(ORDO NEWS) — Viruses are very small, but still, in order to infect a living cell, they have to become even smaller.
Using the example of a virus that causes cancerous tumors in monkeys, scientists were able to fix exactly how the pathogen penetrates the wall of the cell nucleus and makes the cell’s genetic apparatus work for its own good.
To reproduce their own kind, viruses use the genetic apparatus of living cells – bacterial, plant, fungal or animal – to create the nucleic acids and proteins necessary to build new viral particles.
And if in the case of a bacterium, a non-nuclear organism, it is not difficult for a virus to get to its circular DNA molecule , then in all other cases the pathogen must first penetrate into the nucleus.
It is worth noting here that the nuclear membrane is not a solid wall at all: there are passages in it called nuclear pores.
Through these pores, the nucleus exchanges various molecules with the rest of the cell: proteins, RNA, and others.
Many viruses also enter the nucleus through pores, but how do they do it if the pore is not the right size?
To understand this, scientists looked at how the SV40 virus , which causes cancerous tumors in monkeys, interacts with the nuclear pore.
The whole virus is small, but definitely larger than the diameter of the nuclear pore – and yet somehow gets inside the nucleus so that its genetic material is integrated into the cellular DNA and begins to produce viral DNA and proteins.
It turned out that to solve this problem, the virus literally destroys itself: it gets rid of most of its protein shell, leaving only a couple of proteins and its own DNA.
In such a “thinner” form, SV40 binds to the nuclear pore protein and penetrates into the nucleus, after which it is freely integrated into cellular DNA.
The authors of the work emphasize: although SV40 is most likely not dangerous to humans, it belongs to carcinogenic viruses that can cause cancerous tumors in the host body.
Understanding exactly how viruses enter the nuclei of cells could help researchers develop new ways to protect against these pathogens by drug-blocking or genetically modifying nuclear pore proteins.
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