Acyclovir or Aβ42 peptides attenuate HSV-1-induced miRNA-146a levels in human primary brain cells.

Published

Journal Article

Human brains harbor herpes simplex virus type-1 (HSV-1) DNA, which normally remains quiescent throughout many decades of life. HSV-1 is associated with viral encephalopathy and with the amyloid beta 42 (Abeta42) peptide-enriched lesions that characterize Alzheimer's disease neuropathology. Here we report that infection of human neuronal-glial cells in primary co-culture with HSV-1 induces an irregular hypertrophy of human neuronal-glial cell bodies, an induction of HSV-1 DNA polymerase, and an up-regulation of micro-RNA-146a associated with altered innate-immune responses. Presence of the antiviral acyclovir or soluble Abeta42 peptide significantly attenuated these neuropathological responses. The inhibitory effects of Abeta42 peptide were also observed in an HSV-1-infected CV-1 cell-based viral plaque assay. The results suggest that soluble Abeta42 peptide can invoke non-pathological and anti-viral effects through inactivation of an HSV-1 challenge to human brain cells by simple viral sequestration, viral destruction, or by complex neurogenetic mechanisms.

Full Text

Duke Authors

Cited Authors

  • Lukiw, WJ; Cui, JG; Yuan, LY; Bhattacharjee, PS; Corkern, M; Clement, C; Kammerman, EM; Ball, MJ; Zhao, Y; Sullivan, PM; Hill, JM

Published Date

  • October 2010

Published In

Volume / Issue

  • 21 / 14

Start / End Page

  • 922 - 927

PubMed ID

  • 20683212

Pubmed Central ID

  • 20683212

Electronic International Standard Serial Number (EISSN)

  • 1473-558X

International Standard Serial Number (ISSN)

  • 0959-4965

Digital Object Identifier (DOI)

  • 10.1097/WNR.0b013e32833da51a

Language

  • eng