**3. Trigger**

Although spontaneous recurrences are possible, a wide variety of internal and external triggers may lead to transformation of the HSV from a dormant to a proliferative state [30].

Some of the following factors may trigger herpes symptoms:


**15**

*Sunlight and Herpes Virus*

titers [39, 45–47].

time [5].

*DOI: http://dx.doi.org/10.5772/intechopen.82643*

chronically stressed low socioeconomic status individuals have higher antibody titers to latent HV. Additionally, dementia caregivers have greater HSV-1 anti-

• Nerve damage: minimal stimulation or inapparent trauma to the trigeminal sen-

• Radiotherapy: the example of radiation therapy against a brain tumor initiating HSV encephalitis suggests that other trigger factors also should be studied [43].

• Immunosuppression: when the immune system is dysregulated, by HIV or chemotherapy or corticosteroid administration, people generally exhibit greater disease susceptibility and latent HSV or VZV reactivation [43, 44]. Maladaptive alterations in cellular immune function can enhance herpesvirus reactivation and replication, resulting in elevated herpesvirus antibody titers. For instance, organ transplant patients have elevated herpesvirus antibody

• Sexual intercourse: some people find that the friction of sexual intercourse irritates the skin and brings on symptoms of HG. Even if the friction of intercourse seems to be a trigger for symptoms, it won't probably cause a flare-up every

• Hormonal changes, like those that occur in the menstrual cycle, can affect herpes outbreaks. There is a significant association of development of recurrence

Whether a common pathway exists for pathogenetic processes induced by these

The skin is continually subjected to the action of external agents including solar radiation. One of the scientifically documented triggers for herpes outbreaks is the

The Sun is a G-type main-sequence star and is the largest and the most massive object in the solar system. The Sun is the source of the overwhelming majority of light, heat, and energy on Earth's surface, and is powered by nuclear fusion of hydrogen nuclei into helium. As a result of these nuclear reactions a continuous flow of particles and electromagnetic waves called the solar wind is released in the cosmos. Solar wind is a constant stream of plasma and particles emanating from the sun and is the extension of solar corona into interplanetary space. The solar wind invests all the planets, can reach speeds above 700 km/s and have a density that

ionizing radiation (cosmic, gamma, and X-rays) and long wavelength non-ionizing

. Sunlight consists mostly of short wavelength

HSV and the luteal phase of the menstrual cycle [5].

• Change in antiviral activity of the saliva [5].

disparate reactivating factors remains to be determined.

**4. The Sun radiation and interaction whit skin**

**4.1 The Sun as origin of the electromagnetic energy**

ultraviolet (UV) light found in direct sunlight.

varies from 10 to 100 particles/cm3

radiation (UV, visible, and infrared) [48].

body titers compared with demographically matched controls [40, 41].

• Physical stress: fever[5], illness (infection, septicaemia).

sory root is sufficient to activate latent HSV in humans [42].

*Human Herpesvirus Infection - Biological Features, Transmission, Symptoms, Diagnosis...*

delivery of the viral nucleocapsid to the cytoplasm accomplished either by membrane fusion or endocytosis/phagocytosis-like uptake. Beside membrane fusion, mechanisms of endocytosis and/or a phagocytosis-like uptake have been proposed. The endocytosis of HSV particles is atypical, because not mediated by clathrin-coated pits or caveolae. The phagocytosis process requires a cytoskeletal rearrangement with activation of Rho GTPases [18].

After fusion between the cellular membrane with the infecting virus, a viral transactivator tegument protein (VP16), is released into the cytoplasm. The viral capsid is then transported to the nuclear membrane along the microtubule network and, through nuclear pore, the viral DNA is released into the nucleus. VP16 forms a transactivation complex binding in the cytoplasm host cell factor-1 (HCF-1) (protein that contains a nuclear localization sequence), and in the nucleus the homeodomain protein Octamer binding protein-1 (Oct-1). These proteins form a trimeric complex able to activate the immediate early (IE) gene expression [19]. Successful lytic replication is dependent on the expression of the viral IE genes within all infected cells. While this model of VP16 activation of IE gene expression is well understood, the mechanisms implicated in neuronal latency are debated and considerable gaps remain in our knowledge of how different signaling pathways act on the latent genome for reactivation. Following the establishment of latent infection, viral lytic gene expression is silenced, and the lytic gene promoters are associated with repressive heterochromatin [20]. Key experiments performed in the 1980s indicated that latent genomes in the brain stems of infected mice have a nucleosomal structure [21]. Later studies confirmed that the latent viral genome associates with cellular histones in the trigeminal ganglia of mice [22, 23]. Coinciding with the silencing of lytic transcripts, the viral lytic gene promoters become enriched with characteristic heterochromatic histone modifications [24, 25]. While it appears that factors intrinsic to neurons play a key role in the transcriptional silencing of the virus, viral gene products expressed during latent infection can also modulate the chromatin structure [23, 26, 27]. This modulation likely promotes long-term latency, while priming

the genome for reactivation following the appropriate stimuli [28, 29].

Some of the following factors may trigger herpes symptoms:

seems that HZ can be stimulated by sun exposure [8, 31].

Although spontaneous recurrences are possible, a wide variety of internal and external triggers may lead to transformation of the HSV from a dormant to a

• Sunlight: some study demonstrates UVR as a powerful trigger for HL and it also

• Local tissue trauma may make herpes symptoms appear such as: undergoing a surgery [33], laser surgery [34], dental procedures [35], and Tattoos [36]. Another unusual form of traumatic triggering of HSV reactivation may be neurosurgery: after a delay of approximately 1 week, destructive encephalitis may develop with fever and seizures, and with typical viral inclusion bodies demon-

• Persistent mental stress and fatigue [33, 38]. Psychological stress can also dysregulate cellular immunity, and enhance latent αHV reactivation [39]. Importantly,

**14**

**3. Trigger**

proliferative state [30].

• Exposure to heat or cold [5, 32].

strated by histopathology [37].

chronically stressed low socioeconomic status individuals have higher antibody titers to latent HV. Additionally, dementia caregivers have greater HSV-1 antibody titers compared with demographically matched controls [40, 41].


Whether a common pathway exists for pathogenetic processes induced by these disparate reactivating factors remains to be determined.
