PLOS ONE: Alzheimer's Associated β-Amyloid Protein Inhibits Influenza A Virus and Modulates Viral Interactions with Phagocytes

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.

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