Cited by 196Influenza Virus Research StudiesAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

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

Open access
White, Mitchell R., Kandel, Ruth, Tripathi, Shweta, Condon, David, Qi, Li, Taubenberger, Jeffrey, Hartshorn, Kevan L.·2014·PLoS ONE

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0101364

Cites

28 of 28 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
White, M. R., Kandel, R., Tripathi, S., Condon, D., Qi, L., Taubenberger, J., & Hartshorn, K. L.
Affiliations
  • Boston University (US)
  • Harvard University (US)
  • National Institute of Allergy and Infectious Diseases (US)
Corresponding author
Hartshorn, Kevan L.
Venue
PLoS ONE
Published
2014-07-02
Volume
9
Issue
7
Pages
e101364
ISSN
1932-6203 (ISSN-L)
OpenAlex
W2164223927
Cited by
193
References
28
Citations by year
2026: 13 · 2025: 19 · 2024: 15 · 2023: 13 · 2022: 32 · 2021: 23 · 2020: 18 · 2019: 13 · 2018: 12 · 2017: 12 · 2016: 15 · 2015: 4 · 2014: 4
FWCI
8.84
Type
journal article
Language
en
Open access
Locations
  • PLoS ONE (publishedVersion, public-domain)
  • Europe PMC (PubMed Central) (publishedVersion, public-domain)
  • PubMed Central (publishedVersion, public-domain)
  • PubMed (publishedVersion)
  • Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL069031, HL-069031)
  • National Institute of Allergy and Infectious Diseases (AI-83222, P01AI083222)
Topics
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid-beta, Alzheimer's disease, influenza A virus, antiviral activity, amyloid-beta 42, H3N2, H1N1, viral replication inhibition, viral uptake, virus aggregation, neutrophils, neutrophil extracellular traps, hydrogen peroxide, monocytes, interleukin-6, phagocytes
MeSH terms
Animals, Antiviral Agents, Cell Line, Humans, Influenza, Human, Monocytes, Neutrophils, Orthomyxoviridae Infections, Influenza A virus, Peptide Fragments, Phagocytes, Amyloid beta-Peptides, Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype, Host-Pathogen Interactions

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review