Morphine enhances HIV infection of neonatal macrophages
Morphine enhances HIV infection of neonatal macrophages
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DOI：
10.1203/01.pdr.0000074973.83826.4c
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发表时间：
2003-08-01
影响因子：
3.6
通讯作者：
Ho, WZ
中科院分区：
文献类型：
--
作者：
Li, Y;Merrill, JD;Ho, WZ
艾滋病毒的围产期传播几乎是所有儿童新感染艾滋病毒的原因。在母亲滥用非法药物的情况下，艾滋病毒围产期传播的风险增加。关于新生儿免疫系统的改变以及在接触吗啡后对艾滋病毒感染的易感性，人们知之甚少。我们研究了吗啡对新生儿单核细胞来源的巨噬细胞(MDM)感染HIV的影响。吗啡显著增加新生儿MDM的HIV感染。吗啡诱导的新生儿MDM中的HIV复制是完全的。被阿片受体拮抗剂纳曲酮抑制。吗啡显著上调新生MDM中CCR5受体的表达，抑制巨噬细胞炎性蛋白-1β的内源性产生。因此，吗啡很可能通过改变β-趋化因子和CCR5受体的表达，增加新生儿MDM对HIV感染的易感性，并可能在围产期HIV传播和感染中起辅助作用。
Perinatal transmission of HIV accounts for almost all new HIV infections in children. There is an increased risk of perinatal transmission of HIV with maternal illicit substance abuse. Little is known about neonatal immune system alteration and subsequent susceptibility to HIV infection after morphine exposure. We investigated the effects of morphine on HIV infection of neonatal monocyte-derived macrophages (MDM). Morphine significantly enhanced HIV infection of neonatal MDM. Morphine-induced HIV replication in neonatal-MDM was completely. suppressed by naltrexone, the opioid receptor antagonist. Morphine significantly up-regulated CCR5 receptor expression and inhibited the endogenous production of macrophage inflammatory protein-1beta in neonatal MDM. Thus, morphine, most likely through alteration of beta-chemokines and CCR5 receptor expression, enhances the susceptibility of neonatal MDM to HIV infection, and may have a cofactor role in perinatal HIV transmission and infection.