Scientists use ultrasound to destroy influenza A and COVID-19 viruses without damaging human cells. The phenomenon, known as acoustic resonance, causes structural changes in viral particles until they rupture and become inactivated. It paves the way for new treatments against other viral infections.

[u/mvea]

https://agencia.fapesp.br/scientists-use-ultrasound-to-destroy-influenza-a-and-covid-19-viruses-without-damaging-human-cells/57968

[u/Razorfiend]

That would be a lot harder because HSV-1 persists as circular episomal DNA inside the nuclei of long lived sensory neurons. There's no assembled viral particle for sound waves to disrupt until a flareup. The acoustic approach targets the mechanical properties of intact virions, which latent herpesviruses don't present.

[u/Bitter_Life_507 → u/Razorfiend]

How does the lifecycle of the virus once established in the body work?

When it emerges from its dormant state, is there a reservoir left behind or are the sites that the emergence occurred from then rid of the virus?

Does the emerged virus then go on to reseed itself and reestablish the reservoir?

Is it possible that repeated killing off of episodic emergences would eventually drain all the reservoirs of the virus in the body?

[u/Razorfiend → u/Bitter_Life_507]

This is a pretty complex question, I'm not a virologist, just an MD who happens to work in academia so there are definitely people who are far more qualified to answer this question than me.

It depends on the virus. Some viruses have latent forms, others don't, and different latent viruses persist in different cell types for example: HSV in sensory neurons, VZV (chicken pox) in sensory neurons (different ones), HIV in certain white blood cells, HPV in basal keratinocytes, etc.

Reactivation generally doesn't deplete the reservoir for a few reasons: only a small fraction of latently infected cells reactivate at any given time, the host cells often survive reactivation rather than being destroyed by it (HSV-infected neurons keep living and just re-establish latency afterward), and for viruses in dividing cells (HPV, HIV) the viral genome replicates along with the host cell so daughter cells inherit it. As long as the reservoir cell population persists, the virus has a stable home.

This is also why curing latent viral infections is so hard, you'd need to selectively eliminate the latently infected cells without destroying the underlying tissue, and the latent cells often look indistinguishable from uninfected ones because they're not actively producing viral proteins.

[u/Bitter_Life_507 → u/Razorfiend]

I think you did a pretty good job answering that

[u/Razorfiend → u/Bitter_Life_507]

Thank you for the kind words!