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肿瘤可能引发更多的肿瘤
 
Viruses may be causing more cancers than previously thought, according to a new study.

Scientists know that a few cancers, such as cervical cancer, are caused by viruses, because researchers have isolated the viral genomes from the cancerous cells. But some viruses may take a "hit and run" approach - inducing cancer and then vanishing before the disease is caught, the researchers say.

The new study, performed in mice, showed that a particular mouse herpesvirus could trigger cancer but then practically disappear from the cancer cells. Herpesviruses belong to a family of viruses called Herpesviridae that can infect humans and include chicken pox and the Epstein-Barr virus - a virus that virtually everyone is infected with, yet only causes cancer in rare cases.

"We're saying that herpes viruses could cause a lot more disease than you would guess if you limited your suspicion to just to cancers that came out having the virus genome in them," said study author Philip Stevenson, a researcher at the University of Cambridge in the United Kingdom. "We're saying that they might cause orders of magnitude more cancers," he told LiveScience.

However, it is important to note that the cancers induced in the mice are different from the cancers that occur in people, and so the findings might not hold true for humans.

The results are published in the September issue of the Journal of General Virology.

Hit and run

Cancers occur when the genetic material within cells, the cells' DNA, develops mutations that cause the cell to divide uncontrollably. These mutations sometimes arise when the DNA is damaged. However, viruses can have effects similar to these mutations when they insert themselves into the DNA, and the end result is the same - uncontrolled cell growth. Two types of human papillomaviruses (HPV) are thought to cause cervical cancer this way.

By inserting itself into the cells' DNA, the virus "hides" from the body's immune system, so the body's defenses can't eliminate it. This means that researchers can later find evidence that HPV was indeed the culprit behind cervical cancer - the virus leaves its genes behind like fingerprints at a crime scene. About 20 percent of cancers are thought to be caused by viruses, according to Stevenson.

However, cells have several defense mechanisms to prevent tumor growth. Sometimes cells with certain mutations will self-destruct so they don't turn cancerous.

But viruses can interfere with these defenses.

"Viruses don't set out to cause cancer, but their replication uses all the same functions. So they tend to inhibit the whole set of these protective mechanisms," Stevenson said. "So they're kind of ideal agents for causing cancer."

The "hit and run" hypotheses proposes that a virus can cause cancer without integrating itself into the cell's DNA. In this case, a cell develops a genetic mutation, but the virus present in the cell overrides the defense mechanisms and allows the cell to continue to live. Over time, more and more genetic mutations develop, and the cell turns cancerous. However, by the time the cancer is discovered, the virus has been eliminated by the immune system, leaving no "fingerprints" behind.

For many years scientists have suspected viruses could cause cancer through this mechanism, but it was difficult to prove.

Cancer vaccines

Stevenson and his colleagues wanted to know: if a virus triggers cancer without integrating into the cells' DNA, how often can you still find traces of the virus inside the cancer cells?

They genetically engineered mice so that they would develop cancer if infected with the herpesvirus (the virus has a gene that triggers mouse cells to divide uncontrollably).

But when they later checked the tumors that grew in the mice, they found no trace of the virus. If the findings hold true for humans, that would mean viruses such as Epstein-Barr trigger more cancers than previously thought.

Further, the researchers found evidence that vaccinating against these viruses might prove effective in preventing cancers. When the researchers vaccinated the mice against the herpesvirus, none of the mice developed cancer.

While a vaccine against Epstein-Barr and other herpes viruses could theoretically be made, companies would not be willing to take the risk to develop them unless there was some significant disease threat, Stevenson said.

"With every vaccine there's a balance between the risk and the benefits," Stevenson said. Because cancers that have the Epstein-Barr virus genome in them are thought to be relatively rare, the benefits are seen as small, so no one wants to take the risk, he said. "If people recognize that these viruses may cause an awful lot more cancers, then the benefits [become greater]."

The current study suggests that a clinical trial of an Epstein-Barr vaccine or similar vaccine might be worthwhile, Stevenson said.
 
