Marc Veldhoen
@marcveld.bsky.social
Professor of Immunology 🇳🇱 🇬🇧
Lisbon, 🇵🇹
#Immunology
Time for Science, not silence
https://scholar.google.co.uk/citations?user=7vG1jLIAAAAJ&hl=en
https://orcid.org/0000-0002-1478-9562
threads.net/@marc_veld
mastodon.online/@marc_veld
Lisbon, 🇵🇹
#Immunology
Time for Science, not silence
https://scholar.google.co.uk/citations?user=7vG1jLIAAAAJ&hl=en
https://orcid.org/0000-0002-1478-9562
threads.net/@marc_veld
mastodon.online/@marc_veld
Any expert sees through this. Sees this is a bad paper, low impact journal, the authors are no experts, the data not sound. Looking at total PBMC without knowing the cell composition? No infection controls?
It does not hold up, it is not evidence of anything.
bsky.app/profile/marc...
It does not hold up, it is not evidence of anything.
bsky.app/profile/marc...
Investigating apoptosis in peripheral blood mononuclear cells among the elderly in the post-COVID-19 era
Very bad paper, no conclusions possible. The authors do not even know which cells they are looking at!
bmcimmunol.biomedcen...
1/7
Very bad paper, no conclusions possible. The authors do not even know which cells they are looking at!
bmcimmunol.biomedcen...
1/7
Investigating apoptosis in peripheral blood mononuclear cells among the elderly in the post-COVID-19 era - BMC Immunology
Background and aim The COVID-19 pandemic has left a lasting imprint on immune function, particularly in the elderly—a population already vulnerable to immunosenescence. While acute and long-COVID immune responses have been widely studied, the long-term apoptotic behavior of peripheral blood mononuclear cells (PBMCs) remains underexplored. This study aims to investigate the legacy of SARS-CoV-2 on PBMC apoptosis in elderly individuals during the post-COVID era, shedding light on potential persistent immune dysregulation. Materials and methods In this cross-sectional study, PBMCs were isolated from peripheral blood samples of elderly individuals (> 65 years old) with a documented history of COVID-19 infection at least six months prior. Using multiparametric flow cytometry, we quantified early and late apoptosis markers (Annexin V/PI), mitochondrial membrane potential disruption (ΔΨm), and expression of pro-apoptotic (Bax, Caspase-3) and anti-apoptotic (Bcl-2) proteins. Statistical analyses were performed to assess intergroup differences and correlations with clinical history. This study was conducted in 2025. Results Elderly post-COVID individuals exhibited a significantly elevated proportion of apoptotic PBMCs compared to controls (p < 0.01), particularly within the CD4 + and CD8 + T-cell subsets. Mitochondrial depolarization and increased Bax/Bcl-2 ratios indicated a shift toward intrinsic apoptotic pathways. Caspase-3 activation was also heightened in the post-COVID group. Notably, apoptotic burden correlated with time since infection and severity of initial illness. Discussion Our findings suggest a prolonged apoptotic signature in the immune cells of elderly individuals following recovery from COVID-19. These alterations may reflect a sustained immune exhaustion or maladaptive remodeling of lymphocyte populations, potentially contributing to impaired immunosurveillance and increased vulnerability to secondary infections or chronic inflammatory conditions. Conclusion COVID-19 may cast a long immunological shadow in the elderly, with persistent PBMC apoptosis representing a novel facet of post-viral immune dysregulation. Flow cytometry reveals a unique apoptotic phenotype that could serve as a biomarker for long-term immune health and guide post-pandemic clinical management strategies for aging populations.
bmcimmunol.biomedcentral.com
November 11, 2025 at 3:02 PM
Any expert sees through this. Sees this is a bad paper, low impact journal, the authors are no experts, the data not sound. Looking at total PBMC without knowing the cell composition? No infection controls?
It does not hold up, it is not evidence of anything.
bsky.app/profile/marc...
It does not hold up, it is not evidence of anything.
bsky.app/profile/marc...
It would be great if someone would actually come with evidence. The primary solid publications, the figures where this is evident and the context that this is the norm for all. Is that too much to ask for those claiming "right"? If it is, than "right" is simply: wrong.
November 11, 2025 at 2:37 PM
It would be great if someone would actually come with evidence. The primary solid publications, the figures where this is evident and the context that this is the norm for all. Is that too much to ask for those claiming "right"? If it is, than "right" is simply: wrong.
There is no T cell "damage", "exhaustion" or "dysfunction".
-T cells are extremely specific, which T cells does this apply to?
-If there was anything wrong, how come we do not see any of it? We see very good immunity, against SARS-CoV-2 and all other infections, just as pre-2020.
-T cells are extremely specific, which T cells does this apply to?
-If there was anything wrong, how come we do not see any of it? We see very good immunity, against SARS-CoV-2 and all other infections, just as pre-2020.
