Influence of NAD+ as an ageing-related immunomodulator on COVID 19 infection: A hypothesis
Open accessAbstract
The aging-associated decline of biological functions represents an important contributor to the increase in morbidity and mortality of human beings. Of these biological functions deterioration; there is a significant decline in the heart function, impairments in the lungs gas exchange, and impairments in the immune function. Many alterations in the body humeral and cellular immune response were observed with ageing process: The circulating pro-inflammatory cytokines are increased, the naive lymphocytes are decreased, the numbers of the antigen-presenting cells areelevated and the overall response is impaired. In addition, ageing is associated with a progressive restriction in the telomere length. Telomeres are located at chromosomes ends and play an essential role in preserving chromosome stability. Also, telomere length is very important to the immune system, because of the high sensitivity of the immune cells to the shortening of telomeres. Telomeres shortening adversely affect the immune cells' function and developments. These adverse changes increased the susceptibility for severe infection, risk of hospitalization, and even death. Elderly COVID-19 patients are at a real risk of complications due to impaired immune function, cytokine storm and defective respiratory function. Administration of anti-ageing immunomodulation factors like Nicotinamide Adenine Dinucleotide NAD+ can minimize these changes through its potent immunomodulation and longevity effects. NAD+ has a direct inhibitory effect on PARP-1 and can prevent pro-inflammatory cytokines over-activation. Increasing the NAD+ level will also result in stabilizing telomeres and this has a positive impact on immune cells function.
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Excessive PARP activation compensates for ADPR hydrolysis and consumes NAD+, suggesting that increasing NAD+ may restore antiviral PARP functions to support immunity to SARS-CoV-2.
“Consequently, excessive activation of PARPs occurs to compensate for ADPR hydrolysis, accompanied by NAD+ consumption, suggesting that increasing NAD+ levels may restore the antiviral functions of PARPs to support immunity to SARS-CoV-2 [16, 106].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [106]
In “Role of NAD+ in infection and autoimmune diseases” (page unavailable), the paper says coronavirus-mediated ADP-ribose hydrolysis can prompt excessive PARP-1 activation and NAD+ consumption. It also describes PARP-1 as antiviral and says exogenous NAD+ can reverse its overactivation, but it does not say that increasing NAD+ restores PARP’s antiviral function against SARS-CoV-2; it emphasizes inhibiting PARP-1 overactivation and inflammation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTelomere shortening and a decrease in naïve lymphocytes impair immune function and increase circulating pro-inflammatory cytokines, contributing to worsening of COVID-19.
“The shortening of telomeres and decrease in naïve lymphocytes leading to impaired immune function and a rise in circulating pro-inflammatory cytokines are factors contributing to the worsening of COVID-19 cases [105, 106].”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [106]
PARPs play a critical antiviral role by inhibiting translation of viral transcripts through ADP-ribosylation, requiring NAD+.
“PARPs are known to play a critical antiviral role in inhibiting the translation of transcripts through ADP-Ribosylation in the viral genome, with NAD+ requirement.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [106]
Several viral families including SARS-CoV encode a macrodomain protein that hydrolyses ADPR units, inhibiting PARPs and facilitating replication and virulence.
“However, several viral families, including SARS-CoV, encode a macrodomain protein that hydrolyses the ADPR units of proteins and nucleic acids, inhibiting PARPs protective effect and then facilitating replication and virulence.”
From NAD+ Precursors Nicotinamide Mononucleotide (NMN) and Nicotinamide Riboside (NR): Potential Dietary Contribution to Health (2023) · cites this paper as [106]
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- Authors
- Omran, H. M., & Almaliki, M. S.
- Corresponding author
- Omran, Huda M.
- Venue
- Journal of Infection and Public Health
- Publisher
- Elsevier BV
- Published
- 2020-09
- Volume
- 13
- Issue
- 9
- Pages
- 1196-1201
- ISSN
- 1876-0341 (ISSN-L)
- PMC
- PMC7275989
- OpenAlex
- W3033048015
- Cited by
- 45
- References
- 86
- Citations by year
- 2025: 2 · 2024: 9 · 2023: 9 · 2022: 9 · 2021: 13 · 2020: 3
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Infection and Public Health (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Keywords
- NAD+, COVID-19 pandemic, immunosenescence, aging, immunomodulation, telomere shortening, PARP1 inhibition, inflammatory cytokines, cytokine storm, elderly patients
- MeSH terms
- Poly (ADP-Ribose) Polymerase-1, Betacoronavirus, COVID-19, SARS-CoV-2, Aging, Autoimmune Diseases, Humans, NAD, Pneumonia, Viral, Cytokines, Coronavirus Infections, Pandemics, Telomere Shortening
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