Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors (2021)

Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.

Abstract

The SARS-CoV-2 infection determines the COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, pulmonary and cardiac fibrosis, inflammatory cytokine release, and immunosuppression. This condition has led to the death of about 2.15% of the total infected world population so far. Among survivors, the presence of the so-called persistent post-COVID-19 syndrome (PPCS) is a common finding. In COVID-19 survivors, PPCS presents one or more symptoms: fatigue, dyspnea, memory loss, sleep disorders, and difficulty concentrating. In this study, a cohort of 117 COVID-19 survivors (post-COVID-19) and 144 non-infected volunteers (COVID-19-free) was analyzed using pyrosequencing of defined CpG islands previously identified as suitable for biological age determination. The results show a consistent biological age increase in the post-COVID-19 population, determining a DeltaAge acceleration of 10.45 ± 7.29 years (+5.25 years above the range of normality) compared with 3.68 ± 8.17 years for the COVID-19-free population (p < 0.0001). A significant telomere shortening parallels this finding in the post-COVID-19 cohort compared with COVID-19-free subjects (p < 0.0001). Additionally, ACE2 expression was decreased in post-COVID-19 patients, compared with the COVID-19-free population, while DPP-4 did not change. In light of these observations, we hypothesize that some epigenetic alterations are associated with the post-COVID-19 condition, particularly in younger patients (< 60 years).

Keywords: biological age; COVID-19; post-COVID-19; telomeres; epigenetics; DNA methylation; ACE2; DPP-4; DeltaAge

Full paper:

https://www.mdpi.com/1422-0067/22/11/6151/htm

Particularly hard on the under 60’s there. Epigenetic changes caused by methylation (ie long term gene silencing) + ACE2 depletion are suspected as contributory.

I would also add DNA damage caused by ROS generation and immune exhaustion to the list, as covered previously:

Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #4:Telomere Dynamics in Immune Senescence and Exhaustion Triggered by Chronic Viral Infection

https://doorlesscarp953.substack.com/p/spike-protein-inc-vax-induced-immunodeficiency-655/comments

---

Is HIV a Model of Accelerated or Accentuated Aging? (2014)

"Accumulated comorbidities in multiple systems lead to geriatric syndromes—multimorbidity, polypharmacy, frailty, and even falls an average of 15–20 years earlier than in HIV-uninfected participants."

"For example, cardiovascular risk factors and rates of acute coronary syndromes are markedly increased in HIV-infected versus age-matched control participants (28), and coronary artery “age” assessed by coronary artery calcium score is accelerated on average by about 15 years."

"ART-treated patients with a fully suppressed viral load (median age 56 years, <50 HIV-1 RNA copies/mL, median CD4 count 724 cells/mm3) have frequencies of senescent CD8+ T cells (CD57+CD28− phenotype) similar to HIV-negative individuals decades older (median age 88 years)"

"Young HIV-infected men exhibit age-related changes to the monocyte phenotype and levels of innate immune activation that resemble those observed in HIV-uninfected individuals aged approximately 30 years older."

"Long-term successfully treated HIV-infected individuals have high levels of CMV-specific effector cells, similar to that observed in the elderly participants, but occurring about 40 years earlier."

https://academic.oup.com/biomedgerontology/article/69/7/833/661915?login=false

---

And in cancer patients:

Accelerated aging?

We may not be imagining it

https://doorlesscarp953.substack.com/p/accelerated-aging?s=w