Format

Send to

Choose Destination
PLoS One. 2014 Jul 2;9(7):e101364. doi: 10.1371/journal.pone.0101364. eCollection 2014.

Alzheimer's associated β-amyloid protein inhibits influenza A virus and modulates viral interactions with phagocytes.

Author information

1
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America.
2
Hebrew Senior Life, Harvard Medical School, Boston, Massachusetts, United States of America.
3
National Institute of Allergy and Infectious Disease, Bethesda, Maryland, United States of America.

Abstract

Accumulation of β-Amyloid (βA) is a key pathogenetic factor in Alzheimer's disease; however, the normal function of βA is unknown. Recent studies have shown that βA can inhibit growth of bacteria and fungi. In this paper we show that βA also inhibits replication of seasonal and pandemic strains of H3N2 and H1N1 influenza A virus (IAV) in vitro. The 42 amino acid fragment of βA (βA42) had greater activity than the 40 amino acid fragment. Direct incubation of the virus with βA42 was needed to achieve optimal inhibition. Using quantitative PCR assays βA42 was shown to reduce viral uptake by epithelial cells after 45 minutes and to reduce supernatant virus at 24 hours post infection. βA42 caused aggregation of IAV particles as detected by light transmission assays and electron and confocal microscopy. βA42 did not stimulate neutrophil H2O2 production or extracellular trap formation on its own, but it increased both responses stimulated by IAV. In addition, βA42 increased uptake of IAV by neutrophils. βA42 reduced viral protein synthesis in monocytes and reduced IAV-induced interleukin-6 production by these cells. Hence, we demonstrate for the first time that βA has antiviral activity and modulates viral interactions with phagocytes.

PMID:
24988208
PMCID:
PMC4079246
DOI:
10.1371/journal.pone.0101364
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center