Post-COVID-19 immune competence
A short reference for those facing arguments of immune damage, exhaustion, lymphopenia or immunodeficiency.
marcveldhoen.substack.com
November 11, 2025 at 2:37 PM
There is no T cell "damage", "exhaustion" or "dysfunction".
-T cells are extremely specific, which T cells does this apply to?
-If there was anything wrong, how come we do not see any of it? We see very good immunity, against SARS-CoV-2 and all other infections, just as pre-2020.
-T cells are extremely specific, which T cells does this apply to?
-If there was anything wrong, how come we do not see any of it? We see very good immunity, against SARS-CoV-2 and all other infections, just as pre-2020.
It is a gimmick. Thinking outside the box can be beneficial, but only if it is realistic and supported by data.
November 11, 2025 at 12:53 PM
It is a gimmick. Thinking outside the box can be beneficial, but only if it is realistic and supported by data.
Epidemiologist Michael Osterholm talks about efforts by the Center for Infectious Disease Research and Policy to inform vaccine recommendations and maintain public-health awareness during the Trump administration.
2/2
2/2
November 11, 2025 at 11:28 AM
Epidemiologist Michael Osterholm talks about efforts by the Center for Infectious Disease Research and Policy to inform vaccine recommendations and maintain public-health awareness during the Trump administration.
2/2
2/2
Again this data shows SARS-CoV-2 was naturally sufficiently adjusted to humans that infection was relatively easy.
Nevertheless, it went through rapid cycles of optimalisation thereafter, eventually and so far, ending with Omicron subvariants.
4/4
Nevertheless, it went through rapid cycles of optimalisation thereafter, eventually and so far, ending with Omicron subvariants.
4/4
November 10, 2025 at 11:07 PM
Again this data shows SARS-CoV-2 was naturally sufficiently adjusted to humans that infection was relatively easy.
Nevertheless, it went through rapid cycles of optimalisation thereafter, eventually and so far, ending with Omicron subvariants.
4/4
Nevertheless, it went through rapid cycles of optimalisation thereafter, eventually and so far, ending with Omicron subvariants.
4/4
When hACE2 and TMPRSS2 are placed in the bat cells, infection is very easy.
Why? The virus clealy can infect bats. The cells in isolation may not express sufficient receptors has been suggested.
journals.asm.org/doi...
3/4
Why? The virus clealy can infect bats. The cells in isolation may not express sufficient receptors has been suggested.
journals.asm.org/doi...
3/4
Species-Specific Molecular Barriers to SARS-CoV-2 Replication in Bat Cells | Journal of Virology
Bats are host ancestors of several viruses that cause serious disease in humans, as
illustrated by the ongoing SARS-CoV-2 pandemic. Progress in investigating bat-virus
interactions has been hampered by a limited number of available bat cellular models.
journals.asm.org
November 10, 2025 at 11:07 PM
When hACE2 and TMPRSS2 are placed in the bat cells, infection is very easy.
Why? The virus clealy can infect bats. The cells in isolation may not express sufficient receptors has been suggested.
journals.asm.org/doi...
3/4
Why? The virus clealy can infect bats. The cells in isolation may not express sufficient receptors has been suggested.
journals.asm.org/doi...
3/4
in Rhinolophus cells. BANAL-236 did not replicate in wild-type Rhinolophus cell lines.
The S protein of BANAL-236 interacts more efficiently with hACE2 than with its Rhinolophus counterpart..
Like SARS-COV-2, "well adjusted to humans'?
2/4
The S protein of BANAL-236 interacts more efficiently with hACE2 than with its Rhinolophus counterpart..
Like SARS-COV-2, "well adjusted to humans'?
2/4
November 10, 2025 at 11:07 PM
in Rhinolophus cells. BANAL-236 did not replicate in wild-type Rhinolophus cell lines.
The S protein of BANAL-236 interacts more efficiently with hACE2 than with its Rhinolophus counterpart..
Like SARS-COV-2, "well adjusted to humans'?
2/4
The S protein of BANAL-236 interacts more efficiently with hACE2 than with its Rhinolophus counterpart..
Like SARS-COV-2, "well adjusted to humans'?
2/4
"The significant increase in self-reported cognitive disability, particularly after 2016, suggests changing perceptions or experiences of cognitive challenges in the US population."
8/8
8/8
November 10, 2025 at 9:31 PM
"The significant increase in self-reported cognitive disability, particularly after 2016, suggests changing perceptions or experiences of cognitive challenges in the US population."
8/8
8/8
There was no difference between men and women. Cognitive disability demonstrates substantial and persistent disparities across racial, ethnic, and socioeconomic groups.
7/8
7/8
November 10, 2025 at 9:31 PM
There was no difference between men and women. Cognitive disability demonstrates substantial and persistent disparities across racial, ethnic, and socioeconomic groups.
7/8
7/8