Psychological stress exacerbates primary vaginal herpes simplex virus type 1 (HSV-1) infection by impairing both innate and adaptive immune responses

Ashcraft, Kathleen A.; Bonneau, Robert H.

doi:10.1016/j.bbi.2008.06.008

Cited by 28 publications

(26 citation statements)

References 68 publications

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“…Prior work has shown that levels of Ach increase during stress (Schlereth et al, 2007), and stressed individuals appear to be more susceptible to a wide range of opportunistic infections (Ashcraft and Bonneau, 2008; Wu et al, 2005). The elements responsible for increasing infection after stress are incompletely understood.…”

Section: Resultsmentioning

confidence: 99%

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Neuroendocrine Nicotinic Receptor Activation Increases Susceptibility to Bacterial Infections by Suppressing Antimicrobial Peptide Production

Radek

Elias

Taupenot

et al. 2010

Cell Host & Microbe

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SUMMARY Stress mobilizes elements from the neuroendocrine system to modulate immune responses. Cholinergic stimulation via nicotinic receptor (nAchR) is a major neuroendocrine signaling axis associated with the stress response whose specific effects on the immune system are unknown. Here, we show that nAchR activation by topical agonist application or deletion of the nAChR antagonist catestatin (Chga−/−) reduced antimicrobial peptide (AMP) activity in skin extracts and increased susceptibility to methicillin-resistant Staphylococcus aureus and Group A Streptococcus infections. The adverse effects on AMP expression and infection were rescued by topical application of a nAChR antagonist. Stress-induced nAChR activation increased infection in wild-type, but not Chga−/− or cathelicidin-deficient, mice. These data identify a mechanism for the negative regulation of host-innate AMP response to infection through cholinergic activation and indicate nAChR-mediated cathelicidin dysregulation as a potential mechanism for increased susceptibility to infection following prolonged stress or nicotine use.

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Section: Resultsmentioning

confidence: 99%

“…Stress mobilizes various elements from the neuroendocrine system to modulate immune responses. Acute stress was typically thought to be immunoenhancing as part of the “fight-or-flight” response, while sustained stress tends to be immunosuppressive (Aberg et al, 2007; Ashcraft and Bonneau, 2008; Dhabhar, 2009). …”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine Nicotinic Receptor Activation Increases Susceptibility to Bacterial Infections by Suppressing Antimicrobial Peptide Production

Radek

Elias

Taupenot

et al. 2010

Cell Host & Microbe

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“…Psychological stress results in the enhanced production of corticosteroids and catecholamines [21] which are potent immunomodulators [22]. In animal models, high-stress environments have been associated with increased morbidity and mortality following bacterial and viral infection [23,24]. People experiencing stressful life events, such as marital problems or caring for a sick relative, have been shown to have altered immunity such as a lower antibody response to influenza vaccination [25] and reactivation of latent viral infections [26].…”

Section: Introductionmentioning

confidence: 99%

The Impact of Self-Reported Psychological Stress Levels on Changes to Peripheral Blood Immune Biomarkers in Recreational Marathon Runners during Training and Recovery

Rehm

Elci²,

Hahn

et al. 2013

Neuroimmunomodulation

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Objective: Marathon training is both physically and psychologically stressful, both of which can lead to altered immunity. The purpose of this study was to determine if the overall immunoregulatory changes associated with the physical stress of marathon training are affected by psychological stress. Methods: Nineteen recreational marathoners completed the Perceived Stress Scale (PSS), State-Trait Anxiety Inventory (STAI) and Penn State Worry Questionnaire (PSWQ), and had levels of T cell subpopulations and cytokine (IFNγ, IL4 and IL10) production determined 4 weeks before (baseline), 24-48 h before (prerace) and 1 week after (recovery) participation in a marathon. Results: PSS scores decreased at the prerace visit compared to baseline and remained low at recovery. Compared to baseline, there were significant changes to numerous immune measures at the prerace visit, including decreases in Th1/Th2 ratio, Tc1/Tc2 ratio, Tr1 and Th3 cell populations as well as decreases in IFNγ/IL4 cytokine ratio and IL10 production. Most immune parameters had returned to near baseline values at the recovery visit. Higher levels of perceived stress, anxiety and worry exacerbated many of the alterations in immunity that were observed at the prerace visit. Higher levels of perceived stress and worry had significant effects on changes to Treg, IL4 production and the IFNγ/IL4 cytokine ratio. Stress had an additional impact on changes in IL10 production. High anxiety levels resulted in significant changes to Treg, Tr1 and Th3. Conclusion: These data suggest that recreational marathon runners with higher levels of psychological stress may be more at risk for the immune alterations that are common during periods of prolonged physical training.

