Gessani S, Puddu P, Varano B, Borghi P, Conti L, Fantuzzi L, Gherardi G, Belardelli F
Department of Virology, Istituto Superiore di Sanità, Rome, Italy.
J Leukoc Biol. 1994 Sep;56(3):358-61. doi: 10.1002/jlb.56.3.358.
In vitro culture of human monocytes results in a time-dependent differentiation into macrophages. Monocyte/macrophages were infected with HIV-1Ba-L at different times after isolation and subsequent culture. When 7-day macrophages were infected in the presence of antibodies to interferon-beta (IFN-beta), 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-beta. The overall results indicate that the infection of monocyte/macrophages with HIV-1 results in the induction of IFN-beta, 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-beta) in macrophages underlines the complex physiological function of these cells in maintaining normal homeostasis in vivo in response to virus infection.
人单核细胞的体外培养会导致其随时间推移分化为巨噬细胞。单核细胞/巨噬细胞在分离及后续培养后的不同时间用HIV-1Ba-L进行感染。当在存在β干扰素（IFN-β）抗体的情况下感染7天的巨噬细胞时，观察到HIV-1 p24释放显著增加。在1天的单核细胞中未检测到这种效应。用HIV-1重组糖蛋白120（rgp120）处理培养7天的巨噬细胞会使其对水疱性口炎病毒感染产生抗性。这种rgp120诱导的抗病毒状态在存在IFN-β抗体的情况下被中和。总体结果表明，HIV-1感染单核细胞/巨噬细胞会导致IFN-β的诱导，而IFN-β反过来又会抑制巨噬细胞中HIV-1的表达。HIV-1自身（可能通过其gp120）能够在巨噬细胞中诱导一种强效抗病毒因子（IFN-β）这一发现，突显了这些细胞在体内应对病毒感染以维持正常内环境稳定方面的复杂生理功能。
