The evolution of the placenta

An interesting hypothesis postulates that the placenta was shaped by mammalian co-evolution with mutualistic, symbiotic viruses.

Placentalia

Animals can be viviparous (bearing live young inside the parents) or oviparous (storing young inside eggs). Mammals in the group placentalia have evolved to have a placenta. The placenta is a temporary organ, which provides new capabilities to assist viviparity. It facilitates the exchange of gas, nutrients, and waste between the foetus and the mother.

The placenta arises from the blastocyst. This develops into an embryoblast (which becomes the embyro) and a trophoblast. The trophoblast burrows into the blood supply in the uterine wall of the mother, and it develops into the placenta.

Placental viviparous species, such as humans, gained unique advantages compared to oviparous species and even other viviparous species. This allowed them to evolve down new avenues, to behave differently, and to exploit new ecological niches.

Viruses

The placenta is a relatively immune-privileged zone, making it ideal for viral replication, survival and proliferation. It is also a potential bridge for viruses to pass from parent to offspring.
The placenta confers competitive advantages to the placentalial host.
Therefore the placenta could support the continued existence of both parties.

Viruses are strongly mutagenic, with strong genetic engineering capabilities. Many years of research have confirmed that retroviruses can infect germline DNA, to produce offspring with a genome containing a new endogenous retrovirus element. 5–8% of the human genome is believed to be composed of endogenous retroviruses.

The genes necessary for placental generation and development may have been implanted by viruses into the genome of placentalia animals.  Such a process would have occured gradually over the course of countless generations, with continous selection pressure and mutagenesis caused by the symbiotic viruses.

Trial and error 

There are four possible outcomes to a de novo mutation.

1. A host is born with a new mutation in their genome. Their genome produces a functional placenta. The host is able to reproduce successfully and passes the functional genotype on to future generations. 
2. A host is born with a new mutation in their genome. Their genome produces a dysfunctional placenta. The host is unable to reproduce successfully, and fails to pass the faulty genotype onto future generations.
3. A host is born with a new mutation in their genome. Their genome produces a functional placenta with a small advantageous variation. This variation could be a loss of a redundant feature, or a gain of a beneficial feature. As this genotype has an advantage compared to their peers in the gene pool, they would be more likely to reproduce successfully. This is a competitive advantage. Over many generations, their offspring will have a higher rate of survival and successful reproduction. The prevalence of the new genotype will expand and become the majority in the gene pool. 
4. A host is born with a new mutation in their genome. Their genome produces a functional placenta with a small disadvantageous variation. This variation could be a loss of a beneficial feature, or a gain of a redundant feature. As this genotype has a disadvantage compared to their peers in the gene pool, they would be less likely to reproduce successfully. This is a competitive disadvantage. Over many generations, their offspring will have a lower rate of survival and successful reproduction. The prevalence of the new genotype will remain low in the gene pool. Eventually it may cease to exist. 

You can see how over time, the placenta could develop rapidly from nothing, to become a complex and useful organ.

 

Strength in mutualism

Why didn't the virus evolve to harm the hosts? Why didn't the host kill the viruses like it normally would? Consider the three potential outcomes here:

1. The viruses caused harm to the host, so the host and viruses died out.
2. The host caused harm to the viruses, or failed to transmit them to offspring, so the viruses died out. The host lost the advantage of the symbiosis and they lost the evolutionary arms race.
3. The viruses supported the hosts, so they were replicated and continued to exist. The host nurtured the viruses, so they kept a useful tool and won the evolutionary race.

 

Remember the microbiota

If you needed further convincing of this co-evolution, consider the mutualistic relationship between humans and other organisms. The human gut contains so many bacteria that the ratio of bacterial cells to human cells is estimated to be 1:1, or even 10:1. These bacteria have been extensively proven to be a blend of harmless commensals and useful mutualists. Humans and gut microbiota have co-evolved so intimately, that there is a proven two-way interaction between the microbiome and various human systems. Mood, metabolism and immunity are examples of such systems.

 

Nice hypothesis, but where is the proof? Read more:

• virology.ws: Retroviruses turned egg-layers into live-bearers
• discovermagazine.com: Mammals Made By Viruses
• pbs.org: The Viruses That Made Us Human
• journals.plos.org: The placenta goes viral: Retroviruses control gene expression in pregnancy
• sciencedirect.com: Retroviruses and the Placenta

I first wrote an essay about this hypothesis in 2014. I am pleased to see that by 2019, researchers have built a mountain of evidence to support this hypothesis. I'm also sad that the field has advanced so much, whilst I still haven't finished medical school.