Herpesvirus: an underestimated virus

Rechenchoski, Daniele Zendrini; Faccin-Galhardi, Lígia Carla; Linhares, Rosa Elisa Carvalho; Nozawa, Carlos

doi:10.1007/s12223-016-0482-7

Cited by 79 publications

(45 citation statements)

References 22 publications

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“…The icosahedral capsid-enveloped HSV-1 is a neurotropic, neuroinvasive group 1 member of the herpes virus family Herpesviridae ( 18 – 20 ). As a 155,000 base pair double-stranded DNA (dsDNA) virus, HSV-1 contains at least 74 genes and is known to be capable of establishing a persistent and lifelong latency in human CNS and PNS tissues ( 21 – 28 ).…”

Section: Hsv-1 and Sporadic Admentioning

confidence: 99%

Microbiome-Mediated Upregulation of MicroRNA-146a in Sporadic Alzheimer’s Disease

Zhao

Lukiw

2018

Front. Neurol.

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The first indication of a potential mechanistic link between the pathobiology of the human gastrointestinal (GI)-tract microbiome and its contribution to the pathogenetic mechanisms of sporadic Alzheimer’s disease (AD) came a scant 4 years ago (1). Ongoing research continues to strengthen the hypothesis that neurotoxic microbial-derived components of the GI tract microbiome can cross aging GI tract and blood–brain barriers and contribute to progressive proinflammatory neurodegeneration, as exemplified by the AD-process. Of central interest in these recent investigations are the pathological roles played by human GI tract resident Gram-negative anaerobic bacteria and neurotropic viruses—two prominent divisions of GI tract microbiome-derived microbiota—which harbor considerable pathogenic potential. It is noteworthy that the first two well-studied microbiota—the GI tract abundant Gram-negative bacteria Bacteroides fragilis and the neurotropic herpes simplex virus-1 both share a final common pathway of NF-κB (p50/p65) activation and microRNA-146a induction with ensuing pathogenic stimulation of innate-immune and neuroinflammatory pathways. These appear to strongly contribute to the inflammation-mediated amyloidogenic neuropathology of AD. This communication: (i) will review recent research contributions that have expanded our understanding of the nature of the translocation of microbiome-derived neurotoxins-across biophysiological barriers; (ii) will assess multiple-recent investigations of the induction of the proinflammatory pathogenic microRNA-146a by these two prominent classes of human microbiota; and (iii) will discuss the role of molecular neurobiology and mechanistic contribution of polymicrobial infections to AD-type neuropathological change.

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Section: Hsv-1 and Sporadic Admentioning

confidence: 99%

Microbiome-Mediated Upregulation of MicroRNA-146a in Sporadic Alzheimer’s Disease

Zhao

Lukiw

2018

Front. Neurol.

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“…However, some pathogens infect DCs, thus subverting the immune system and spreading infection in the host [ 166 , 167 ]. This is the case of Herpes simplex virus type 1 (HSV-1), a member of the α-herpesvirus family that persists in a latent state in sensory neurons and ganglia after primary infection and can lead to severe local and systemic disease in immunosuppressed patients [ 168 , 169 ].…”

Section: Lamin A/c In Innate Immunitymentioning

confidence: 99%

Lamin A/C and the Immune System: One Intermediate Filament, Many Faces

Saéz

Herrero‐Fernández

Gómez-Bris

et al. 2020

IJMS

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Nuclear envelope lamin A/C proteins are a major component of the mammalian nuclear lamina, a dense fibrous protein meshwork located in the nuclear interior. Lamin A/C proteins regulate nuclear mechanics and structure and control cellular signaling, gene transcription, epigenetic regulation, cell cycle progression, cell differentiation, and cell migration. The immune system is composed of the innate and adaptive branches. Innate immunity is mediated by myeloid cells such as neutrophils, macrophages, and dendritic cells. These cells produce a rapid and nonspecific response through phagocytosis, cytokine production, and complement activation, as well as activating adaptive immunity. Specific adaptive immunity is activated by antigen presentation by antigen presenting cells (APCs) and the cytokine microenvironment, and is mainly mediated by the cellular functions of T cells and the production of antibodies by B cells. Unlike most cell types, immune cells regulate their lamin A/C protein expression relatively rapidly to exert their functions, with expression increasing in macrophages, reducing in neutrophils, and increasing transiently in T cells. In this review, we discuss and summarize studies that have addressed the role played by lamin A/C in the functions of innate and adaptive immune cells in the context of human inflammatory and autoimmune diseases, pathogen infections, and cancer.

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“…Herpes simplex virus-1 (HSV-1) is a neurotropic double-stranded DNA virus, which is the leading cause of infectious blindness in the developed world (Rechenchoski et al, 2017). Epidemiology shows that HSV-1 has been recognized as a ubiquitous human pathogen, infecting 50-90% of the world population (Smith and Robinson, 2002).…”

Section: Introductionmentioning

confidence: 99%

TRIM21 Aggravates Herpes Simplex Virus Epithelial Keratitis by Attenuating STING-IRF3-Mediated Type I Interferon Signaling

Tan

Xia

2020

Front. Microbiol.

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Herpes simplex virus-1 (HSV-1) is the leading cause of infectious blindness in the developed world. HSV-1 infection can occur anywhere in the eye, and the most common presentation is epithelial keratitis. In the HSV epithelial keratitis mice model, we detected the expression of TRIM21 and then investigated the clinical relationship between TRIM21 and HSV epithelial keratitis by silencing TRIM21. Through the clinical scores and histopathology examination, we found that TRIM21 can effectively reduce the severity of HSV epithelial keratitis. Furthermore, silencing TRIM21 significantly controlled the virus particle release at 1, 3, and 5 days post-HSV-1 infection. Notably, the production of IFNβ was enhanced, and the secretion of pro-inflammatory cytokines (IL-6 and TNF-a) was inhibited. Next, human corneal epithelial cells were pretreated with lentivirus or siRNA, respectively, so that TRIM21 expression was overexpressed or silenced. We focused on the regulation of STING-IRF3 and type I interferon signaling after infected with HSV-1. In conclusion, our results have identified that TRIM21 is abnormally high expressed in HSV epithelial keratitis. TRIM21 enhances the replication of HSV-1 in corneal epithelial cells via suppressing the production of type I IFN by inhibiting STING/IRF3 signaling. It also promotes the secretion of IL-6 and TNF-a, thereby aggravating the severity of HSV epithelial keratitis.

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Herpesvirus: an underestimated virus

Cited by 79 publications

References 22 publications

Microbiome-Mediated Upregulation of MicroRNA-146a in Sporadic Alzheimer’s Disease

Microbiome-Mediated Upregulation of MicroRNA-146a in Sporadic Alzheimer’s Disease

Lamin A/C and the Immune System: One Intermediate Filament, Many Faces

TRIM21 Aggravates Herpes Simplex Virus Epithelial Keratitis by Attenuating STING-IRF3-Mediated Type I Interferon Signaling

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