SARS-CoV-2 Infected Macrophages Found to Release Deadly Vesicles That Age Cells and Cripple Bacterial Defenses!
Nikhil Prasad Fact checked by:Thailand Medical News Team Apr 25, 2025 4 hours, 13 minutes ago
Medical News: A new study out of Brazil has uncovered a previously unknown mechanism by which SARS-CoV-2, the virus responsible for COVID-19, may be causing long-term damage to the human body—even long after the virus has left the system. Scientists have discovered that the virus can hijack immune cells and force them to release microscopic particles, or extracellular vesicles (EVs), that drive cellular aging and weaken the body’s ability to fight off bacterial infections.
Schematic representation of SASP induction by EVs treatment, focusing on TREM-1, miRNA, and inflammatory mediator expression. This supports the hypothesis that MφV-EVs carry early immunosenescence markers and influence SASP modulation. Additionally, miRNAs delivered by EVs may regulate the immune response and the senescence process, as evidenced by miR-155 increases.
This
Medical News report focuses on the role of specialized vesicles produced by infected immune cells—specifically, macrophages—that carry inflammatory molecules and aging-related signals into other cells. These “booby-trapped” vesicles not only provoke inflammation, but also shut down normal immune defenses, effectively sabotaging the body from within.
The groundbreaking research was conducted by scientists from several departments within the University of São Paulo in Brazil, including the Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Faculdade de Medicina de Ribeirão Preto, Faculdade de Zootecnia e Engenharia de Alimentos in Pirassununga, and Instituto de Ciências Biológicas at the Universidade Federal do Amazonas in Manaus.
Hijacked Macrophages Become Agents of Inflammation and Immune Collapse
Macrophages are essential immune cells that act as the body’s cleanup crew, detecting and destroying invading pathogens. However, the researchers found that when macrophages are exposed to SARS-CoV-2 particles, they undergo disturbing changes. These infected macrophages begin producing abnormal extracellular vesicles—tiny lipid-encased packets that are normally used for healthy cell communication.
But in this case, the SARS-CoV-2-altered macrophages released vesicles loaded with dangerous cargo, including a receptor called TREM-1 (Triggering Receptor Expressed on Myeloid cells 1), pro-inflammatory cytokines such as IL-8, and a particularly troubling molecule: microRNA-155, which is known to fuel inflammation and cellular aging.
Even more alarming, when these altered EVs interacted with other healthy immune cells, they triggered gene activity associated with cellular senescence. Cells that become senescent stop dividing, begin to secrete harmful inflammatory substances, and can damage tissues around them. Essentially, these vesicles were sending “aging signals” to healthy immune cells, disrupting their normal function and pushing them toward dysfunction.
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Key Findings Show Link Between Viral Vesicles and Long COVID Symptoms
Among the most striking findings, the researchers observed that:
-The SARS-CoV-2-influenced vesicles were significantly larger than those produced by normal or even classically activated macrophages.
-These vesicles carried a distinctive molecular signature with elevated TREM-1 expression, high levels of inflammatory mediators like MMP-9 and IL-8, and abnormal miRNA content, particularly miR-155.
-When these vesicles were introduced to healthy immune cells, they triggered overexpression of two critical genes involved in aging and cell cycle arrest: CDKN2A (which encodes the protein p16) and TP53 (which encodes the tumor suppressor protein p53).
-These gene activations are classic signs of cellular senescence, a condition associated with aging, chronic disease, and weakened immune response.
Furthermore, in functional assays, the macrophages exposed to these SARS-CoV-2-modified EVs lost much of their ability to produce inflammatory cytokines like TNF and IL-1β in response to bacterial threats. Even more concerning, their ability to kill bacteria such as E. coli was significantly impaired, indicating a collapse in innate immune defense mechanisms.
Implications for Long COVID and Post-Infection Vulnerability
This research provides a critical missing link in understanding why many people continue to suffer lingering symptoms months or even years after the initial infection, regardless of whether they were vaccinated or had a mild form of COVID-19. The production and spread of these senescence-inducing EVs could explain symptoms such as:
-Fatigue
-Brain fog
-Chronic inflammation
-Susceptibility to other infections
-Exacerbation of aging-related illnesses
In essence, the virus may be sowing seeds of long-term immune dysfunction by instructing infected cells to manufacture these toxic vesicles, which continue to cause damage even after the virus is cleared.
Conclusions Offer Alarming Insights into How SARS-CoV-2 Causes Lasting Harm
This study offers compelling evidence that SARS-CoV-2 is not just a respiratory virus but a master manipulator of the immune system. By hijacking macrophages and converting them into producers of dangerous EVs, the virus initiates a self-sustaining cycle of inflammation, cellular aging, and immune suppression. The presence of molecules like TREM-1 and miRNA-155 in these vesicles amplifies this effect, driving neighboring immune cells into a dysfunctional, senescent state.
More importantly, the infected cells' vesicles impair the immune system’s ability to perform its most basic task—destroying harmful bacteria. This raises serious concerns about patients' vulnerability to post-COVID infections, whether bacterial, fungal, or opportunistic.
In a broader context, these findings suggest that COVID-19 is not merely an acute illness, but one with long-lasting cellular and molecular consequences. The chronic damage inflicted by these virus-induced vesicles may underlie many of the symptoms observed in Long COVID sufferers and could potentially accelerate aging processes or trigger the onset of age-related diseases.
Future treatments might target the TREM-1 pathway or find ways to neutralize these inflammatory vesicles. Doing so could provide relief for those with lingering post-COVID symptoms and reduce the risk of long-term immune compromise. However, more in vivo research is urgently needed to translate these findings into clinical interventions.
The study findings were published in the peer reviewed journal: Viruses.
https://www.mdpi.com/1999-4915/17/5/610
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https://www.thailandmedical.news/news/individuals-exposed-to-covid-19-age-faster-at-a-molecular-level-and-face-higher-risk-of-age-related-diseases-and-shorter-lifespans
https://www.thailandmedical.news/news/sars-cov-2-alters-blood-formation-and-triggers-immune-aging-in-stem-cells
https://www.thailandmedical.news/news/sars-cov-2-spike-protein-induces-the-formation-of-senescent-cells-particularly-in-heart-tissues
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