# HSV-1 and beta-amyloid deposition

> **NIH NIH R01** · UNIVERSITY OF ILLINOIS AT CHICAGO · 2021 · $381,045

## Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder with progressive decline in cognitive
functions leading to memory loss and dementia. It affects millions of Americans and causes significant
morbidity and mortality. AD is characterized by the accumulation of amyloid-β-containing neuritic
plaques and intracellular tau protein tangles in the brain. Growing evidence pinpoints a link between
herpes simplex virus 1 (HSV-1) infection and AD. Notably, HSV-1 DNA is detectable in AD amyloid
plaques in human brains, and antiviral acyclovir is reported to block the accumulation of the AD-
associated proteins beta-amyloid. Multiscale transcriptome analysis of independent Alzheimer's
cohorts in the USA suggests that AD pathology traits are closely coupled with neurovirulence factor
γ134.5 encoded by HSV-1. However, the way through which HSV-1 is functionally involved remains
largely unknown. We recently found that γ134.5 recruits and activates protein kinase Cδ, a host
serine/threonine kinase that upregulates β-secretase and facilitates AD pathology. As viral γ134.5 also
targets Beclin1 in the autophagy pathway, we hypothesize that viral activities mediated by HSV-1 may
alter homeostasis of amyloid precursor protein and its metabolites through γ134.5 and facilitates the
development of AD. As such, we will study viral regulation of amyloid-β generation a 3D human neural
cell culture model of Alzheimer's disease. Recombinant HSV will be constructed to interrogate the
expression of β-secretase. Furthermore, we will investigate amyloid-β clearance. Genetic studies will
be carried out to assess viral interference of autophagy machineries. The proposed research will
systematically explore pathological features of AD linked to HSV-1 infection. If successful, it will inform
design of new therapeutic approach for AD.

## Key facts

- **NIH application ID:** 10283982
- **Project number:** 3R01AI148148-02S1
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **Principal Investigator:** BIN HE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $381,045
- **Award type:** 3
- **Project period:** 2020-05-15 → 2022-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10283982

## Citation

> US National Institutes of Health, RePORTER application 10283982, HSV-1 and beta-amyloid deposition (3R01AI148148-02S1). Retrieved via AI Analytics 2026-05-29 from https://api.ai-analytics.org/grant/nih/10283982. Licensed CC0.

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