A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Topical treatment of herpes simplex virus infection with enzymatically created siRNA swarm
Tekijät: Henrik Paavilainen, Jenni Lehtinen, Alesia Romanovskaya, Michaela Nygårdas, Dennis H Bamford, Minna M Poranen, Veijo Hukkanen
Julkaisuvuosi: 2017
Journal: Antiviral Therapy
Tietokannassa oleva lehden nimi: Antiviral therapy
Lehden akronyymi: Antivir Ther
Vuosikerta: 22
Numero: 7
Aloitussivu: 631
Lopetussivu: 637
Sivujen määrä: 7
ISSN: 2040-2058
DOI: https://doi.org/10.3851/IMP3153
Tiivistelmä
Abstract
Background: Herpes simplex virus (HSV) is a common human
pathogen. Despite current antivirals, it causes a significant medical
burden. Drug resistant strains exist and they are especially prevalent
in immunocompromised patients and in HSV eye infections. New treatment
modalities are needed.
Methods: BALB/c mice were corneally
infected with HSV and subsequently treated with a swarm of enzymatically
created, Dicer-substrate small interfering RNA (siRNA) molecules that
targeted the HSV gene UL29. Two infection models were used, one in which
the infection was predominantly peripheral and another in which it
spread to the central nervous system. Mouse survival, as well as viral
spread, load, latency and peripheral shedding, was studied.
Results:
The anti-HSV-UL29 siRNA swarm alleviated HSV infection symptoms,
inhibited viral shedding and replication and had a favourable effect on
mouse survival.
Conclusions: Treatment with anti-HSV-UL29 siRNA
swarm reduced symptoms and viral spread in HSV infection of mice and
also inhibited local viral replication in mouse corneas.
Abstract
Background: Herpes simplex virus (HSV) is a common human
pathogen. Despite current antivirals, it causes a significant medical
burden. Drug resistant strains exist and they are especially prevalent
in immunocompromised patients and in HSV eye infections. New treatment
modalities are needed.
Methods: BALB/c mice were corneally
infected with HSV and subsequently treated with a swarm of enzymatically
created, Dicer-substrate small interfering RNA (siRNA) molecules that
targeted the HSV gene UL29. Two infection models were used, one in which
the infection was predominantly peripheral and another in which it
spread to the central nervous system. Mouse survival, as well as viral
spread, load, latency and peripheral shedding, was studied.
Results:
The anti-HSV-UL29 siRNA swarm alleviated HSV infection symptoms,
inhibited viral shedding and replication and had a favourable effect on
mouse survival.
Conclusions: Treatment with anti-HSV-UL29 siRNA
swarm reduced symptoms and viral spread in HSV infection of mice and
also inhibited local viral replication in mouse corneas.
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