🕷️ Crawler Inspector

URL Lookup

Direct Parameter Lookup

Raw Queries and Responses

1. Shard Calculation

Query:

Response:

Calculated Shard: 137 (from laksa138)

2. Crawled Status Check

Query:

curl -X POST \
  'http://laksa137.int.ahrefs:8124/' \
  -H 'Content-Type: text/plain' \
  -H 'X-ClickHouse-Database: crawler3' \
  -H 'Authorization: Basic YXBpOg==' \
  -d 'SELECT getAhrefsURLFromUnparsed(src_unparsed) AS found_url, ifNull(toUnixTimestamp(download_stamp), 0) AS crawl_time, ifNull(toUnixTimestamp(props_url_first_seen), 0) AS first_indexed_time, download_http_code AS http_code, src_unparsed AS src_unparsed, src_root_hash AS src_root_hash, history_drop_reason AS history_drop_reason, meta_title AS meta_title, meta_descriptions AS meta_descriptions, attrs_boilerpipe_text AS attrs_boilerpipe_text, attrs_markdown AS attrs_markdown, attrs_readable_markdown AS attrs_readable_markdown, meta_canonical AS meta_canonical FROM crawler3.page_info_local FINAL PREWHERE (src_root_hash, src_unparsed) IN ((getAhrefsRootHashFromUnparsed(getAhrefsUnparsedNoserviceFromURL(\'https://neurosciencenews.com/covid-flu-brain-fog-inflammation-30192/\')), getAhrefsUnparsedNoserviceFromURL(\'https://neurosciencenews.com/covid-flu-brain-fog-inflammation-30192/\'))) FORMAT JSONEachRow'

Response:

