of viruses by acting at various stages of the life cycle and may play a role in protecting against vertical transmission of HIV-1. In addition the beta-chemokines RANTES (regulated on activation T cell expressed and secreted), macrophage inflammatory protein-1-alpha (MIP-1alpha), and MIP-1beta can block HIV-1 entry into cells by preventing the binding of the macrophage-trophic HIV-1 strains to the coreceptor CCR5. In this study the production of IFNs and beta-chemokines by placental trophoblasts of HIV-1-infected women who were HIV-1 non-transmitters was examined.

Methods: Placental trophoblastic cells were isolated from 29 HIV-1-infected and 10 control subjects. Supernatants of trophoblast cultures were tested for the production of IFNs and beta-chemokines by enzyme linked immunosorbent assay (ELISA). Additionally, HIV-1-gag and IFN-beta transcripts were determined by a semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) assay.

Results: All placental trophoblasts of HIV-1-infected women contained HIV-1-gag transcripts. There were no statistical differences in the median constitutive levels of IFN-alpha and IFN-gamma produced by trophoblasts of HIV-1 infected and control subjects. In contrast, trophoblasts of HIV-1-infected women constitutively produced significantly higher levels of IFN-beta protein than trophoblasts of control subjects. Furthermore, the median levels of beta-chemokines produced by trophoblasts of HIV-infected and control women were similar.

Conclusions: Since there was no correlation between the placental HIV load and the production of interferons or beta-chemokines, the role of trophoblast-derived IFNs and beta-chemokines in protecting the fetus from infection with HIV-1 is not clear.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • CD4 Lymphocyte Count
  • Chemokines, CC / genetics
  • Chemokines, CC / immunology
  • Chemokines, CC / metabolism*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • HIV Infections / immunology
  • HIV Infections / metabolism*
  • HIV Infections / transmission*
  • HIV-1 / genetics
  • HIV-1 / immunology
  • HIV-1 / metabolism*
  • Humans
  • Infant, Newborn
  • Infectious Disease Transmission, Vertical*
  • Interferon-beta / genetics
  • Interferon-beta / immunology
  • Interferon-beta / metabolism
  • Interferon-gamma / genetics
  • Interferon-gamma / immunology
  • Interferon-gamma / metabolism
  • Interferons / genetics
  • Interferons / immunology
  • Interferons / metabolism*
  • Pregnancy
  • Pregnancy Complications, Infectious / immunology
  • Pregnancy Complications, Infectious / metabolism*
  • Pregnancy Outcome
  • Reverse Transcriptase Polymerase Chain Reaction
  • Trophoblasts / immunology
  • Trophoblasts / metabolism*
  • Viral Load
  • Virus Replication / genetics
  • Virus Replication / immunology


  • Chemokines, CC
  • Interferon-beta
  • Interferon-gamma
  • Interferons