The standard model of a virus is that it is non-living, it is a strand of RNA and is inherently destructive. While some parts of these descriptors may be correct in some scenarios, it would not be wise to tarnish all viruses with the same brush. Because our understanding of viruses is pretty recent, we have yet to wrap our mind around it and misconceptions remain. Recent scientific discoveries are challenging our basic assumptions.
Connecting humans and viruses: We share around 9% of our DNA with viruses. Called human endogenous retroviruses (HERV), these trace their origin from retroviruses. Unlike viruses, retroviruses, however, use a slower, stealthier approach. After entering the cell, the retrovirus uses an enzyme called reverse transcriptase to turn its RNA into DNA before making its way to the nucleus. Once in the nucleus, it inserts its DNA into the host’s genome. The virus, however, wasn’t actively transmitted from animal to the other. Instead, a retrovirus had embedded itself in the germline and passed from parent to child. While such insertion typically happened millions of years ago, researchers in the year 2000, saw this happening on Koalas right before their eyes. This is remarkable considering that retroviruses have introduced themselves only 30-40 times into the human genome in the past 60 million years.
Oxford Professor Aris Katzourakis, remarks “It (HERV) is changing how we think of ourselves as a species. Such an intimate interaction between ourselves and these viruses, and exchanging DNA that’s useful for us, has really molded how we’re now thinking of ourselves as a dynamic soup of DNA that’s now infiltrated by viruses,”
Let us begin by discussing HERV-K. According to research, HERV-K may also have played an important role in separating some of the first humans from their primate ancestors by making small adjustments in when certain genes were switched on or off. It activates key genes that help transform a single cell into a fully-formed infant. These HERV-K viral particles and proteins also help protect the tiny ball of cells from being infected by other viruses. HERV-H plays an instrumental in switching embryo cells into adult cells and vice-versa. A protein Syncytin is produced only by certain cells in the placenta, and it directs the formation of the cellular boundary between the placenta and maternal tissue. When scientists looked closer at the DNA sequence of syncytin, they found that it was nearly identical to a viral protein called env that caused the virus to fuse with its host cell. In the placenta, syncytin performed helped the fetus fuse with its mother. Humans aren’t the only species with a placenta, however. All mammals have placentas, including marsupials and egg-laying mammals. Although all of these mammals have a syncytin gene, they don’t all have the same syncytin gene. The syncytin produced by mice is completely different from the two syncytins found in humans and other primates. At numerous points in mammalian evolution, symbiotic retroviruses entered the genome and steered different groups of mammals along different evolutionary paths.
Transposons: 44% of all genetic material in humans is made of transposable elements also called transposons or jumping genes. These molecular parasites behave very much like viruses and ensure their own replication at every cost to the host cell. Just one transposon, the ALU sequence alone is estimated to make up 15–17% of the human genome. ALU insertions have been implicated in various types of cancers, sarcoma, hemophilia, diabetes and Alzheimer’s disease. At the same time, ALU insertions have also helped with the evolution of color vision in primates. Similar double agent roles of transposons include helping animal cells get immunity from microbes and also helping microbes get immunity from antibiotics. Paradoxically, transposons have played a key role in the formation of the placenta, formation of embryos, DNA methylation and aging.
Polintons: Also called Mavericks, they are DNA transposons that are widespread in cellular genomes. Polintons were the first group of cellular double-stranded DNA viruses to evolve from phages and that they gave rise to most large DNA viruses in cells like the Adenovirus and various other selfish genetic elements. Plasmids are very important component of all cells in the animal kingdom including animals and humans. Plasmids come from Polintons, the adenovirus ancestors. An old Polinton somehow left the nucleus with the new proteins and then evolved into Magavirales and these plasmids in the cytoplasm.
It is estimated that Adenoviruses which emerged from Polintons had started to coevolve with the vertebrates 450 million years ago, before the divergence of fish from other vertebrates. The fact that they exist in the genomes of protists, fungi, and all animals shows that Polintons are extremely ancient, with research indicating at least a billion years old. Evidence of even older ancestry comes from the fact that Polintons make proteins that are similar to the Major and Minor Capsid Proteins. These proteins construct the complex icosahedral geometric forms of the common double-stranded DNA virus covers for all three cellular kingdoms. The Polinton major capsid protein is similar to the large Megavirales family of viruses. This connects Polintons with the largest viruses and with smaller double-stranded viruses.
Let me close with a funny and thought provoking discussion. Humans are not only part virus but also part banana. Researchers from Cambridge reveal that while we share around 50% of our DNA with our parents, we share 50% of our genes with bananas. This interesting conundrum is resolved when you understand that genes – the regions of DNA that code for proteins – only make up about 2% of your DNA. “So sharing 50% of our genes with bananas means we only actually share 1% of our DNA with them. But animals and plants share a common ancestor – a single-celled life form which probably lived about 1.6 billion years ago. The genes that we share with bananas would have been present in that ancestor, and have been passed down to all animals and plants alive today. And the reason that we’ve kept these genes, is that they’re involved in fundamental cell processes – like making energy and repairing damage. Just like that single-celled ancestor, and our banana relatives, we need these processes to survive – and so we share half of our genes, but not half of our DNA with bananas.”
“The boundaries between organisms are a bit more merged now, a bit more shadowy. We need to break down those boundaries,” says University of Queensland virologist Paul Young. “The more we look, the more we find overlap.”
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