{"found_url":"https:\/\/neurosciencenews.com\/covid-flu-brain-fog-inflammation-30192\/","crawl_time":1776277767,"first_indexed_time":1772046087,"http_code":200,"src_unparsed":"com,neurosciencenews!\/covid-flu-brain-fog-inflammation-30192\/ s443","src_root_hash":"5108634008265956737","history_drop_reason":null,"meta_title":"COVID-19 Uniquely Rewires the Brain Compared to the Flu - Neuroscience News","meta_descriptions":["Researchers discover that COVID-19 uniquely causes brain inflammation and disrupts serotonin\/dopamine pathways, explaining \"brain fog\" in Long COVID."],"attrs_boilerpipe_text":"Summary:\nWhile both the flu and COVID-19 are respiratory viruses that can leave lasting lung damage, only COVID-19 appears to leave a persistent, inflammatory footprint on the brain. New research reveals that SARS-CoV-2 causes small blood vessel injury and ongoing brain inflammation even after the virus is cleared.\nThis study found that COVID-19 specifically disrupts serotonin and dopamine signaling—neurotransmitters critical for mood, cognition, and energy. These findings provide a biological explanation for why “brain fog” and fatigue are hallmark symptoms of Long COVID, but are rarely seen after the seasonal flu.\nKey Facts\nVascular Injury:\nCOVID-19, but not the flu, causes tiny areas of bleeding and inflammation in the brain’s small blood vessels, even in mild cases.\nNeurotransmitter Disruption:\nSARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, which explains the persistent cognitive and mood changes in Long COVID.\nLung Repair Failure:\nWhile both viruses cause lung scarring (collagen buildup), the lungs switch into “repair mode” after the flu. Following COVID-19, this natural healing response is largely missing.\nAbsence of Virus:\nStrikingly, the brain inflammation occurred despite the fact that no actual virus was detected in the brain tissue, suggesting the damage is caused by the body’s overactive immune response.\nSubchronic Effects:\nThe study focused on the “subchronic” phase—weeks after the initial infection—to specifically map out the transition from acute illness to long-term symptoms.\nSource:\nTulane University\nEven a mild case of COVID-19 or the flu can impact the body long after the fever and cough fade, according to new Tulane University research that may help explain why some people struggle to feel fully recovered weeks or months later.\nTulane researchers found that while both viruses can leave lasting lung damage, only SARS-CoV-2 infection caused persistent brain inflammation and small blood vessel injury, even after the virus was no longer detectable.\nNew evidence suggests that Long COVID’s neurological symptoms are driven by persistent vascular inflammation and the disruption of key neurotransmitter pathways that are unaffected by influenza. Credit: Neuroscience News\nThe findings, published in \nFrontiers in Immunology\n, help explain why long COVID often includes neurological symptoms such as brain fog, fatigue and mood changes, while influenza is more commonly associated with respiratory complications.\n“Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” said Dr. Xuebin Qin, lead author and professor of microbiology and immunology at the Tulane National Biomedical Research Center.\nTo separate effects common to severe respiratory infections from those unique to COVID-19, researchers used a mouse model to examine lung and brain tissue after infection had cleared.\nIn the lungs, both viruses left behind a similar picture: immune cells that failed to fully stand down and increased buildup of collagen, a protein associated with scarring. Those changes can stiffen lung tissue and make breathing feel more labored — a possible biological explanation for why some people report lingering shortness of breath after respiratory infections.\nBut when the researchers looked more closely, they found a key difference. After the flu, the lungs appeared to switch into repair mode, sending specialized cells into damaged areas to help rebuild the lining of the airways. That repair response was largely missing after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing process.\nThe most striking differences appeared in the brain.\nAlthough neither virus was found in brain tissue, mice that had COVID-19 showed signs of persistent brain inflammation weeks later, along with tiny areas of bleeding. Gene expression analysis revealed ongoing inflammatory signaling and disruption of pathways involved in serotonin and dopamine regulation, systems closely tied to mood, cognition and energy levels. These persistent changes were largely absent in influenza-infected animals.\n“In both infections, we observed lasting lung injury,” Qin said. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.”\nThis study was supported by an American Heart Association award Qin received as part of a national effort to understand the long-term cardiovascular and cerebrovascular effects of COVID-19. The findings shed new light on how vascular and immune changes may contribute to persistent neurological symptoms.\nBy defining these biological changes, the research offers a clearer foundation for monitoring patients and developing treatments aimed at preventing lasting damage. As lingering symptoms continue to complicate recovery for some, understanding what is driving them is essential to reducing long-term health consequences.\nFunding:\nThis research was supported by the American Heart Association Long COVID Impact Project (AHA962950), the National Institutes of Health, including P51OD011104-62 and R01HL165265, and institutional funding.\nKey Questions Answered:\nQ: Why does COVID feel so different from the flu during recovery?