Herpes simplex virus encephalitis in a mouse model: PCR evidence for CNS latency following acute infection

Drummond, Cláudia; Eglin, Roger; Esiri, Margaret M.

doi:10.1016/0022-510x(94)90068-x

Cited by 42 publications

(21 citation statements)

References 32 publications

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“…After a primary infection, the virus becomes latent mainly in the ganglia but viral DNA can be found in the neurons of several areas of the central nervous system (Cabrera et al, 1980;Drummond et al, 1994). The reactivation of HSV-1 in the brain by stress factors (Drummond et al, 1994;Kastrukoff et al, 1981;Whitley, 1996) might contribute to neurodegenerative development. Itzhaki and coworkers suggest that HSV-1 in the brain and the presence of the apolipoprotein E allele 4 (the recognized risk factor for AD) together confer high risk for AD (Lin et al, 2002).…”

Section: Resultsmentioning

confidence: 99%

Mortalin – a multipotent chaperone regulating cellular processes ranging from viral infection to neurodegeneration

Flachbartova¹,

Kováčech²

2013

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Summary. -Heat shock 70kDa protein 9 (HSPA9)/mortalin is a heat-uninducible member of the heat shock 70 protein family. This protein has been attributed many cellular functions, including energy generation, stress response, carcinogenesis and involvement in neurodegenerative diseases, which is well documented by many names it has been given (CSA, MOT, MOT2, GRP75, PBP74, GRP-75, HSPA9B, MGC4500, MTHSP75, and mortalin). As an immortalization marker (hence the name "mortalin") in mouse embryonic fibroblasts cybrids it preferentially segregated with loss of immortality in passaged cells. Mortalin regulates the functions of the tumor suppressor protein p53 and plays important roles in stress response and maintenance of the mitochondria and endoplasmic reticulum. Furthermore, mortalin appears to have roles in membrane trafficking and viral release regulation, since it interacts with Nef protein it is necessary for secretion of exosomal negative factor (Nef) and HIV-1 virus release. Recently, mortalin has been described as a significant player in neurodegenerative diseases. Mutations in HSPA9 gene have been found in Parkinson΄s disease patients; mortalin isoform expression differs in hippocampus of patients with Alzheimer΄s disease and could regulate the β-amyloid toxicity pathway. In this review we summarize the functions of mortalin, its pathological implications in neuronal dysfunction and possible roles in neurodegenerative diseases.Keywords: HSPA9/mortalin/GRP75; mitochondria; cancer; Alzheimer΄s disease * Corresponding author: E-mail: Branislav.Kovacech@savba.sk; phone: +412-2-54788100. Abbreviations: Aβ = beta-amyloid; AD = Alzheimer΄s disease; PD = Parkinson΄s disease; HSPA9 = heat shock 70 kDa protein 9; Hsp = chaperone; MAC = membrane attack complex; Net = negative factor Contents:

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Section: Resultsmentioning

confidence: 99%

Mortalin – a multipotent chaperone regulating cellular processes ranging from viral infection to neurodegeneration

Flachbartova¹,

Kováčech²

2013

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“…The largely described mouse model of HSV intranasal infection has been used for studying HSV induced pneumonia and encephalitis [Kern et al, 1982;Erlich et al, 1987Erlich et al, , 1989Drummond et al, 1994;Lamade et al, 1996;Adler et al, 1997Adler et al, , 1999Meyding-Lamade et al, 1998, 1999Haas et al, 1999]. Herewith, we investigated the effect of inhibiting NO production during the first steps of HSV intranasal infection.…”