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“…The mechanism through which these stress factors impact HSV disease severity and recurrences is thought to be suppression of the immune system, permitting the viruses to escape immune surveillance (2,7,12,19). However, the receptors for the two major stress hormones, epinephrine and cortisol, are expressed selectively by the different types of neurons infected by HSV, including sensory and autonomic neurons (20,21).…”

mentioning

confidence: 99%

“…Psychosocial stress has been correlated with oral herpes recurrences in humans (8). Psychological stress at the time of infection increases HSV-1 titers and pathology following intranasal or vaginal infection in mice (7,9). Epinephrine (EPI), a catecholaminergic hormone secreted by the adrenal medulla to induce the "short-term" fight-or-flight stress response, is regulated by the sympathetic nervous system.…”

mentioning

confidence: 99%

Stress Hormones Epinephrine and Corticosterone Selectively Modulate Herpes Simplex Virus 1 (HSV-1) and HSV-2 Productive Infections in Adult Sympathetic, but Not Sensory, Neurons

Ives

Bertke

2017

J Virol

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Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) infect and establish latency in peripheral neurons, from which they can reactivate to cause recurrent disease throughout the life of the host. Stress is associated with the exacerbation of clinical symptoms and the induction of recurrences in humans and animal models. The viruses preferentially replicate and establish latency in different subtypes of sensory neurons, as well as in neurons of the autonomic nervous system that are highly responsive to stress hormones. To determine if stress-related hormones modulate productive HSV-1 and HSV-2 infections within sensory and autonomic neurons, we analyzed viral DNA and the production of viral progeny after treatment of primary adult murine neuronal cultures with the stress hormones epinephrine and corticosterone. Both sensory trigeminal ganglion (TG) and sympathetic superior cervical ganglion (SCG) neurons expressed adrenergic receptors (activated by epinephrine) and the glucocorticoid receptor (activated by corticosterone). Productive HSV infection colocalized with these receptors in SCG but not in TG neurons. In productively infected neuronal cultures, epinephrine treatment significantly increased the levels of HSV-1 DNA replication and production of viral progeny in SCG neurons, but no significant differences were found in TG neurons. In contrast, corticosterone significantly decreased the levels of HSV-2 DNA replication and production of viral progeny in SCG neurons but not in TG neurons. Thus, the stress-related hormones epinephrine and corticosterone selectively modulate acute HSV-1 and HSV-2 infections in autonomic, but not sensory, neurons.IMPORTANCE Stress exacerbates acute disease symptoms resulting from HSV-1 and HSV-2 infections and is associated with the appearance of recurrent skin lesions in millions of people. Although stress hormones are thought to impact HSV-1 and HSV-2 through immune system suppression, sensory and autonomic neurons that become infected by HSV-1 and HSV-2 express stress hormone receptors and are responsive to hormone fluctuations. Our results show that autonomic neurons are more responsive to epinephrine and corticosterone than are sensory neurons, demonstrating that the autonomic nervous system plays a substantial role in HSV pathogenesis. Furthermore, these results suggest that stress responses have the potential to differentially impact HSV-1 and HSV-2 so as to produce divergent outcomes of infection.KEYWORDS herpes simplex virus, HSV-1, HSV-2, epinephrine, corticosterone, stress, reactivation

show abstract

Psychological stress exacerbates primary vaginal herpes simplex virus type 1 (HSV-1) infection by impairing both innate and adaptive immune responses

Cited by 28 publications

References 68 publications

Neuroendocrine Nicotinic Receptor Activation Increases Susceptibility to Bacterial Infections by Suppressing Antimicrobial Peptide Production

Neuroendocrine Nicotinic Receptor Activation Increases Susceptibility to Bacterial Infections by Suppressing Antimicrobial Peptide Production

The Impact of Self-Reported Psychological Stress Levels on Changes to Peripheral Blood Immune Biomarkers in Recreational Marathon Runners during Training and Recovery

Stress Hormones Epinephrine and Corticosterone Selectively Modulate Herpes Simplex Virus 1 (HSV-1) and HSV-2 Productive Infections in Adult Sympathetic, but Not Sensory, Neurons

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