NH4Cl 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.

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.
Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
Acetaminophen Harmful Increased risk of severe outcomes and mortality.
Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.

NH4Cl may be beneficial for COVID-19 according to the studies 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 NH4Cl in detail.

Studies suggesting benefit with NH4Cl

Zhang et al., SARS-CoV-2 spike protein dictates syncytium-mediated lymphocyte elimination, Cell Death & Differentiation, doi:10.1038/s41418-021-00782-3

Hansen et al., Getting in on the action: New tools to see SARS-CoV-2 infect a cell, Cell Chemical Biology, doi:10.1016/j.chembiol.2023.02.010

Cesar-Silva et al., Lipid compartments and lipid metabolism as therapeutic targets against coronavirus, Frontiers in Immunology, doi:10.3389/fimmu.2023.1268854

Lipids perform a series of cellular functions, establishing cell and organelles’ boundaries, organizing signaling platforms, and creating compartments where specific reactions occur. Moreover, lipids store energy and act as secondary messengers whose distribution is tightly regulated. Disruption of lipid metabolism is associated with many diseases, including those caused by viruses. In this scenario, lipids can favor virus replication and are not solely used as pathogens’ energy source. In contrast, cells can counteract viruses using lipids as weapons. In this review, we discuss the available data on how coronaviruses profit from cellular lipid compartments and why targeting lipid metabolism may be a powerful strategy to fight these cellular parasites. We also provide a formidable collection of data on the pharmacological approaches targeting lipid metabolism to impair and treat coronavirus infection.

Shang et al., Inhibitors of endosomal acidification suppress SARS-CoV-2 replication and relieve viral pneumonia in hACE2 transgenic mice, Virology Journal, doi:10.1186/s12985-021-01515-1

Abstract Background Coronavirus disease 2019 (COVID-19) is caused by SARS-CoV-2 and broke out as a global pandemic in late 2019. The acidic pH environment of endosomes is believed to be essential for SARS-CoV-2 to be able to enter cells and begin replication. However, the clinical use of endosomal acidification inhibitors, typically chloroquine, has been controversial with this respect. Methods In this study, RT-qPCR method was used to detect the SARS-CoV-2N gene to evaluate viral replication. The CCK-8 assay was also used to evaluate the cytotoxic effect of SARS-CoV-2. In situ hybridization was used to examine the distribution of the SARS-CoV-2 gene in lung tissues. Hematoxylin and eosin staining was also used to evaluate virus-associated pathological changes in lung tissues. Results In this study, analysis showed that endosomal acidification inhibitors, including chloroquine, bafilomycin A1 and NH4CL, significantly reduced the viral yields of SARS-CoV-2 in Vero E6, Huh-7 and 293T-ACE2 cells. Chloroquine and bafilomycin A1 also improved the viability and proliferation of Vero E6 cells after SARS-CoV-2 infection. Moreover, in the hACE2 transgenic mice model of SARS-CoV-2 infection, chloroquine and bafilomycin A1 reduced viral replication in lung tissues and alleviated viral pneumonia with reduced inflammatory exudation and infiltration in peribronchiolar and perivascular tissues, as well as improved structures of alveolar septum and pulmonary alveoli. Conclusions Our research investigated the antiviral effects of endosomal acidification inhibitors against SARS-CoV-2 in several infection models and provides an experimental basis for further mechanistic studies and drug development.