Section: Introductionmentioning

confidence: 95%

Early inhibition of nitric oxide production increases HSV‐1 intranasal infection

Gamba

Cavalieri

Courrèges

et al. 2004

Journal of Medical Virology

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Here, we studied the role of nitric oxide (NO) production during the first steps of the respiratory infection of BALB/c mice with herpes simplex virus type 1 (HSV-1), strain F. Nitric oxide synthase II (NOS-II) mRNA and protein were detected by reverse transcription (RT)-PCR and dot blot, respectively in samples of lungs and turbinates early post-infection (p.i.). Immunohistochemical analysis revealed pulmonar macrophages and PMN expressing NOS-II in the lungs of infected animals. Animals intranasally treated with aminoguanidine (AG), a NOS inhibitor, during the first steps of infection, showed a dose-dependent increase in pneumonitis compared to controls. Viral titres in turbinates, lungs, and brains were higher in AG treated mice. Finally, histopathology studies revealed a stronger inflammation in eyes, and lungs of these animals. Taken together, these results suggest a role of NO in controlling primary HSV intranasal infection.

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“…The murine model has been used to study HSV-1 reactivation, because the virus establishes latency and then reactivates following stimulation in a way similar to that in humans (6)(7)(8)(9)(10). In the past 3 decades, numerous ex vivo studies documented that viral reactivation occurs efficiently and consistently in the ganglia but extremely rarely in the CNS (such as the brain) when assessed with a conventional assay by cocultivating minced tissue explants with monolayers of cells that support viral growth (6,9,(11)(12)(13).…”

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confidence: 99%

In Vivo Reactivation of Latent Herpes Simplex Virus 1 in Mice Can Occur in the Brain before Occurring in the Trigeminal Ganglion

Yao

Ling

Tung

et al. 2014

J Virol

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Herpes simplex virus 1 (HSV-1) establishes latency in neurons of the brains and sensory ganglia of humans and experimentally infected mice. The latent virus can reactivate to cause recurrent infection. Both primary and recurrent infections can induce diseases, such as encephalitis. In humans, the majority of encephalitis cases occur as a recurrent infection. However, in the past, numerous mouse studies documented that viral reactivation occurs efficiently in the ganglion, but extremely rarely in the brain, when assessed ex vivo by cultivating minced tissue explants. Here, we compare the brains and the trigeminal ganglia of mice latently infected with HSV-1 (strain 294.1 or McKrae) for levels of viral genomes and in vivo reactivation. The numbers of copies of 294.1 and McKrae genomes in the brain stem were significantly greater than those in the trigeminal ganglion. Most importantly, 294.1 and McKrae reactivation was detected in the brain stems earlier than in the trigeminal ganglia of mice treated with hyperthermia to reactivate latent virus in vivo. In addition, the brain stem yielded reactivated virus at a high frequency compared with the trigeminal ganglion, especially in mice latently infected with 294.1 after hyperthermia treatment. These results provide evidence that recurrent brain infection can be induced by the reactivation of latent virus in the brain in situ. IMPORTANCEHerpes simplex virus 1 (HSV-1) establishes latency in neurons of the brains and sensory ganglia of humans and experimentally infected mice. The latent virus can reactivate to cause recurrent infection. In the past, studies of viral reactivation focused on the ganglion, because efficient viral reactivation was detected in the ganglion but not in the brain when assessed ex vivo by cultivating mouse tissue explants. In this study, we report that the brain contains more viral genomes than the trigeminal ganglion in latently infected mice. Notably, the brain yields reactivated virus early and efficiently compared with the trigeminal ganglion after mice are stimulated to reactivate latent virus. Our findings raise the potential importance of HSV-1 latent infection and reactivation in the brain.

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Herpes simplex virus encephalitis in a mouse model: PCR evidence for CNS latency following acute infection

Cited by 42 publications

References 32 publications

Mortalin – a multipotent chaperone regulating cellular processes ranging from viral infection to neurodegeneration

Mortalin – a multipotent chaperone regulating cellular processes ranging from viral infection to neurodegeneration

Early inhibition of nitric oxide production increases HSV‐1 intranasal infection

In Vivo Reactivation of Latent Herpes Simplex Virus 1 in Mice Can Occur in the Brain before Occurring in the Trigeminal Ganglion

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