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前列腺素A在急性感染期间抑制人类免疫缺陷病毒的复制。

Prostaglandin A inhibits replication of human immunodeficiency virus during acute infection.

作者信息

Ankel H, Turriziani O, Antonelli G

机构信息

Institute of Virology, University La Sapienza, Rome, Italy.

出版信息

J Gen Virol. 1991 Nov;72 ( Pt 11):2797-800. doi: 10.1099/0022-1317-72-11-2797.

DOI:10.1099/0022-1317-72-11-2797
PMID:1940869
Abstract

An antiviral effect of prostaglandins (PGs) of the A series on the replication of human immunodeficiency virus (HIV) has been determined. In the T cell line C8166 under single growth cycle conditions, PGA1 reduced the number of infectious progeny 1000-fold in the absence of cytotoxicity. Thus, inhibition of HIV replication by PGA1 represents a true antiviral phenomenon. The number and size of virus-induced syncytia, and the amount of viral antigen were also drastically reduced. The effect was specific for PGAs because PGA2 was also inhibitory, whereas PGB1, PGE1 and PGE2 were inactive. Virus adsorption and penetration do not appear to be targets of antiviral action because PGA1 substantially reduced virus replication, even when added 5 h post-infection. PGA1 did not inhibit viral reverse transcriptase, as determined by in vitro assays, suggesting that its antiviral action is not the consequence of a direct inhibitory effect on this enzyme. PGA1 also inhibited the replication of HIV-1 in CEM x 174 cells, but with less potency. Previously, intravenous infusion of PGA1 into human volunteers has shown no significant deleterious side-effects and thus these observations suggest that PGAs might have potential as antiviral agents in humans.

摘要

已确定A系列前列腺素(PGs)对人类免疫缺陷病毒(HIV)复制具有抗病毒作用。在单生长周期条件下的T细胞系C8166中,PGA1在无细胞毒性的情况下将感染性子代数量减少了1000倍。因此,PGA1对HIV复制的抑制代表了一种真正的抗病毒现象。病毒诱导的多核巨细胞的数量和大小以及病毒抗原的量也大幅减少。这种作用对PGAs具有特异性,因为PGA2也具有抑制作用,而PGB1、PGE1和PGE2则无活性。病毒吸附和穿透似乎不是抗病毒作用的靶点,因为即使在感染后5小时添加PGA1,它也能大幅减少病毒复制。体外试验表明,PGA1不抑制病毒逆转录酶,这表明其抗病毒作用不是对该酶直接抑制作用的结果。PGA1也抑制HIV-1在CEM x 174细胞中的复制,但效力较低。此前,向人类志愿者静脉输注PGA1未显示出明显的有害副作用,因此这些观察结果表明,PGAs可能具有作为人类抗病毒药物的潜力。

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