Human herpes simplex virus infections: Epidemiology, pathogenesis, symptomatology, diagnosis, and management

Fatahzadeh, Mahnaz; Schwartz, Robert A.

doi:10.1016/j.jaad.2007.06.027

Cited by 453 publications

(486 citation statements)

References 253 publications

(787 reference statements)

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“…17 Periodically, dormant HSV-1 may reactivate from latency, and virus particles are then transported along sensory neurons to the skin or other mucosa, causing recurrent HSL. 18 Although HSV-1 allows itself to be silenced in neurons, reactivated virus may prevail by overcoming various host defenses 19 to cause disseminated disease, 18,20 which will be discussed later. An important cellular defense mechanism against HSV-1 infection is the lysosome degradation pathway of autophagy, which constitutes a quality control of intracellular entities of eukaryotic cells.…”

Section: Herpes Simplex Virus Type-1 Primary Infectionmentioning

confidence: 99%

Autophagy interaction with herpes simplex virus type-1 infection

O’Connell

Liang

2016

Autophagy

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More than 50% of the U.S. population is infected with herpes simplex virus type-I (HSV-1) and global infectious estimates are nearly 90%. HSV-1 is normally seen as a harmless virus but debilitating diseases can arise, including encephalitis and ocular diseases. HSV-1 is unique in that it can undermine host defenses and establish lifelong infection in neurons. Viral reactivation from latency may allow HSV-1 to lay siege to the brain (Herpes encephalitis). Recent advances maintain that HSV-1 proteins act to suppress and/or control the lysosome-dependent degradation pathway of macroautophagy (hereafter autophagy) and consequently, in neurons, may be coupled with the advancement of HSV-1-associated pathogenesis. Furthermore, increasing evidence suggests that HSV-1 infection may constitute a gradual risk factor for neurodegenerative disorders. The relationship between HSV-1 infection and autophagy manipulation combined with neuropathogenesis may be intimately intertwined demanding further investigation.

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Section: Herpes Simplex Virus Type-1 Primary Infectionmentioning

confidence: 99%

Autophagy interaction with herpes simplex virus type-1 infection

O’Connell

Liang

2016

Autophagy

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“…2) [3,4]. Les complications sont rares chez le sujet immunocompétent bien que la fréquence des récurrences puisse être élevée, perturbant la vie sociale du patient en raison notamment des répercussions esthétiques.…”

Section: Commentairesunclassified

Cellulite à partir d’un herpès labial chez un patient immunocompétent

Samot¹,

Catros²,

Fricain³

2010

Med Buccale Chir Buccale

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Mots clés : herpès récurrent / celluliteRésumé -L'herpès labial récurrent est une lésion fréquente dont les manifestations cliniques se limitent le plus souvent à une gêne et à la présence de croûtes disgracieuses. La surinfection des lésions herpétiques a été décrite mais elle reste le plus souvent subclinique. Le cas rapporté décrit une cellulite labiale en rapport avec une ulcération due à un herpès récurrent. Cela souligne la possibilité d'une surinfection potentiellement invalidante dans l'herpès labial récurrent. Key words: recurrent herpes / cellulitisAbstract -Labial cellulitis secondary to recurrent herpes labialis in non immunocompromised patient. Recurrent herpes labialis is a frequent lesion that induces a discomfort and the presence of ungraceful crusts. Secondary infections of herpetic lesions were represented but usually they do not provide clinical manifestations. This case report shows a labial cellulitis secondary to herpetic recurrence. This case underlines the possibility of potentially disabling secondary infections in herpetic recurrences.Les infections à HSV1 et HSV2 (herpès simplex virus) sont fréquentes et peuvent intéresser l'ensemble du revêtement cutanéomuqueux. La primo-infection herpétique correspond au premier contact infectant pour les cellules épithéliales. Elle génère une réaction immunitaire qui n'entraîne pas la clairance du virus ; ce dernier persiste à l'état latent. Une réac-tivation virale (réplication) favorisée par un épisode fébrile, une exposition aux ultra-violets, une asthénie, un stress, une lésion tissulaire. . . entraîne une récurrence (symptomatique) ou une excrétion virale asymptomatique mais contaminante. Le traitement de l'infection herpétique fait l'objet de recommandations [1]. Le traitement de la primo-infection repose sur l'acyclovir (200 mg × 5 . j −1 × 5 à 10 j), celui des récur-rences avant tout sur la prévention ; l'intérêt de l'utilisation d'antiseptiques locaux est discuté. Les infections herpétiques sont le plus souvent bénignes en dehors des complications classiques : méningo-encéphalite, atteintes systémiques, syndrome de Kaposi-Juliusberg, érythème polymorphe. La surinfection des lésions herpétiques a été exceptionnellement rapportée dans la littérature [2]. Le cas clinique présenté est la première description d'une cellulite labiale ayant pour porte d'entrée une ulcération due à un herpès labial récurrent.

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“…In people who are immunocompromised, e.g. people living with AIDS, neonates or stem cell recipients, the symptoms are often severe (Fatahzadeh & Schwartz, 2007). Many questions remain regarding the spread of infection within the host, which has hindered the development of treatments to prevent recurrent infections.…”

Section: Introductionmentioning

confidence: 99%

Mutation of UL24 impedes the dissemination of acute herpes simplex virus 1 infection from the cornea to neurons of trigeminal ganglia

Rochette

Bourget

Sanabria-Solano

et al. 2015

Journal of General Virology

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Herpes simplex virus 1 (human herpesvirus 1) initially infects epithelial cells of the mucosa and then goes on to infect sensory neurons leading ultimately to a latent infection in trigeminal ganglia (TG). UL24 is a core herpesvirus gene that has been identified as a determinant of pathogenesis in several Alphaherpesvirinae, although the underlying mechanisms are unknown. In a mouse model of ocular infection, a UL24-deficient virus exhibited a reduction in viral titres in tear films of 1 log 10 , whilst titres in TG are often below the level of detection. Moreover, the efficiency of reactivation from latency was also severely reduced. Herein, we investigated how UL24 contributed to acute infection of TG. Our results comparing the impact of UL24 on viral titres in eye tissue versus in tear films did not reveal a general defect in virus release from the cornea. We also found that the impairment of replication seen in mouse primary embryonic neurons with a UL24-deficient virus was not more severe than that observed in an epithelial cell line. Rather, in situ histological analyses revealed that infection with a UL24-deficient virus led to a significant reduction in the number of acutely infected neurons at 3 days post-infection (p.i.). Moreover, there was a significant reduction in the number of neurons positive for viral DNA at 2 days p.i. for the UL24-deficient virus as compared with that observed for WT or a rescue virus. Our results supported a model whereby UL24 functions in the dissemination of acute infection from the cornea to neurons in TG.

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Human herpes simplex virus infections: Epidemiology, pathogenesis, symptomatology, diagnosis, and management

Cited by 453 publications

References 253 publications

Autophagy interaction with herpes simplex virus type-1 infection

Autophagy interaction with herpes simplex virus type-1 infection

Cellulite à partir d’un herpès labial chez un patient immunocompétent

Mutation of UL24 impedes the dissemination of acute herpes simplex virus 1 infection from the cornea to neurons of trigeminal ganglia

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