原來上帝真的有設定一鍵刪除功能ㄝ？
https://is.gd/EO6B9y
一份新研究發現，數千年前、甚至數百萬年前混入人類基因組的古老的病毒基因，即便整
體病毒處於休眠狀態，可是其某些基因仍然是活躍的，可以產生病毒蛋白質。而這些蛋白
質似乎隨時在準備啟用病毒，一旦外界的條件合適，這些病毒就會在人體中起破壞作用。
一份由美國華盛頓大學醫學院和加拿大拉瓦爾大學（Laval University）醫學院聯合完成
的研究稱，這項發現可能有助於解釋為什麼繼承了這些古老病毒基因的人群罹患多發性硬
化症和老年失智症（Alzheimer’s）的風險更高。
華盛頓大學實驗醫學助理教授格雷寧格（Alex Greninger）說：「曾發現過皰疹病毒6（
HHV-6）在人體內被重新啟用的案例，但是很罕見，我們想知道，在整個病毒不被啟用的
情況下，這些病毒中的單個基因是否會被啟用。」
這份研究關注的是皰疹病毒6的兩個版本HHV-6B和HHV-6A。前者引發小兒急疹（roseola，
俗稱奶疹、假麻疹），90%的兒童都會遇到的常見兒童疾病，症狀為發燒和紅疹等；對後
者的了解目前甚少。兩種病毒感染人體後都可以保持休眠狀態，以後在合適的情況下又會
重新啟用，比如在免疫系統受抑制的情況下。
這次研究對像體內的病毒不是通過感染得到，而且從基因中遺傳而來，大約1%的人都會遺
傳這種病毒。人體基因中約8%來自遠古時期混入的病毒，很多時候可以追溯到數百萬年前
的遠古人類。
研究者對650位志願者進行了基因測序，結合40份器官組織細胞RNA樣本進行分析。
結果顯示其中6人攜帶HHV-6基因，兩人攜帶HHV-6A，四人攜帶HHV-6B。RNA測序分析顯示
，這些人體內兩種病毒基因U90和U100是活躍的。
在大多數組織樣本中，這些病毒基因的表徵水平很低，然而在食道、睪丸、腎上腺和大腦
這些組織樣本中表徵水平最高。U100掌管病毒外殼的部分蛋白質，U90是一種蛋白啟用劑
，負責促進其它基因的表徵。
格雷寧格說，尚不明確這些蛋白質可能對人體細胞產生哪些影響，然而鑒於U90的主要作
用是啟用病毒基因組，「它幾乎就是這些遠古病毒嘗試在啟用自己的表現」。
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原文轉載：
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.