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一份新研究发现，数千年前、甚至数百万年前混入人类基因组的古老的病毒基因，即便整
体病毒处于休眠状态，可是其某些基因仍然是活跃的，可以产生病毒蛋白质。而这些蛋白
质似乎随时在准备启用病毒，一旦外界的条件合适，这些病毒就会在人体中起破坏作用。
一份由美国华盛顿大学医学院和加拿大拉瓦尔大学（Laval University）医学院联合完成
的研究称，这项发现可能有助于解释为什么继承了这些古老病毒基因的人群罹患多发性硬
化症和老年失智症（Alzheimer’s）的风险更高。
华盛顿大学实验医学助理教授格雷宁格（Alex Greninger）说：“曾发现过疱疹病毒6（
HHV-6）在人体内被重新启用的案例，但是很罕见，我们想知道，在整个病毒不被启用的
情况下，这些病毒中的单个基因是否会被启用。”
这份研究关注的是疱疹病毒6的两个版本HHV-6B和HHV-6A。前者引发小儿急疹（roseola，
俗称奶疹、假麻疹），90%的儿童都会遇到的常见儿童疾病，症状为发烧和红疹等；对后
者的了解目前甚少。两种病毒感染人体后都可以保持休眠状态，以后在合适的情况下又会
重新启用，比如在免疫系统受抑制的情况下。
这次研究对像体内的病毒不是通过感染得到，而且从基因中遗传而来，大约1%的人都会遗
传这种病毒。人体基因中约8%来自远古时期混入的病毒，很多时候可以追溯到数百万年前
的远古人类。
研究者对650位志愿者进行了基因测序，结合40份器官组织细胞RNA样本进行分析。
结果显示其中6人携带HHV-6基因，两人携带HHV-6A，四人携带HHV-6B。RNA测序分析显示
，这些人体内两种病毒基因U90和U100是活跃的。
在大多数组织样本中，这些病毒基因的表征水平很低，然而在食道、睾丸、肾上腺和大脑
这些组织样本中表征水平最高。U100掌管病毒外壳的部分蛋白质，U90是一种蛋白启用剂
，负责促进其它基因的表征。
格雷宁格说，尚不明确这些蛋白质可能对人体细胞产生哪些影响，然而鉴于U90的主要作
用是启用病毒基因组，“它几乎就是这些远古病毒尝试在启用自己的表现”。
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原文转载：
Genes From ‘Fossil’ Virus In Human DNA Found To Be Active
November 11, 2019
Genes from a virus that was stitched into the human genome thousands of years
ago are active, producing proteins in the human brain and other tissues,
according to researchers at the University of Washington School of Medicine
and the Laval University School of Medicine in Quebec, Canada.
Their finding might help explain why people who inherit this “fossil virus”
appear to have a higher risk of developing neurodegenerative diseases such
as multiple sclerosis and Alzheimer’s.
“There have been some reports that the virus, called human herpesvirus-6,
can reactivate, but if it does, it’s rare,” said Dr. Alex Greninger, UW
assistant professor of laboratory medicine. “What we wanted to know whether
some of the virus’ individual genes were being turned on without full
reactivation of the virus.”
Genes from ‘fossil’ virus in human DNA found to be active
Alex Greninger of the UW School of Medicine, left, and Louis Flamand of Laval
University in Quebec were research project co-leads.
The Journal of Virology published the article recently. Its lead authors were
Vikas Peddu, a bioinformatician in the Greninger lab, and Isabelle Dubuc of
Laval University. The project was led by Greninger and Louis Flamand,
professor in the microbiology and immunology at Laval.
The researchers were interested in two versions of human herpesvirus-6
(HHV-6) that can integrate into chromosomes and be inherited like any other
human gene. HHV-6B causes the common childhood illness, roseola. This
infection affects about 90 percent of children early in life, causing high
fevers and rash. However, relatively little is known about the second virus,
HHV-6A. After infection, both viruses can remain dormant in the body and
reactivate later, particularly in people whose immune systems are suppressed.
In the new study, the researchers looked at a form of the virus that is not
acquired by infection but which about one in a hundred people inherit as part
of their genome. About 8 percent of human DNA comes from viruses inserted
into our genomes in the distant past, in many cases into the genomes of our
pre-human ancestors millions of years ago.
Most of these viral genes come from retroviruses, RNA viruses that insert DNA
copies of their own genes into our genomes when they infect cells. HHV-6 is
unique because it is the only known human DNA herpesvirus that integrates
into the human genome and can be routinely inherited. HHV-6’s genome may
have been accidentally copied into the human genome because it has repeating
DNA sequences that resemble those found in human chromosomes.
In conducting the study, the investigators analyzed a database of genome
sequences of 650 people who gave consent before they died for their DNA
genomes to be researched. The scientists also had access to cellular RNA in
up to 40 tissue samples.
Since cells must convert the instructions of active genes into RNA before
they can be used to make proteins, different RNA sequences in different
tissues reveal which genes are active and inactive in different cell types.
“A lot of human genomicists have overlooked these integrated HHV-6 sequences
in human genomes. They’re not in the human reference sequences and they’re
not common enough to rise on the radar,” Greninger said.
The researchers identified six individuals who had HHV-6 integrated in their
genomes: two with HHV-6A and four with HHV-6B. The RNA sequences revealed
that in these individuals, a number of viral genes were being actively
expressed, in particular one gene called U90 and another called U100.
In most tissues, the level of expression was low and sporadic, but the
highest expressions were found in the esophagus, testes, adrenal gland and
brain. The gene U100 codes for a viral protein that is part of the viral
outer shell, or envelope. U90 codes for a protein known as a transactivator,
which means it promotes the expression of other genes.
Working with samples they had collected as part of another study, the
Canadian researchers showed that individuals with the inherited HHV-6 genes
mounted a greater immune response to viral proteins.
“This suggests that even though the viral genes had been long been part of
their genome, the immune systems of people who carried the genes still
recognized the viral proteins as foreign,” said Flamand. “We still need to
know more how the immune system gets educated by or against these endogenous
viruses to understand what this increased immune response against HHV-6
proteins means.”
What biological effect these proteins may be having on human cells is
unknown, Greninger said. “The transactivator protein U90 is primarily
responsible for turning on the viral genome. It almost as though this
fossilized virus is trying to reactivate itself.”
“One question we want answer is, ‘What effect does having this 150 kb viral
genome present enact on expression of your human genes? We don’t know
because it is present only in about 1% of the population. It will require
analysis of data from very large biobanks that have associated RNA
transcription sequences and the full medical records of the participants to
identify which diseases these inherited HHV-6 genomes may play a role in,”
he said.
This work was made possible with grants from the Heart and Stroke Foundation
of Canada and Canadian Institutes of Health Research.