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A Treatise on the Role of Herpesvirus in Neurodegeneration
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi, Kenneth Blum
Herpesviruses have been demonstrated to exert significant neurological morbidity. Herpes simplex virus type 1 (HSV-1), HSV-2, and varicella zoster viruses, three of the nine known human herpesviruses, demonstrate latency in the peripheral sensory ganglia and exist in the host for lifetime. Primary infection takes place at a mucocutaneous surface with a declining transportation of the virus to the peripheral sensory ganglia, conserving the integrity of the viral genome within the peripheral sensory ganglia, as well as regular reactivation with antegrade transmission to the nerve endings and mucocutaneous surface. HSV-1 is primarily transmitted by oral-to-oral contact and in most cases causes orolabial herpes or “cold sores” around the mouth. HSV-2 is almost entirely sexually transmitted through skin-to-skin contact, causing genital herpes.
Infections Related to Steroids and Immunosuppressive Agents in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Herpes zoster (HZ) is a significant global problem that results from reactivation of the latent varicella zoster virus within the sensory ganglia. Older age, female gender, ethnicity, and depression are the potential risk factors. In addition, cellular immune dysfunction in certain conditions (e.g., HIV infection or lymphomas) is another risk factor triggering the HZ infection. In half of HZ-infected patients, some complications such as postherpetic neuralgia (PHN), ophthalmic zona, meningoencephalitis, and secondary bacterial infections occur.
Baroreflex Failure
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
The glossopharyngeal nerve has two sensory ganglia. The superior ganglion is a small swelling of the nerve at the level of the jugular foramen, while the somewhat larger petrosal ganglion lies in the fossula petrosa, just beneath the jugular foramen. The otic ganglion is situated just below the foramen ovale and receives parasympathetic preganglionic fibers from the tympanic branch of the glossopharyngeal nerve where the former courses anteriorly as the lesser superficial petrosal nerve (Brodal, 1957). Postganglionic parasympathetic fibers then enter the auriculotemporal nerve (a branch of the trigeminal nerve) and innervate the parotid gland.
Disseminated herpes zoster in an immunocompetent young adult: A rare complication of Ramsay Hunt syndrome
Published in Acta Oto-Laryngologica Case Reports, 2023
Naoyuki Matsumoto, Makiko Toma-Hirano, Takuya Yasui, Ken Ito
Ramsay Hunt syndrome (RHS) is a complication of latent varicella-zoster virus (VZV) infection, and is considered as a form of herpes zoster occurring in the otic region. It is usually identified clinically as a triad of facial paralysis, otalgia and herpetiform vesicles on the ear or in the mouth, frequently accompanied by vestibulocochlear symptoms, such as tinnitus, sensorineural hearing loss, and vertigo [1]. Herpes zoster is caused by reactivation of VZV which may be dormant in sensory ganglia of the dorsal root ganglia after a previous varicella infection. Although grouped vesiculobullous skin lesions usually appear along only one or two dermatomes, it is occasionally disseminated hematogenously in patients with decreased immunity [2]. We report a rare case of Ramsay Hunt syndrome developing disseminated herpes zoster in an immunocompetent young adult, in whom discrimination from drug eruption was important for clinical decision-making.
The Role of Nervous System and Immune System in Herpes Zoster Ophthalmicus Dissemination and Laterality – Current Views
Published in Ocular Immunology and Inflammation, 2023
Yue Li, Louis Tong, Chrystie Quek, Yun Feng
In immunocompetent individuals, VZV-specific cell-mediated immune responses inhibit the spread of the virus between cells, thereby preventing the reactivation of VZV. When the local immune response becomes insufficient to contain the virus, the underlying VZV in a sensory ganglion reactivates. Currently, the nature of this local immune anomaly that is limited to one sensory ganglion is not known. VZV spreads within the ganglion to the sensory nerve and the skin. This causes the characteristic rash and pain in the area of skin innervated by the affected ganglion. As sensory nerves associated with one ganglion do not cross the midline, dermatomes supplied by these nerves also respect the vertical midline. Therefore, reactivation of VZV in a ganglion produces unilateral lesions in the dermatome subserved by that affected ganglion.15
Current vaccine approaches and emerging strategies against herpes simplex virus (HSV)
Published in Expert Review of Vaccines, 2021
Vindya Nilakshi Wijesinghe, Isra Ahmad Farouk, Nur Zawanah Zabidi, Ashwini Puniyamurti, Wee Sim Choo, Sunil Kumar Lal
Both HSV-1 and HSV-2 are able to enter a dormant state in the peripheral neurons; thus, establishing a latent infection where the viral genetic component remains intact though no new virions are formed until the onset of viral reactivation [17]. The primary infection in hosts arises upon entry via a mucosal surface or damaged skin, where the virus then undergoes intracellular replication at the initial site of exposure [18]. Nerve terminals in the mucosal tissue or infected skin provide a portal for viral entry into the peripheral nervous system (PNS). Viral particles undergo retrograde transport via axons, and the virion genetic component is unloaded into the nucleus [19]. This process is key in achieving a latent state in the sensory ganglia until viral reactivation occurs [20]. Upon reactivation, newly formed virions migrate from the ganglia toward the nerve endings of innervated mucocutaneous sites (dermis or innervated tissue) via anterograde transport, causing reinfection [19]. The most efficient reactivation of HSV-1 and HSV-2 usually occurs from the trigeminal ganglia (TG) and lumbosacral dorsal root ganglia (DRG) of the nervous system, respectively [20]. Though reactivation is often spontaneous, certain internal and external factors have been identified as triggers including fatigue, subjection to bright light [2] psychological stress and menstruation [21].