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The therapeutic potential of RANTES/CCL5 across diverse infections and its synergistic enhancement by ezrin peptide RepG3 for long COVID

Rupert Holms1*
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1 Newal R&D Ltd., London, United Kingdom
MI 2024, 1(1), 1–24; https://doi.org/10.36922/mi.2474
Submitted: 19 December 2023 | Accepted: 4 February 2024 | Published: 6 March 2024
© 2024 by the Author (s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
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Abstract

The amplification of anti-infective immunity against a wide spectrum of acute and chronic infections caused by various pathogens is mediated by RANTES/CCL5. This chemokine controls infections caused by viruses, bacteria, fungi, and protozoans. In addition, RANTES/CCL5 exhibits anti-cancer effects by increasing NK-cell activity and targeting tumors. RANTES/CCL5 acts by amplifying antigen-specific immunity on mucosal surfaces, programmed T-cell responses, cytotoxic T lymphocytes (CTL), B-cell activation, and antibody production. RANTES/CCL5 exerts its effects by binding to C-C receptors, thereby triggering JAK/STAT signaling and inducing the migration of lymphocytes, NK cells, and monocytes. In the brain, RANTES/CCL5 activates astrocytes and upregulates anti-inflammatory interleukin (IL)-10 expression. Inflammatory cytokines rapidly induce RANTES/CCL5 expression in fibroblasts, epithelial cells, and monocytes/macrophages. In T-cells, RANTES/CCL5 expression is mediated by translational control of the transcription factor RFLAT-1/KLF13, which is responsible for a 3-day delay in RANTES/CCL5 secretion after T-cell activation. A cell membrane multi-protein complex containing CFTR, EBP50, ezrin, and PKC is a dominant regulator of both RANTES/CCL5 and inflammatory cytokine expression. Treatment of a volunteer patient suffering from long COVID/vaccine injury with the ezrin peptide RepG3 alleviated symptoms, substantially reduced serum proinflammatory cytokines to normal levels, and enhanced the expression of RANTES/CCL5. The immune amplification activities of RANTES/CCL5 and the ezrin peptide RepG3 exhibit striking similarities. In contrast, the ezrin peptide RepG3 differs from RANTES/CCL5 in its ability to significantly inhibit the expression of proinflammatory cytokines IL-1β, IL-6, IL-8, IL-13, TNF-α, and proinflammatory chemokines MIP-1α and MIP-1β. The mechanism through which the ezrin peptide RepG3 enhances adaptive immunity likely involves its induction of systemic elevation of RANTES/CCL5 expression and the simultaneous inhibition of proinflammatory cytokine expression.

Keywords
RANTES
CCL5
CCR5
Ezrin peptide
Immune amplification
Anti-inflammatory
SARS-CoV-2
Long COVID
Funding
Newal R&D Ltd., London, UK.
Conflict of interest
The author, Dr. Rupert Holms, is the inventor of ezrin peptide therapy and owns the controlling majority of shares in Newal R&D Limited, which owns granted patents related to ezrin peptide technology in the following territories: Canada, Finland, France, Germany, Greece, Hong Kong, Hungary, Iceland, Indonesia, Ireland, Italy, Japan, Latvia, Lithuania, Luxembourg, Macedonia, Malaysia, Malta, Mexico, Moldova, Monaco, Montenegro, Morocco, Netherlands, New Zealand, Norway, Poland, Portugal, Republic of Korea, Romania, Russian Federation, San Marino, Serbia, Singapore, Slovakia, Slovenia, South Africa, Spain, Sweden, Switzerland, Turkey, United Kingdom, and the United States of America.
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