\nA:\nThis study shows that while both can scar your lungs, only COVID-19 effectively “sets fire” to your brain’s communication lines. By damaging small blood vessels and disrupting serotonin and dopamine, COVID creates a biological environment for depression, fatigue, and “fog” that the flu simply doesn’t.\nQ: If the virus isn’t in my brain, how is it causing damage?\nA:\nIt’s an immune “echo.” Even after the virus is gone, your body’s inflammatory signals stay turned on in the brain. This ongoing inflammation causes small leaks in blood vessels and messes with the chemicals that help you think and feel happy.\nQ: Can the lung damage be reversed?\nA:\nThe research found that after the flu, the body sends in a “repair crew” to fix the airway lining. After COVID, that crew never shows up. This suggests we may need specific treatments to jumpstart the healing process in Long COVID patients.\nEditorial Notes:\nThis article was edited by a Neuroscience News editor.\nJournal paper reviewed in full.\nAdditional context added by our staff.\nAbout this COVID-19 and neurology research news\nAuthor:\nAndrew Yawn\nSource:\nTulane University\nContact:\nAndrew Yawn – Tulane University\nImage:\nThe image is credited to Neuroscience News\nOriginal Research:\nOpen access.\n“\nCharacterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice\n” by Joshua Currey, Chenxiao Wang, Meredith G. Mayer, Yilin Chen, Ana Karina Nisperuza Vidal, Michaela J. Allen, Mst Shamima Khatun, Calder R. Ellsworth, Mohammad Islamuddin, Jefferson Evangelista, Skye M. Minor, Nadia Golden, Kevin J. Zwezdaryk, Nicholas J. Maness, Robert V. Blair, Jay K. Kolls, Derek A. Pociask, Tracy Fischer, and Xuebin Qin.\nFrontiers in Immunology\nDOI:10.3389\/fimmu.2026.1755141\nAbstract\nCharacterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice\nIntroduction: \nSARS-CoV-2 and, to a lesser extent, influenza A can lead to long-term complications in the respiratory and nervous systems. However, the mechanisms driving post-viral sequelae remain poorly understood.\nMethods: \nTo address this gap, we longitudinally characterized C57BL\/6 mice infected with sublethal doses of mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). Lung and brain tissues were analyzed at 14-, 21-, and 28-days post-infection (DPI) using histological analysis and bulk-RNA sequencing.\nResults: \nIn the lungs, both infections caused prolonged inflammation and fibrosis. MA30-infected lungs showed persistent upregulation of inflammation, coagulation, complement, as well as fibrotic, and extracellular matrix (ECM) remodeling pathways at 21 DPI, alongside downregulation of epithelial junction and metabolic program pathways.\nIn contrast, PR8-infected lungs exhibited a strong acute interferon response and chronic upregulation of basal epithelial markers (e.g., \nKrt5\n, \nKrt14\n), consistent with epithelial regeneration. Notably, only PR8-infected mice displayed KRT5+ progenitor cell migration into damaged lung regions, indicating divergence in repair mechanisms.\nNeither MA30-infected, nor PR8-infected mice had detectable brain infection. However, MA30 mice, but not PR8-infected mice exhibited an elevated frequency of microhemorrhages at early timepoints and marked neuroinflammation at all timepoints. Transcriptomic profiling of MA30-infected brains showed enrichment for up-regulation of ECM remodeling, vascular dysfunction, IL6-signaling pathways along with a virus-specific disruption of the hypothalamic–pituitary axis with MA30 infection not seen in PR8-infected brains.\nThese included genes linked to neuroinflammation, sensory processing disruption, and microvascular injury, mirroring clinical features of Long COVID.\nDiscussion: \nTogether, these findings establish distinct tissue-specific trajectories of long-term pathology following SARS-CoV-2 and influenza infection and provide a foundation for dissecting the mechanisms of post-viral lung and brain disease.","attrs_markdown":"[![Neuroscience News logo for mobile.](https:\/\/neurosciencenews.com\/files\/2020\/07\/Neuroscience-News_AZ_RevNewest-scaled-e1596228355273-1.jpg)](https:\/\/neurosciencenews.com\/)\n\n[![Neuroscience News Logo](https:\/\/neurosciencenews.com\/files\/2020\/07\/Neuroscience-News_AZ_RevNewest-scaled-e1596228355273.jpg)](https:\/\/neurosciencenews.com\/)\n\n# COVID-19 Uniquely Rewires the Brain Compared to the Flu\n[Featured](https:\/\/neurosciencenews.com\/neuroscience-topics\/featured\/)[Neurology](https:\/\/neurosciencenews.com\/neuroscience-topics\/neurology\/)[Neuroscience](https:\/\/neurosciencenews.com\/neuroscience-topics\/neuroscience\/)\n\n·\n\nFebruary 25, 2026\n\n**Summary:** While both the flu and COVID-19 are respiratory viruses that can leave lasting lung damage, only COVID-19 appears to leave a persistent, inflammatory footprint on the brain. New research reveals that SARS-CoV-2 causes small blood vessel injury and ongoing brain inflammation even after the virus is cleared.\n\nThis study found that COVID-19 specifically disrupts serotonin and dopamine signaling—neurotransmitters critical for mood, cognition, and energy. These findings provide a biological explanation for why “brain fog” and fatigue are hallmark symptoms of Long COVID, but are rarely seen after the seasonal flu.\n\n**Key Facts**\n\n- **Vascular Injury:** COVID-19, but not the flu, causes tiny areas of bleeding and inflammation in the brain’s small blood vessels, even in mild cases.\n- **Neurotransmitter Disruption:** SARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, which explains the persistent cognitive and mood changes in Long COVID.\n- **Lung Repair Failure:** While both viruses cause lung scarring (collagen buildup), the lungs switch into “repair mode” after the flu. Following COVID-19, this natural healing response is largely missing.