期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 24, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/ijms24054673
关键词
oxidative stress; immunomodulation; reactive oxygen and nitrogen species; redox homeostasis; antioxidant; innate immunity; adaptive immunity; antiviral therapy; plasma
Herpes simplex virus type 1 (HSV-1) is a contagious pathogen that causes lifelong infections. Current antiviral therapies are effective against HSV-1 replication in epithelial cells but not in neurons where the virus can remain dormant. Non-thermal plasma (NTP) therapy shows promise in controlling HSV-1 by manipulating oxidative stress responses and stimulating antiviral immune responses. NTP application can decrease the size of the viral reservoir in the nervous system, addressing the challenge of latency.
Herpes simplex virus type 1 (HSV-1) is a contagious pathogen with a large global footprint, due to its ability to cause lifelong infection in patients. Current antiviral therapies are effective in limiting viral replication in the epithelial cells to alleviate clinical symptoms, but ineffective in eliminating latent viral reservoirs in neurons. Much of HSV-1 pathogenesis is dependent on its ability to manipulate oxidative stress responses to craft a cellular environment that favors HSV-1 replication. However, to maintain redox homeostasis and to promote antiviral immune responses, the infected cell can upregulate reactive oxygen and nitrogen species (RONS) while having a tight control on antioxidant concentrations to prevent cellular damage. Non-thermal plasma (NTP), which we propose as a potential therapy alternative directed against HSV-1 infection, is a means to deliver RONS that affect redox homeostasis in the infected cell. This review emphasizes how NTP can be an effective therapy for HSV-1 infections through the direct antiviral activity of RONS and via immunomodulatory changes in the infected cells that will stimulate anti-HSV-1 adaptive immune responses. Overall, NTP application can control HSV-1 replication and address the challenges of latency by decreasing the size of the viral reservoir in the nervous system.
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