HIV-1 infection in infants severely impairs the immune response induced by Bacille Calmette-Guérin vaccine.

نویسندگان

  • Nazma Mansoor
  • Thomas J Scriba
  • Marwou de Kock
  • Michele Tameris
  • Brian Abel
  • Alana Keyser
  • Francesca Little
  • Andreia Soares
  • Sebastian Gelderbloem
  • Silvia Mlenjeni
  • Lea Denation
  • Anthony Hawkridge
  • W Henry Boom
  • Gilla Kaplan
  • Gregory D Hussey
  • Willem A Hanekom
چکیده

BACKGROUND Worldwide, most infants born to mothers infected with human immunodeficiency virus (HIV) receive bacille Calmette-Guérin (BCG) vaccine. Tuberculosis is a major cause of death among infants infected with HIV in sub-Saharan Africa, and it should be prevented. However, BCG may itself cause disease (known as "BCGosis") in these infants. Information regarding the immunogenicity of BCG is imperative for the risk/benefit assessment of BCG vaccination in HIV-infected infants; however, no such data exist. METHODS We compared BCG-induced CD4 and CD8 T cell responses, as assessed by flow cytometry, in HIV-infected (n=20), HIV-exposed but uninfected (n=25), and HIV-unexposed (n=23) infants, during their first year of life. RESULTS BCG vaccination of the 2 HIV-uninfected groups induced a robust response, which was characterized by CD4 T cells expressing interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and/or interleukin (IL)-2. In contrast, HIV-infected infants demonstrated a markedly lower response throughout the first year of life. These infants also had significantly reduced numbers of polyfunctional CD4 T cells coexpressing IFN-gamma, TNF-alpha, and IL-2, a finding that is thought to indicate T cell quality. CONCLUSIONS Infection with HIV severely impairs the BCG-specific T cell response during the first year of life. BCG may therefore provide little, if any, vaccine-induced benefit in HIV-infected infants. Considering the significant risk of BCGosis, these data strongly support not giving BCG to HIV-infected infants.

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عنوان ژورنال:
  • The Journal of infectious diseases

دوره 199 7  شماره 

صفحات  -

تاریخ انتشار 2009