A Nurse Practitioner's Guide to the Management of Herpes Simplex Virus-1 in Children

Janel M. Drugge, MSM, RN, PNP; Patricia Jackson Allen, MS, RN, PNP, FAAN


Dermatology Nursing. 2008;20(6):455-466. 

In This Article

Endogenous and Exogenous Triggers to HSV-1 Outbreaks

Factors believed to trigger recurrent HSV-1 infections have not been completely identified, but endogenous factors, such as immune suppression or deficiency (Logan, Lutgendorf, Hartwig, Lilly, & Berberich, 1998), emotional and physical stress (Buske-Kirschbaum, Geiben, Wermke, Pirke, & Hellhammer, 2001; Logan et al., 1998), menstruation (Raborn & Grace, 1999), illness (Dalkvist, Wahlin, Bartsch, & Forsbeck 1995; Ichihashi, Nagai, & Matsunga, 2004), and fatigue (Dalkvist et al., 1995; Yeung-Yue et al., 2002) have been noted. Exogenous factors, including ultra-violet radiation (Dalkvist et al., 1995; Femiano, Gombos, & Scully, 2005), tissue damage (Yeung-Yue et al., 2002), severe cold and hot weather (Raborn & Grace, 1999; Yeung-Yue et al., 2002), wind (Raborn & Grace, 1999), and trauma to the mouth (Femiano et al., 2005), have been associated with recurrent HSV-1 infections.

A few studies have tried to determine the exact mechanism stress has on herpes outbreaks. Logan et al. (1998) reported emotional stress was most often stated by persons with secondary HSV-1 infections as the main cause of recurrent outbreaks. Logan and colleagues (1998) conducted a prospective and longitudinal study to compare daily mood states and weekly changes in plasma levels of three immune and neuroendocrine markers of persons with recurrent herpes labialis lesions. Nine healthy participants between the ages of 20 and 40 years old with a history of recurrent herpes labialis were included in the study. Each participant had baseline and weekly blood draws; kept daily diaries of mood, alcohol intake, stress, and sleep; and participated in two psychological assessment tools. The authors concluded that an increased level of emotional arousal leads to an elevation in epinephrine levels that correlates with recurrent HSV-1 lesions (Logan et al., 1998). A major limitation to the study was the small sample size of nine participants.

By contrast, Dalkvist and colleagues (1995) conducted a prospective study on 28 participants with recurrent oral herpes to determine if mood, the common cold, amount of sleep, and sunshine correlated with recurrent HSV outbreaks. Each participant kept a daily log for 3 months of his/her individual herpes outbreaks or symptoms of HSV infection, emotional and physical states using mood dimension scales, changes of daily routine, illnesses, medications, and unintended events. The authors concluded that stress and emotional well-being are not related to HSV-1 recurrence (Dalkvist et al., 1995). A limitation to the study was the short time frame of only 3 months.

Dalkvist and colleagues (1995) also examined the role of illness on recurrent HSV-1 infections. In this same prospective study, the authors concluded the common cold was the most critical factor in recurrent HSV-1 outbreaks. The authors speculated that local immunological changes, as opposed to systemic changes of the immune system, correlate with secondary outbreaks of HSV-1 infections. More research studies are needed to understand the relationship that the immune system and the common cold have with recurrent HSV-1 infections.

Other researchers examined the role of sunlight on recurrent HSV-1 infections. Boon and colleagues (2000) conducted a randomized, double-blind, placebo-controlled clinical trial of 541 participants to determine the effect sunlight has on inducing recurrent herpes labialis. The authors confirmed their previous assumptions that UV radiation is a trigger for recurrent oral HSV-1 infections. Strengths of the study were the large sample size and the study design.

In conclusion, further evidence-based research is needed to determine exactly which exogenous and endogenous triggers are involved in recurrent HSV-1 infections and the physiological mechanisms of these triggers. The role of local and systemic changes in the immune system of persons with recurrent HSV-1 infections needs to be further examined to help understand the role of both exogenous and endogenous triggers.


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