Why Do Our Cells Have Receptors For Viruses?

Shin

It's the reverse: Viruses evolve to fit our cell receptors.

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Viruses lack the machinery to reproduce on its own. They hijack on the host cell’s machinery instead. That’s why viruses are parasitic in nature.

Before the hijack, the virus must first attach to the cell surface. If the virus manages to bind to the proper receptor on it, virus entry is initiated. And virus replication and infection are established. This is a prerequisite for all known viruses.

One may ponder, why the receptor that binds to viruses exist in the first place?

In reality, it’s the virus that has evolved to fit the cell receptor. Viruses are clever in targetting the ‘conserved’ one to bind to. Conserved means conserved in function — that the cell receptor performs vital functions. Removing this conserved receptor might as well renders the cell useless. It can’t be removed and that's why viruses target it.

Example 1: HSPG Receptors

Heparan sulfate proteoglycan (HSPG) receptors are necessary for neural stem cells of the hippocampus — a brain area specialized for memory and learning — to receive growth signals for neurogenesis. HSPG receptors are, therefore, highly expressed when our brain is actively making new neurons.

Herpes simplex virus type-1 (HSV-1) exploits this conserved phenomenon — attaching to HSPG receptors prior to cell entry. This explains why HSV-1 easily sneaks into the hippocampus and creates disaster. And why HSV-1 has been gaining worldwide acknowledgment for its contribution to Alzheimer’s disease — a hippocampal disorder.

Other herpes viruses also interact with HSPG receptors: HSV-2, varicella-zoster virus (VZV), pseudorabies virus (PRV), human cytomegalovirus (HCMV), human herpesvirus 7 (HHV-7), and Kaposi’s sarcoma herpesvirus (KSHV or HHV-8).

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Example 2: Transferrin Receptors

This example is by far the most studied one. Transferrin receptor uptakes iron into the cell — a conserved receptor fundamental in life. Yet it facilitates the entry of viruses from 3 families — out of 23 families — known to infect mammals (e.g., herpesviruses is one type of family).

Here’s the interesting part: Although transferrin receptors can’t be removed, they can modify themselves at some intricate spots. This changes its structure slightly but sufficient to prevent the binding of viruses without compromising its original function.

By comparing the DNA sequences of the transferrin receptor from 7 different species of rodents, researchers have identified an ‘evolution hotspot’ at a small DNA section. This section has 3 amino acids which are binding sites for retroviruses (e.g., HIV, leukemia virus, lentivirus) and arenaviruses (e.g., Lassa, Junin, Sabia viruses). Changing any 3 of these amino acids can prevent virus entry while retaining its iron uptake function.

Viruses, however, evolve at a faster rate than a living cell due to their smaller genome yet higher multiplication rates and larger population sizes. The virus can simply change one nucleotide in its genome to tweak its structure to fit the cell receptor again.

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Evolutionary Arms Race

“Natural selection acts only by taking advantage of slight successive variations; she can never take a great and sudden leap, but must advance by short and sure, though slow steps,” Darwin wrote in the Origin of Species.

The evolutionary arms race between host cells and viruses has shaped their structures today, my lecturer — who has published HIV-focused papers in Nature — once explained. Indeed, this arms race is nothing but the competition between two adversaries via natural selection.

As Dr. Peter Kerr, a pioneer in the coevolution of myxoma virus (MYXV) and wild European rabbits, described it:

“The rabbits evolved resistance, the virus evolved ways to combat that resistance, and this continued in a back-and-forth, ever-escalating way,”

Or another explanation by Dr. Rich Berry from Monash Biomedicine Discovery Institute who studied the arms race between cytomegalovirus and human T-cells:

“…evolutionary arms race can be likened to a life or death game of chess. However, in this scenario molecules replace chess pieces and instead of moving pieces to attack or defend, the virus and host evolve or build new pieces tailored to suit their strategy.”

Sadly, it’s clear that viruses always win the arms race. That's why vaccines and antivirals are created. That’s why healthy lifestyles are promoted. That’s why policies to prevent the spread of infection are taught and implemented. All in an attempt to help human biology overcome its flaws.

This article was originally published in Microbial Instincts.

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MSc Biology student | 5x first-author academic papers | 100+ articles on coronavirus | Freelance medical writer

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