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Role of endogenous interferon‐ β in the restriction of HIV replication in human monocyte/macrophages
Author(s) -
Gessani Sandra,
Puddu Patrizia,
Varano Barbara,
Borghi Paola,
Conti Lucia,
Fantuzzi Laura,
Gherardi Giovanni,
Belardelli Filippo
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.56.3.358
Subject(s) - vesicular stomatitis virus , biology , monocyte , interferon , macrophage , antibody , virology , in vitro , in vivo , virus , viral replication , endogeny , immunology , microbiology and biotechnology , endocrinology , biochemistry
In vitro culture of human monocytes results in a time‐dependent differentiation into macrophages. Monocyte/macrophages were infected with HIV‐1 Ba‐L at different times after isolation and subsequent culture. When 7‐day macrophages were infected in the presence of antibodies to interferon‐ β (IFN‐ β ), a significant increase in HIV‐1 p24 release was observed. This effect was not detected in 1‐day monocytes. Treatment of 7‐day cultured macrophages with HIV‐1 rgp120 resulted in resistance to vesicular stomatitis virus infection. This rgp120‐induced antiviral state was neutralized in the presence of antibodies to IFN‐ β . The overall results indicate that the infection of monocyte/macrophages with HIV‐1 results in the induction of IFN‐ β , which, in turn, inhibits HIV‐1 expression in macrophages. The finding that HIV‐1 itself (possibly through its gp120) can induce a potent antiviral factor (IFN‐ β ) in macrophages underlines the complex physiological function of these cells in maintaining normal homeostasis in vivo in response to virus infection. J. Leukoc. Biol. 56: 358–361; 1994.