Abstract
Most adult humans have been infected with Epstein-Barr virus (EBV), which is thought to contribute to the development of chronic fatigue syndrome. Stress is known to influence the immune system and can exacerbate the sickness response. Although a role for psychological stress in the sickness response, particularly in combination with EBV-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) has been established, and the role of physical stressors in these interactions remains unspecified. In this study, we seek to determine the interaction of chronic physical (swim) stress and EBV-encoded dUTPase injection. We hypothesize that a chronic physical stressor will exacerbate the sickness response following EBV-encoded dUTPase injection. To test this hypothesis mice receive daily injections of EBV-encoded dUTPase or vehicle and are subjected to 15 min of swim stress each day for 14 days or left unmanipulated. On the final evening of injections mice undergo behavioral testing. EBV-encoded dUTPase injection alone produces some sickness behaviors. The physical swimming stress does not alter the sickness response.
Highlights
Chronic fatigue syndrome is characterized by extreme fatigue, muscle pain, swollen lymph nodes, loss of memory, sore throat, stress, and depression [1] [2]
Body temperature was not affected by Epstein-Barr virus (EBV)-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) (p > 0.05, Figure 1(a)) on day 1
Body temperature was not altered by EBVencoded dUTPase or swimming averaged over the first seven days (p > 0.05, Figure 1(b))
Summary
Chronic fatigue syndrome is characterized by extreme fatigue, muscle pain, swollen lymph nodes, loss of memory, sore throat, stress, and depression [1] [2]. Stress can exacerbate sickness responses and impede recovery. Acute psychological stress in particular exacerbates immune responses. Chronic restraint stress suppresses cell mediated immunity in rats [8]. There is the immunomodulatory effect of stress responses and there are direct behavioral changes mediated by stress (e.g. stress induced depressive symptoms that may resemble sickness behaviors). In mice, both 28 days of chronic unpredictable stress and predatory stress impairs the response to lipopolysaccharide [9]. EBV-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) induces a sickness response in mice that is exacerbated by chronic restraint stress [10] [11]
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