根據(jù)一篇發(fā)表于1月12日Science的文章指出，細菌的質(zhì)體—環(huán)狀DNA 寄生蟲（DNA parasites）可能攜帶抗生素抗性基因，其編碼的蛋白質(zhì)可以增加細菌在抗生素環(huán)境中的存活率,，這種質(zhì)體是醫(yī)學界使用抗生素的一大障礙,。
有些質(zhì)體可經(jīng)由接合作用從一個細菌轉(zhuǎn)移到另一個細菌，促進了細菌進化,。有趣的是,，有些質(zhì)體在拷貝的同時，還將病原體對抗生素抗性的基因一起拷貝,、轉(zhuǎn)移,。盡管如此，宿主菌得到質(zhì)體后,，宿主菌的生長和適應(yīng)能力都降低,，停止抗生素治療后，新的重組細菌會被適應(yīng)性更強的不含質(zhì)體的野生菌淘汰掉,。
由(Trinity College Dublin大學的Charles J. Dorman博士和英國The Wellcome Trust Sanger研究所的John Wain博士率領(lǐng)的研究小組發(fā)現(xiàn)一組重要的質(zhì)體,，可以利用秘密基因（sfh）潛入新的宿主菌中，而不會削弱宿主菌的適應(yīng)力,。這種在沙門氏菌中發(fā)現(xiàn)的抗藥性質(zhì)體,，可以使抗藥性細菌易于存活，即使在抗生素療法停止后,，抗性基因依然有效,。
研究人員發(fā)現(xiàn)sfh所編碼的蛋白與另一種細菌蛋白H-NS非常相似。H-NS蛋白組織細菌的遺傳物質(zhì),，控制許多基因包括致病基因活性的蛋白,。藉由引入與H-NS相似的stealth蛋白（Sfh），可以避免重組質(zhì)體對細胞中H-NS和DNA之間的天然平衡的干擾,，因此可以幫助質(zhì)體逃避細菌的監(jiān)測,。
細菌可以通過多種途徑獲得、轉(zhuǎn)移抗性基因,，但是此次研究發(fā)現(xiàn)的抗生素抗性基因顯著提高感染成功率,、宿主抗生素抗性以及致病率的機制。這些質(zhì)體在許多致病菌包括會引起傷寒癥和副傷寒發(fā)熱的病原菌中都存在,，現(xiàn)在研究人員希望可以利用這些信息防止質(zhì)體進一步傳播,。
英文原文：
How 'DNA parasites' can increase spread of antibiotic resistance
Pathogens can become superbugs without their even knowing it, research published today in Science shows. 'Stealth' plasmids - circular 'DNA parasites' of bacteria that can carry antibiotic-resistance genes - produce a protein that increases the chances of survival and spread of the antibiotic-resistant strain.
Low-cost plasmids, described for the first time in the study are a threat to use of antibiotics.
Plasmids are naturally occurring 'DNA parasites' of many bacterial species and have been known about for over 30 years. Some are able to transfer themselves from one bacterial cell to another through a sex-like process called conjugation, contributing to bacterial evolution. Worryingly, as well as copying themselves plasmids can pick up and transfer bacterial genes, such as those that make pathogens resistant to antibiotics.
However, the plasmid comes at a cost to the host bacterium: gaining a plasmid can reduce the host's ability to grow and reduce its fitness. When antibiotic treatment is stopped, the new microbe–plasmid combination will be eliminated quickly through fierce competition from more 'fit', plasmid-free bacteria.
The research teams, led by Professor Charles J. Dorman at Trinity College Dublin, Ireland, and Dr John Wain at the Wellcome Trust Sanger Institute in Cambridge, UK, have discovered that an important class of plasmids use a stealth gene (called sfh) to allow entry into a new bacterium with minimal reduction in fitness.
With the low-cost version of the resistance plasmid they have described in Salmonella, resistant bacteria are likely to survive and the resistance genes to persist even if antibiotic therapy is stopped.
Their research shows that sfh codes for a protein that is very similar to another bacterial protein: the role of the protein is to organise the genetic material in bacterium and control activity of many genes, including those involved in causing disease. The sfh protein binds to the new plasmid DNA, preventing its detection by the bacterium.
"The bacterial protein, called H-NS, is a very important molecule and affects the way a bacterial pathogen operates. By bringing in its own supply of the H-NS-like stealth protein (called Sfh), the plasmid avoids interfering with the natural balance of H-NS and DNA in the cell," explained Professor Dorman.
"Our work suggests that bacterial fitness can be manipulated by altering the proportions of H-NS and DNA in the cell, perhaps through the use of drugs, an insight that may be exploited in the future to prevent or to fight infection."
Bringing its own supply of the host-like protein is clearly an advantage for the plasmid, suggesting that the normal supply of H-NS in the bacterium may become limited when new DNA is imported. If a modified plasmid, lacking the sfh gene, is transferred to Salmonella, the effects of the plasmid are very rapidly detected.
Bacteria can acquire and transfer resistance genes through a variety of methods, but this new study shows how a single gene has the potential to increase dramatically the chance of successful - and health-threatening - transfer and survival of a battery of antibiotic-resistance genes.
The consequences for managing disease - especially in developing countries - are significant, explained Dr John Wain: "These plasmids are found in many pathogenic bacteria including those that cause typhoid and paratyphoid fever. Both of these diseases are increasing in the developing world and in the UK we are seeing more and more imported cases.
"But understanding is not enough: we now need to exploit this information to try to prevent the plasmid spreading any further."
