Pressurized DNA state inside herpes capsids-A novel antiviral target
Brandariz-Nuñez, Alberto ; Robinson, Scott J and Evilevitch, Alex LU
(2020)
In PLoS Pathogens
16(7).
- Abstract
Drug resistance in viruses represents one of the major challenges of healthcare. As part of an effort to provide a treatment that avoids the possibility of drug resistance, we discovered a novel mechanism of action (MOA) and specific compounds to treat all nine human herpesviruses and animal herpesviruses. The novel MOA targets the pressurized genome state in a viral capsid, "turns off" capsid pressure, and blocks viral genome ejection into a cell nucleus, preventing viral replication. This work serves as a proof-of-concept to demonstrate the feasibility of a new antiviral target-suppressing pressure-driven viral genome ejection-that is likely impervious to developing drug resistance. This pivotal finding presents a platform for... (More)
Drug resistance in viruses represents one of the major challenges of healthcare. As part of an effort to provide a treatment that avoids the possibility of drug resistance, we discovered a novel mechanism of action (MOA) and specific compounds to treat all nine human herpesviruses and animal herpesviruses. The novel MOA targets the pressurized genome state in a viral capsid, "turns off" capsid pressure, and blocks viral genome ejection into a cell nucleus, preventing viral replication. This work serves as a proof-of-concept to demonstrate the feasibility of a new antiviral target-suppressing pressure-driven viral genome ejection-that is likely impervious to developing drug resistance. This pivotal finding presents a platform for discovery of a new class of broad-spectrum treatments for herpesviruses and other viral infections with genome-pressure-dependent replication. A biophysical approach to antiviral treatment such as this is also a vital strategy to prevent the spread of emerging viruses where vaccine development is challenged by high mutation rates or other evasion mechanisms.
(Less)
- author
- Brandariz-Nuñez, Alberto
; Robinson, Scott J
and Evilevitch, Alex
LU
- organization
- publishing date
- 2020
- type
- Contribution to journal
- publication status
- published
- subject
- in
- PLoS Pathogens
- volume
- 16
- issue
- 7
- article number
- e1008604
- publisher
- Public Library of Science (PLoS)
- external identifiers
-
- pmid:32702029
- scopus:85088517170
- ISSN
- 1553-7374
- DOI
- 10.1371/journal.ppat.1008604
- language
- English
- LU publication?
- yes
- id
- c7b315f4-44aa-4e40-b7eb-bdd51c6e8681
- date added to LUP
- 2020-07-28 20:39:42
- date last changed
- 2025-10-14 08:54:00
@article{c7b315f4-44aa-4e40-b7eb-bdd51c6e8681,
abstract = {{<p>Drug resistance in viruses represents one of the major challenges of healthcare. As part of an effort to provide a treatment that avoids the possibility of drug resistance, we discovered a novel mechanism of action (MOA) and specific compounds to treat all nine human herpesviruses and animal herpesviruses. The novel MOA targets the pressurized genome state in a viral capsid, "turns off" capsid pressure, and blocks viral genome ejection into a cell nucleus, preventing viral replication. This work serves as a proof-of-concept to demonstrate the feasibility of a new antiviral target-suppressing pressure-driven viral genome ejection-that is likely impervious to developing drug resistance. This pivotal finding presents a platform for discovery of a new class of broad-spectrum treatments for herpesviruses and other viral infections with genome-pressure-dependent replication. A biophysical approach to antiviral treatment such as this is also a vital strategy to prevent the spread of emerging viruses where vaccine development is challenged by high mutation rates or other evasion mechanisms.</p>}},
author = {{Brandariz-Nuñez, Alberto and Robinson, Scott J and Evilevitch, Alex}},
issn = {{1553-7374}},
language = {{eng}},
number = {{7}},
publisher = {{Public Library of Science (PLoS)}},
series = {{PLoS Pathogens}},
title = {{Pressurized DNA state inside herpes capsids-A novel antiviral target}},
url = {{http://dx.doi.org/10.1371/journal.ppat.1008604}},
doi = {{10.1371/journal.ppat.1008604}},
volume = {{16}},
year = {{2020}},
}