Recurring Cold Sores – Morning Sign Out at UCI

Written by Christina Young and Edited by Kevin Liu

It is not uncommon to see people with painful blisters at the corner of their mouths, making it hard for them to eat and drink normally. Colloquially called cold sores, these blisters commonly form dry, bleeding, open wounds around one’s mouth, and are typically triggered by stressful situations. They can last anywhere between a couple of days to a month and signify an active viral infection caused by Herpes Simplex Virus 1, or HSV-1. Between 2015-2016, the CDC found that approximately 48% of the U.S. population have HSV-1 in a survey, although this is regarded as a low estimate [1]. In the presence of cold sores, it is quite easy to spread an HSV-1 infection through saliva contact, such as kissing or sharing the same glass, but with the absence of the sores, the risk of transmission through saliva contact is reduced [2]. Rather, cold sores are the product of the viral transmission to new hosts, yet the virus remains dormant when cold sores are absent. The infection caused by HSVs usually are benign and do not cause severe disease, although they can attack the central nervous system in rare cases.

HSV-1 is part of a family of viruses that have DNA as their genetic material, which confers special interactions with the DNA in human cells. Furthermore, the family the HSV-1 virus belongs to includes varicella zoster, known for causing chicken, Kaposi’s sarcoma, herpes simplex virus 2, known for genital herpes, amongst others [3]. As a DNA virus, HSVs can become “latent”—essentially going dormant until some amount of stress reactivates, producing cold sores [3]. Specifically, HSVs will go latent in peripheral regions of the nervous system, hiding until the time is right. Consequently, HSV-1 infections will remain with an infected individual for their entire lives, and there are currently no treatments or vaccines [4]. However, over-the-counter cold sore medications can help reduce inflammation of the blister.

Until recently, it was not understood that different versions of HSV-1, all of which cause cold sores, could differ in their ability to reactivate [4]. A study recently published from the University of Florida evaluated this matter between the HSV-1 strains 17syn+ and KOS(M), two common laboratory strains, in mice and rabbit models [5]. Initially, it was known that KOS(M) spreads throughout the body at a faster rate than 17syn+, each using slightly different proteins in its life cycle, but researchers took this a step further. It was found that KOS(M) invades the nervous system less often than 17syn+, which restricts its harmfulness so that it can stay in the host longer. Since latency occurs mostly in nerve tissue, the study suggested that reactivation of HSV-1 for cold sores is more likely due to 17syn+ than KOS(M) [5]. To the general public, strain differences in infections causing cold sores may not hold much value, but this serves as an example of modeling how herpes infections can be approached in terms of vaccine discovery and preventing infections [4]. These show that even for well-characterized viruses, like HSV-1, strain differences and their effects are important factors in understanding infectivity and developing treatment for specific diseases based on their life cycle.

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