脂肪酸和单甘油酯可以杀死包膜病毒

Inactivation of enveloped viruses and killing of cells by fatty acids and monoglycerides.

　

Antimicrob Agents Chemother. 1987 Jan;31(1):27-31.

　

　

摘要

　

人类的鲜奶中的脂质并不会灭活病毒，但人乳在4度或23度的温度下储存几天后变成抗病毒物质。

　

抗菌活性的出现取决于人奶中的活性脂肪酶并和人奶中的游离脂肪酸的释放有关。

　

一些正常乳脂的脂肪酸成分，进行抗包膜病毒 ，即水泡性口炎病毒，单纯疱疹病毒，和visna病毒，对抗非包膜病毒，脊髓灰质炎病毒 的试验。

　

在最高浓度下，短链和长链饱和脂肪酸没有或只有很小的抗病毒效果。

　

另一方面，中链饱和脂肪酸如月桂酸（Lauric acid)和长链不饱和脂肪酸(如亚油酸Linoleic acid、亚麻酸alpha-linolenic acid) 都对包膜病毒具有很高的活性，尽管最大程度的病毒失活所需的脂肪酸浓度相差超过20倍。

　

　

这些脂肪酸的单甘酸酯(Monoglycerides)也是高度抗病毒的，在某些情况下，浓度比游离脂肪酸低10倍。(单甘油酯是身体在消化大分子脂肪过程中的中间体）

　

　

没有脂肪酸能灭活脊髓灰质炎病毒（poliovirus)。

　

研究发现，抗病毒脂肪酸会影响病毒包膜，导致渗漏，在浓度较高时，包膜和病毒颗粒完全解体。

　

它们还导致组织培养细胞的质膜解体，导致细胞溶解和死亡。

　

同样的现象也发生在与储存的抗病毒人类牛奶孵育的细胞培养中。

　

因此，人乳脂在体外的抗菌作用很可能是由脂肪酸分解细胞和病毒膜引起的。

　

　

需要进行研究，以确定人乳脂是否对婴儿的胃肠有抗菌作用，并确定它们在保护婴儿免受胃肠道感染方面发挥的作用(如果有的话)。

 

Inactivation of enveloped viruses and killing of cells by fatty acids and monoglycerides.

 

Antimicrob Agents Chemother. 1987 Jan;31(1):27-31.

Thormar H, Isaacs CE, Brown HR, Barshatzky MR, Pessolano T.

Abstract

Lipids in fresh human milk do not inactivate viruses but become antiviral after storage of the milk for a few days at 4 or 23 degrees C.

　

The appearance of antiviral activity depends on active milk lipases and correlates with the release of free fatty acids in the milk. A number of fatty acids which are normal components of milk lipids were tested against enveloped viruses, i.e., vesicular stomatitis virus, herpes simplex virus, and visna virus, and against a nonenveloped virus, poliovirus.

　

Short-chain and long-chain saturated fatty acids had no or a very small antiviral effect at the highest concentrations tested.

　

Medium-chain saturated and long-chain unsaturated fatty acids, on the other hand, were all highly active against the enveloped viruses, although the fatty acid concentration required for maximum viral inactivation varied by as much as 20-fold.

Monoglycerides of these fatty acids were also highly antiviral, in some instances at a concentration 10 times lower than that of the free fatty acids.

　

None of the fatty acids inactivated poliovirus.

　

Antiviral fatty acids were found to affect the viral envelope, causing leakage and at higher concentrations, a complete disintegration of the envelope and the viral particles. They also caused disintegration of the plasma membranes of tissue culture cells resulting in cell lysis and death.

　

The same phenomenon occurred in cell cultures incubated with stored antiviral human milk. The antimicrobial effect of human milk lipids in vitro is therefore most likely caused by disintegration of cellular and viral membranes by fatty acids.

　

Studies are needed to establish whether human milk lipids have an antimicrobial effect in the stomach and intestines of infants and to determine what role, if any, they play in protecting infants against gastrointestinal infections.

　

PMID: 3032090 PMCID: PMC174645

https://www.ncbi.nlm.nih.gov/pubmed/3032090