Let's talk about viruses that SWITCH SIDES.
You may know:
~8% of human genome is made up of HERVs (human endogenous retroviruses).
They've thrown their lot in with us: we preserve them in our genome & they protect us from other viruses.
Viruses on 'Team Human'.
Pet Viruses.
You may know:
~8% of human genome is made up of HERVs (human endogenous retroviruses).
They've thrown their lot in with us: we preserve them in our genome & they protect us from other viruses.
Viruses on 'Team Human'.
Pet Viruses.
HERV sequences & products shape & are shaped by our immune systems.
Our cells sometimes recognize them as internal viral invaders & express gene products related to viral immunity, the interferon pathways. This can lead to autoimmunity OR control of excessive immune activity.
Our cells sometimes recognize them as internal viral invaders & express gene products related to viral immunity, the interferon pathways. This can lead to autoimmunity OR control of excessive immune activity.
A particular one, HERV-K(HML10) landed in the Major Histocompatibility Region (MHR) and is responsible for some human variation in tissue donation compatibility.
HERV-W derived syncytin-1 and syncytin-2 (modified retroviral envelope genes) are actively expressed in placenta during embryonic development & help maintain immune feto-maternal tolerance.
pubmed.ncbi.nlm.nih.gov/19407656/
pubmed.ncbi.nlm.nih.gov/19407656/
Finally & most importantly, some HERVs are part of our innate resistance to viruses, directly targeting their pathogenic cousins and defending us against invaders.
This paper is a great starting point on the subject:
journals.asm.org/doi/10.1128/JV…
I'll summarize it.
This paper is a great starting point on the subject:
journals.asm.org/doi/10.1128/JV…
I'll summarize it.
Cells have a class of defenses called pattern recognition receptors (PRRs) that recognize things like double-stranded RNA or RNA/DNA hybrids, hallmarks of viral infection... but these defenses can be tricked/ knocked out by pathogenic viruses.
Say the sneaky bad guy virus (SBGV) finds a way to bind up our double-stranded RNA detector/alarm. The HERV products, normally controlled at low levels, now start to accumulate up to levels that directly trip the alarm to activate viral defenses.
Alternatively, the SBGV could go through a single-stranded RNA intermediate that doesn't trip our innate defenses to double-stranded RNA.
The HERV sequences match the bad virus just enough to form double-stranded stretches that trigger that alarm.
The HERV sequences match the bad virus just enough to form double-stranded stretches that trigger that alarm.
Our HERV's could just be coding for proteins that are part of the inner core of their self-assembly complex (gag)... which, when it encounters a bad guy virus, binds to the outer coat (capsid), trying to make an inside on the outside of the virus and inactivating it.
There are lots of other ways that our pet viruses protect us, shape and are shaped by our innate immunity to viral infection.
I think it helps to be reminded how important viruses have been in our evolution: our comrades-in-arms as well as our enemies.
I think it helps to be reminded how important viruses have been in our evolution: our comrades-in-arms as well as our enemies.
Like a wolf turned guard dog, HERVs didn't so much stop being what they are: they became part of a suite of evolutionary selection tied to human survival & fitness.
It's important that we continue to study and document the impact of viruses on human health, good and bad.
It's important that we continue to study and document the impact of viruses on human health, good and bad.
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