根据一篇发表于1月12日Science的文章指出，细菌的质体—环状DNA 寄生虫（DNA parasites）可能携带抗生素抗性基因，其编码的蛋白质可以增加细菌在抗生素环境中的存活率，这种质体是医学界使用抗生素的一大障碍。
有些质体可经由接合作用从一个细菌转移到另一个细菌，促进了细菌进化。有趣的是，有些质体在拷贝的同时，还将病原体对抗生素抗性的基因一起拷贝、转移。尽管如此，宿主菌得到质体后，宿主菌的生长和适应能力都降低，停止抗生素治疗后，新的重组细菌会被适应性更强的不含质体的野生菌淘汰掉。
由(Trinity College Dublin大学的Charles J. Dorman博士和英国The Wellcome Trust Sanger研究所的John Wain博士率领的研究小组发现一组重要的质体，可以利用秘密基因（sfh）潜入新的宿主菌中，而不会削弱宿主菌的适应力。这种在沙门氏菌中发现的抗药性质体，可以使抗药性细菌易于存活，即使在抗生素疗法停止后，抗性基因依然有效。
研究人员发现sfh所编码的蛋白与另一种细菌蛋白H-NS非常相似。H-NS蛋白组织细菌的遗传物质，控制许多基因包括致病基因活性的蛋白。藉由引入与H-NS相似的stealth蛋白（Sfh），可以避免重组质体对细胞中H-NS和DNA之间的天然平衡的干扰，因此可以帮助质体逃避细菌的监测。
细菌可以通过多种途径获得、转移抗性基因，但是此次研究发现的抗生素抗性基因显著提高感染成功率、宿主抗生素抗性以及致病率的机制。这些质体在许多致病菌包括会引起伤寒症和副伤寒发热的病原菌中都存在，现在研究人员希望可以利用这些信息防止质体进一步传播。
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."
