Here is another article to support the view that was just released.
J. Alzheimers Dis., 2016
Anti-Viral Properties of Amyloid-β Peptides
Bourgade, K; Dupuis, G; Frost, EH; Fülöp, T
Amyloid-β (Aβ) peptides generated by the amyloidogenic pathway of amyloid-β protein precursor processing contribute significantly to neurodegeneration characteristic of Alzheimer's disease (AD). The involvement of Aβ peptides in the etiology of AD remains a subject of debate. Data published in the last 6 years by three different groups have added a new twist by revealing that Aβ peptides could act as antimicrobial peptides (AMP) in in vitro assays against some common and clinically relevant microorganisms, inhibit replication of seasonal and pandemic strains of influenza A and, HSV-1 virus. These observations are of significance with respect to the notion that pathogens may be important contributors to the development of AD, particularly in the case of herpes simplex virus (HSV) infection, which often resides in the same cerebral sites where AD arises. Here, we review the data that support the interpretation that Aβ peptides behave as AMP, with an emphasis on studies concerning HSV-1 and a putative molecular mechanism that suggests that interactions between Aβ peptides and the HSV-1 fusogenic protein gB lead to impairment of HSV-1 infectivity by preventing the virus from fusing with the plasma membrane. A number of avenues for future research are suggested.
And one other
J. Alzheimers Dis., 2016
Herpes Simplex Virus Type 1 Neuronal Infection Elicits Cellular and Molecular Mechanisms of Neuroinflammation and Neurodegeneration in in vitro and in vivo Mice Models
Otth, C; Leyton, L; Salamin, M; Acuña-Hinrichsen, F; Martin, C; Concha, MI
Herpes simplex virus type 1 (HSV-1) is a neurotropic virus able to establish a persistent latent infection in the host. Herpes simplex encephalitis (HSE) is associated with a high mortality rate and significant neurological, neuropsychological, and neurobehavioral sequelae, which afflict patients for life. Currently, it is unclear whether asymptomatic recurrent reactivations of HSV-1 occur in the central nervous systems in infected people, and if these events could lead to a progressive deterioration of neuronal function. In this context, HSV-1 constitutes an important candidate to be included among the risk factors for the development of Alzheimer's disease. Our group have demonstrated that HSV-1 triggers neurodegenerative events in in vitro and in vivo induced neuronal infection, evidenced by increase in tau hyperphosphorylation and caspase-3 dependent cleavage of tau protein, resembling what occurs in neurodegenerative diseases. In addition, in an in vivo model, a reactivation episode during asymptomatic latency of HSV-1 infection in mice was accompanied by upregulation of neuroinflammatory markers (toll-like receptor-4, interferon α/β, and p-IRF3). Besides, previous reports have shown that HSV-1 inhibits apoptosis during early infection, but is pro-apoptotic during productive infection. Taking in consideration that the stress sensors AMPK and Sirt1 are involved in neuronal survival and neuroprotection, we hypothesized that HSV-1 could activate the AMPK/Sirt1 axis as a strategy to establish latency through inhibition of apoptosis and restoration of the energy status. Thus, we demonstrated that HSV-1 modulates the AMPK/Sirt1 axis differentially during infection, interfering with pro-apoptotic signaling and regulating mitochondrial biogenesis, pivotal processes in the lifetime of neurons in the central nervous system. In conclusion, our findings support the idea that HSV-1 could contribute to induce neurodegenerative processes in age-associated pathologies such as Alzheimer's disease.
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