AAV-KLK13 for COVID-19
c19early.org
COVID-19 Treatment Clinical Evidence
COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets.
c19early analyzes 6,000+ studies for 210+ treatments—over 17 million hours of research.
Only three high-profit early treatments are approved in the US.
In reality, many treatments reduce risk,
with 25 low-cost treatments approved across 163 countries.
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Naso/
oropharyngeal treatment Effective Treatment directly to the primary source of initial infection. -
Healthy lifestyles Protective Exercise, sunlight, a healthy diet, and good sleep all reduce risk.
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Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
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Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
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Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
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High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
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Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
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Acetaminophen Harmful Increased risk of severe outcomes and mortality.
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Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.
AAV-KLK13 may be beneficial for
COVID-19 according to the study below.
COVID-19 involves the interplay of 400+ viral and host proteins and factors providing many therapeutic targets.
Scientists have proposed 11,000+ potential treatments.
c19early.org analyzes
210+ treatments.
We have not reviewed AAV-KLK13 in detail.
, Nasal mucus-derived KLK13 restricts SARS-CoV-2 infection via proteolytic cleavage of spike, mBio, doi:10.1128/mbio.02051-25
ABSTRACT The epithelial cilia are the first line of defense against respiratory pathogens. For the first time, we found that Kallikrein-related peptidase 13 (KLK13), a serine protease expressed in airway ciliated epithelial cells with cell type specificity, was secreted into nasal mucus. KLK13 efficiently cleaved the spike of SARS-CoV-2, resulting in the inhibition of SARS-CoV-2 cell entry and spike protein-mediated cell-cell fusion. Recombinant KLK13 protease efficiently cleaved the spike protein as well as virus particles in vitro . Only KLK13, but not other members of the KLK family, specifically cleaved the spike proteins of SARS-CoV-2 as well as other coronaviruses. We also confirmed that endogenous KLK13 stimulated by CRISPR activation (CRISPRa) in A549 cells inhibited SARS-CoV-2 pseudovirus entry. The mRNA level of KLK13 was stimulated by poly (I:C) in both A549 and HeLa cells, and its expression level was also increased in SARS-CoV-2-infected clinical samples. Recombinant adeno-associated virus packaged KLK13 (AAV-KLK13) reduced SARS-CoV-2 replication in a K18-ACE2 mouse model. Collectively, the nasal mucus-derived KLK13 functions as a scissor of coronaviruses and holds the potential to be further developed as a broad-spectrum antiviral against coronaviruses. IMPORTANCE Epithelial cilia directly come into contact with inhaled pathogens. The nasal mucus functions as a formidable barrier against penetration of viral particles. KLK13 is secreted into nasal mucus and efficiently cleaves the spike proteins across different coronavirus species. KLK13-mediated cleavage of spike inhibits SARS-CoV-2 entry and syncytium formation. Intranasally delivered KLK13 also restricts SARS-CoV-2 infection in vivo . The finding that KLK13 acts as a scissor of viral spike in nasal mucus paves the way for the development of new antivirals against respiratory viruses.