Fighting Viruses With Viruses

Study Finds Surprising Benefit of Viral DNA: Fighting Other Viruses

by Carl Zimmer

Have we domesticated viruses? This article from the New Your Times was very enlightening about the history of Viruses and humans. It is stated that viruses start replicating their own DNA once in a host cells, but I already new that much. The incredible thing is that over generations of viral replication, the virus start to lose the ability to burst back out of an infected cell. They become endogenous retroviruses that stay within the host cell, replicating, but unable to escape. It's at this point that the virus's DNA, trapped in close proximity with the DNA of the host cell, co mingle and becomes incorporated into the  DNA of the host cell. It is reported that as much as 8% of all our human DNA is from fragments of viral DNA taken up this way!

If your like me, you'd think having virus DNA incorporated into your own sounds like a bad thing, that the host taking in the fragment of virus DNA into their own would be perpetually sick or die. The weird truth thing is, it a good thing!  According to the article, we have been able to use the viral DNA to help us fight other viruses. They site a British study in which a protein called FV1, which prevents viruses from injecting their DNA into the hosts cells by latching onto the viruses first, was determined to originate from viral DNA.  There are apparently many virus fighting genes in our DNA that we have viruses to thank for. They apparently make it so that our immune system responds to incoming viruses faster and more efficiently, as proven by experiments where they cut out the viral DNA from the cell's DNA, and failed to fight off introduced viruses. 

Ancient Viruses, Once Foes, May Now Serve as Friends

About 8% of our genomes consist of DNA from ancient, dormant endogenous retroviruses; infectious cells that may have once plagued our ancestors. Scientists have recently discovered that these viruses do eventually "wake up", and at a critical time during embryonic development. One of the major proteins involved in maintaining undifferentiated cells during early development is Oct4, and it does so by latching on to DNA and turing genes on or off. One commonly targeted gene is that of the retrovirus HERV-K, and when it attaches it tells HERV-K to synthesize its viral RNA. Although it may seem scary to have these viral cells re-emerge, they don't seem to be infectious, and in fact play a key role in the development of the embryo. It was found that after this viral RNA synthesis occurs, the embryonic cell builds proteins to help ward off other infectious viruses. The viral RNA even aids as a transporter, bringing embryonic RNA to be translated into proteins. 

Human development is already an unbelievably complex and amazing process, having one embryonic cell transform into such a complex life form. I found this discovery pretty baffling, knowing that the remnants of ancient viruses live in us and actually aid our development. I hope they look into this further and find out what is really going on within the embryo, and what other potential affects these retroviral RNA could have. 

primary article- NYTimes

secondary article- Genomebiology

Mobile DNA Elements Can Disrupt Gene Expression and Cause Biological Variation, Study Shows

According to an article on the website of Science Daily,  a group of researchers at the Ohio State University Comprehensive Cancer Center found that transposons are can affect gene expression even if they are thousands of base pairs away from premature stop site in the genomic DNA. Another factor that determined whether or not the transposons affected the expression of gene was gender of the parent that the transposon was inherited from.

Transposons  are movable pieces of DNA, also called “jumping genes” as they can move from one location to another on a chromosome, but unlike viruses they can’t move from one cell to another. Transposons makeup half of the genomic DNA in humans and mice as they have accumulated in the genome over time.



The transposons studied in this research study were that of diverse mouse strains called endogenous retroviruses (ERVs). They found that ERVs disrupted the gene expression by halting gene transcription. If the gene containing an ERV came from the father it produced an incomplete form of mRNA but if it came from the mother a full length mRNA was produced from the gene.

According to an assistant professor of molecular virology, immunology and medical genetics Dr. David E Symer,  this an unusual example of DNA imprinting.They are in the process of determining how the transposon is able to trigger or halt the expression of the gene and also how the transposons affect the gene expression differently based on the gender of the parent that it came from. Dr. Symer says these finding are important in understanding mechanisms of natural variation and human biology also cancer and other diseases.