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Microbes & Immunity RANTES/CCL5 and ezrin peptide RepG3 for long COVID

Figure 3. Structures of RANTES/CCL5 and ezrin peptide RepG3. Structure of RANTES/CCL5, a 68-amino acid natural immune amplifier, compared to
14-amino acid synthetic ezrin peptide RepG3, which induces RANTES/CCL5 (both peptides contain an alpha-helical structure).

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West Nile virus (WNV), and HCV are all more severe and receptor. In addition to CD4, CCR5 is the coreceptor
more likely to become chronic infections if RANTES/ used by (R5) HIV-1 isolates of the AIDS virus for cell
CCL5 signaling is compromised. 23 membrane fusion and invasion of T-cells. Macrophage-
tropic HIV strains infect macrophages through the CCR5
3.2. RANTES/CCL5 and SARS-CoV-2 infection receptor, which is blocked by RANTES/CCL5 occupation,
The expression of RANTES/CCL5 in the upper respiratory as well as by MIP-1α and MIP-1β. 32
tract is essential for an effective mucosal immune response
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to SARS-CoV-2 and is crucial for effective virus clearance. 3.4. RANTES/CCL5, HCV infection, and hepatitis B
After infection with SARS-CoV-2, RANTES/CCL5 virus (HBV) infection
expression inhibits the replication of SARS-CoV-2 and Approximately 300 million people chronically infected with
prevents deterioration to severe acute COVID. In patients, HBV and 60 million people chronically infected with HCV
the gene expression of RANTES/CCL5 is upregulated in are at risk of liver cancer. Amplification of T-cell responses
response to SARS-CoV-2 infection, particularly to viral to HCV infection by RANTES/CCL5 signaling is critical.
spike protein, and higher serum RANTES/CCL5 levels are Serum levels of RANTES/CCL5 are increased in patients
associated with less severe COVID. High levels of RANTES/ to prevent the development of chronic HCV infection
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CCL5 are essential for effective CTL and T-cell help of B-cell- and inflammatory hepatitis. Polymorphisms in the
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mediated production of IgG antibody subclasses. CCL5 gene demonstrate that RANTES/CCL5 is protective
In a retrospective study of 255 SARS-CoV-2-infected against HCV infection. CCR5-Delta-32 polymorphism of
patients in Madrid, Spain, between November 2020 the CCL5 gene promoter at position-40 results in higher
and March 2021, depressed mucosal expression levels systemic RANTES/CCL5 expression, which correlates
of RANTES/CCL5 were the best predictor of COVID with less liver inflammation and less liver fibrosis. Another
severity. Low expression levels of RANTES/CCL5 in study on HBV infection obtained similar results. 34
nasopharyngeal samples were closely associated with high 3.5. RANTES/CCL5 and RSV infection
levels of SARS-CoV-2 viral load and predicted severe
COVID, ICU admission, and death. In contrast, higher RSV is the most common cause of respiratory disease in
levels of RANTES/CCL5 were associated with better children, and it is estimated that 60% of children with
outcomes from COVID. In addition, the nsp1 protein of bronchiolitis and 40% of children with pneumonia are
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SARS-CoV-1 coronavirus is a strong inducer of RANTES/ infected with RSV. RANTES/CCL5 is important for
CCL5 in human lung epithelial cells. 30 T-cell immune amplification to resolve RSV bronchiolitis
and pneumonia. Children respond to infection by RSV
3.3. RANTES/CCL5 and HIV infection by nasal- and adenoid-epithelial cells secreting more
RANTES/CCL5 is highly expressed in some HIV-infected RANTES/CCL5, and the serum concentration of RANTES/
people who do not proceed to AIDS. RANTES/CCL5 can CCL5 is elevated to inhibit RSV virus replication during
inhibit HIV-1 infection in vitro by occupying its CCR5 RSV bronchiolitis. 35

Volume 1 Issue 1 (2024) 5 doi: 10.36922/mi.2474