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Pathogen virus work in a simple way: they inoculate their genes (DNA or RNA) in the host cells and let them replicate huge amounts of the attacker while hampering the host vital functions. As reaction the host fights back, until either the host or the guest is dead.

I am trying to figure out a "smart" virus, which only inoculates its genes and does no alteration of the host metabolism.

It targets any cell, but has a predilection for the gonad cells, so that whenever the host mates will also transfer the virus to the offspring. Bonus of this scenario is that the offspring will see the virus as "self", so won't even try to defeat it.

Is this a realistic scenario or am I neglecting something?

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    $\begingroup$ Sounds an awful lot like herpes to me $\endgroup$ – Joe Bloggs Feb 14 '17 at 9:47
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    $\begingroup$ @JoeBloggs After all it's Valentine's day. $\endgroup$ – PatJ Feb 14 '17 at 10:12
  • $\begingroup$ If you're using a genital-based STD, you may have a hard time getting away with no symptoms. Many of those spread through cysts, cold sores, and other bumps that can release fluid once torn. Not that other fluids don't work. $\endgroup$ – Zxyrra Feb 15 '17 at 2:24
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What you propose is totally reasonable virus strategy and happens all the time. Your description of a stormy viral infection is one edge of a spectrum. Chronic stable viral infections, heritable viruses partly integrated into the genome, and ancient viral fragments all exist. This paper calls ancient viral fragments in the host genome "viral fossils" which I think is cool. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3205384/

A fine example of what you are looking for is hepatitis B. Hundreds of millions of people carry hepatitis B. Many of them are infected at birth from their mothers, and themselves carry the virus lifelong, infecting their own progeny. @PatJ here writes infected cells must die to release virus but this is not true: cells can shed virus and go about their business. Just as I am certain that my sinonasal epithelium is at this moment shedding virus for my coworkers to inhale yet that epithelium is not dying; I would notice the bloody slough coming out my nose.

From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC98986/ Hepatitis B biology.

One of the reasons for chronic HBV infections is that the virus causes chronic, noncytocidal infections of hepatocytes, the principal cell type of the liver. Hepatocytes continuously shed virus into the bloodstream, ensuring that 100% of the hepatocyte population is infected.

Cell and virus have many, many types of coexistence. Viruses are the oldest parasite.

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Use Adenovirus

Gene therapy can use Adenovirus as a vector to modify a cell's DNA.

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In order to replicate, viruses introduce their genetic material into the host cell, tricking the host's cellular machinery into using it as blueprints for viral proteins. Scientists exploit this by substituting a virus's genetic material with therapeutic DNA. (The term 'DNA' may be an oversimplification, as some viruses contain RNA, and gene therapy could take this form as well.) A number of viruses have been used for human gene therapy, including retrovirus, adenovirus, lentivirus, herpes simplex, vaccinia and adeno-associated virus.[3] Like the genetic material (DNA or RNA) in viruses, therapeutic DNA can be designed to simply serve as a temporary blueprint that is degraded naturally or (at least theoretically) to enter the host's genome, becoming a permanent part of the host's DNA in infected cells.

It wouldn't be outside the realms of science to target the adenovirus at a particular cell type (viruses do this anyway).

How you modify the recipient cell's DNA is up to you and your research team.

So, your theory is totally legit.

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    $\begingroup$ The problem is, you lose the "pathogen" part as the virus doesn't reproduce. $\endgroup$ – PatJ Feb 14 '17 at 10:10
  • $\begingroup$ That probably doesn't matter if you're encoding the genes to insert an inoculation that can be passed on to the next generation. You don't really have to pass on a virus when you can pass on the desired effect... $\endgroup$ – user10945 Feb 14 '17 at 10:16
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There are a few little problem.

First, inoculating its gene (and having the cell using them) is in itself a modification of the cell's metabolism. It can be a very minor one, but it's always a modification.

In order to be released and to continue expansion, the virus needs the infected cell to die. Because the new viruses are within the cell, the usual way for them to get out is to over-produce viruses until the cell dies, releasing all the newly-made death machines (note: death machine is not a biological term as far as I know).

If you want your virus to truly be "mild", you'll need it to find a way to escape the cell. It is possible, though it would require a more complex virus. The more complex, the more improbable.

So I would say "not likely, but possible".

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  • $\begingroup$ That's the point I am trying to achieve: renounce to massive spreading on short term in exchange of massive delayed spreading (an offspring body contains billions of infected cells) $\endgroup$ – L.Dutch - Reinstate Monica Feb 14 '17 at 9:25
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My understanding of these issues is cursory at best, but you might be interested in endogenous retroviruses. I cringe when I try to explain this because I am by no means a biologist, but my understanding is that viral infections in our ancestors could permanently transfer genetic material into our DNA which was then passed down the generations in the usual way. The Wikipedia page I linked claims these ERVs comprise some 5-8% of the entire human genome. They're often non-coding (i.e. no known function); I guess they might arise when a viral sequence mutates in such a way that it's no longer pathogenic, but the sequence is nevertheless still there and still propagated by cell replication.

In fact, one of the ways we can see when our evolutionary path diverged from that of various other animals is by seeing which parasitic viral sequences we have in common with them, which must have arisen from infections of our common ancestors.

We've even observed what's called horizontal gene transfer (much more common in single-celled organisms, but relatively recently demonstrated in multicellular life too), where a virus can pick up a fragment of one species' genetic sequence and deposit it in the sequence of another.

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