 
 
病毒引起的肿瘤或许远比想象中的多

科学家们已经知道少数癌症是由病毒引起的,例如宫颈癌,因为研究者们已经在癌细胞中分离得到了病毒的基因组。但是研究者认为一些病毒也许具有滞后的机制(hit and run),首先诱导引起癌症,但是在发病之前病毒确消失了。
一项在鼠中的研究表明,一种特殊的鼠疱疹病毒能引起癌症,但是在癌细胞中确几乎不存在。疱疹病毒是疱疹病毒科家族中的一员,这些病毒能感染人类,进而引发水痘和EB病毒感染。每个人实际上都会感染EB病毒,但是只有在极少数病例中导致癌症。
我们认为疱疹病毒能引起很多疾病,这大大超出了我们的想象,如果你的想象范围只停留在那些能分离出病毒基因组的癌症中英国剑桥大学的研究者,本文的作者Philip Stevenson说,我们认为它能引起数量级以上的癌症
然而,在鼠中引起癌症和在人中引起癌症,是不相同的,所以这个发现在人体中也许是不正确的。

本研究发表于THE JOURNAL OF GENERAL VIROLOGY9月刊中。

后滞作用
当细胞内的遗传物质—DNA发生突变,导致细胞分裂不可控时,癌症就会发生。当DNA发生损伤时,就会出现突变。当病毒插入整合到细胞DNA后,最终就会产生上述突变的作用细胞分裂的不可控。两种乳头瘤状病毒(HPV)被认为通过这种突降导致宫颈癌。
通过插入细胞DNA中,病毒在体内的免疫系统中隐藏起来,所以机体的防御措施不可能清除它们。这意味着,研究者们后来能发现在宫颈癌背后的罪魁—HPV,病毒基因使其向犯罪现场的指纹一样。按照Stevenson的说法,大约有20%的癌症是由病毒引起的。
然而,细胞有很多防卫的机制去阻止肿瘤的生长,一些细胞固有的突变,能使细胞自毁使其不转变为癌。但是病毒却能影响这些防卫措施。
病毒最初不能导致癌症,但是它们的复制且使其具有相同的功能。所以,他们试图抑制所有的保护机制Stevenson病说,所有它们是导致癌症的理想方式
滞后作用假说提出,病毒不通过自身插入细胞DNA,也能导致癌症。这样的话,一个细胞产生突变后,病毒通过抑制本身的防卫机制使得细胞能继续存活,久而久之,积累了越来越多的突变,最后细胞变为癌性。然而,当癌症被发现时,病毒已经被免疫系统清除掉,就留不下指纹
许多年来,科学家们都猜测病毒利用这种机制导致癌症,但是很难被证明。


癌症疫苗
Stevenson
和他的同事希望了解:如果病毒不是通过插入细胞DNA导致癌症,那么我们多久才能找到在癌症细胞里病毒的踪迹。
他们使用基因工程小鼠,以便于感染疱疹病毒(含有能使鼠细胞分裂不可控的基因)后能产生癌症。
但是当他们后期检查鼠生长的肿瘤时,他们并没有检测到病毒。如果这在人类中也如此,那就意味着向EB这样的病毒能导致比原来多的多的癌症。
后来,研究者发现接种抵抗这些病毒的疫苗,能有效的阻止癌症的发生。当对鼠接种抗疱疹病毒疫苗是,所有鼠未发生癌症。
Stevenson
说,尽管在理论上抵抗EB病毒和疱疹病毒的疫苗能被生产,但是公司不想冒很大的风险,除非它们有重大的疾病威胁。

Stevenson
认为所有的疫苗都是风险和收益的平衡,因为含有EB病毒基因的癌症很少见,收益看起来很小,没有人愿意冒风险。但是如果人们知道这个病毒能导致许多可怕的癌症,那收益就会很大了。
Stevenson
提示现今试验证明,进行EB病毒或其他相似病毒疫苗的临床试验是值得的。
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