\n- **Absence of Virus:** Strikingly, the brain inflammation occurred despite the fact that no actual virus was detected in the brain tissue, suggesting the damage is caused by the body’s overactive immune response.\n- **Subchronic Effects:** The study focused on the “subchronic” phase—weeks after the initial infection—to specifically map out the transition from acute illness to long-term symptoms.\n\n**Source:** Tulane University\n\n**Even a mild case of COVID-19 or the flu can impact the body long after the fever and cough fade, according to new Tulane University research that may help explain why some people struggle to feel fully recovered weeks or months later.**\n\nTulane researchers found that while both viruses can leave lasting lung damage, only SARS-CoV-2 infection caused persistent brain inflammation and small blood vessel injury, even after the virus was no longer detectable.\n\n![This shows a brain surrounded by the COVID virus](https:\/\/neurosciencenews.com\/files\/2026\/02\/covid-flu-brain-neuroscience.jpg)\n\nNew evidence suggests that Long COVID’s neurological symptoms are driven by persistent vascular inflammation and the disruption of key neurotransmitter pathways that are unaffected by influenza. Credit: Neuroscience News\n\nThe findings, published in *Frontiers in Immunology*, help explain why long COVID often includes neurological symptoms such as brain fog, fatigue and mood changes, while influenza is more commonly associated with respiratory complications.\n\n“Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” said Dr. Xuebin Qin, lead author and professor of microbiology and immunology at the Tulane National Biomedical Research Center.\n\nTo separate effects common to severe respiratory infections from those unique to COVID-19, researchers used a mouse model to examine lung and brain tissue after infection had cleared.\n\nIn the lungs, both viruses left behind a similar picture: immune cells that failed to fully stand down and increased buildup of collagen, a protein associated with scarring. Those changes can stiffen lung tissue and make breathing feel more labored — a possible biological explanation for why some people report lingering shortness of breath after respiratory infections.\n\nBut when the researchers looked more closely, they found a key difference. After the flu, the lungs appeared to switch into repair mode, sending specialized cells into damaged areas to help rebuild the lining of the airways. That repair response was largely missing after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing process.\n\nThe most striking differences appeared in the brain.\n\nAlthough neither virus was found in brain tissue, mice that had COVID-19 showed signs of persistent brain inflammation weeks later, along with tiny areas of bleeding. Gene expression analysis revealed ongoing inflammatory signaling and disruption of pathways involved in serotonin and dopamine regulation, systems closely tied to mood, cognition and energy levels. These persistent changes were largely absent in influenza-infected animals.\n\n“In both infections, we observed lasting lung injury,” Qin said. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.”\n\nThis study was supported by an American Heart Association award Qin received as part of a national effort to understand the long-term cardiovascular and cerebrovascular effects of COVID-19. The findings shed new light on how vascular and immune changes may contribute to persistent neurological symptoms.\n\nBy defining these biological changes, the research offers a clearer foundation for monitoring patients and developing treatments aimed at preventing lasting damage. As lingering symptoms continue to complicate recovery for some, understanding what is driving them is essential to reducing long-term health consequences.\n\n**Funding:** This research was supported by the American Heart Association Long COVID Impact Project (AHA962950), the National Institutes of Health, including P51OD011104-62 and R01HL165265, and institutional funding.\n\n### Key Questions Answered:\n**Q: Why does COVID feel so different from the flu during recovery?**\n\n**A:** This study shows that while both can scar your lungs, only COVID-19 effectively “sets fire” to your brain’s communication lines. By damaging small blood vessels and disrupting serotonin and dopamine, COVID creates a biological environment for depression, fatigue, and “fog” that the flu simply doesn’t.\n\n**Q: If the virus isn’t in my brain, how is it causing damage?**\n\n**A:** It’s an immune “echo.” Even after the virus is gone, your body’s inflammatory signals stay turned on in the brain. This ongoing inflammation causes small leaks in blood vessels and messes with the chemicals that help you think and feel happy.\n\n**Q: Can the lung damage be reversed?**\n\n**A:** The research found that after the flu, the body sends in a “repair crew” to fix the airway lining. After COVID, that crew never shows up. This suggests we may need specific treatments to jumpstart the healing process in Long COVID patients.\n### Editorial Notes:\n- This article was edited by a Neuroscience News editor.\n- Journal paper reviewed in full.\n- Additional context added by our staff.\n## About this COVID-19 and neurology research news\n**Author:** [Andrew Yawn](https:\/\/neurosciencenews.com\/cdn-cgi\/l\/email-protection#9bfae2faecf5dbefeef7faf5feb5feffee)  \n**Source:** [Tulane University](https:\/\/tulane.edu\/)  \n**Contact:** Andrew Yawn – Tulane University  \n**Image:** The image is credited to Neuroscience News\n\n**Original Research:** Open access.  \n“[Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice](https:\/\/dx.doi.org\/10.3389\/fimmu.2026.1755141)” by Joshua Currey, Chenxiao Wang, Meredith G. Mayer, Yilin Chen, Ana Karina Nisperuza Vidal, Michaela J. Allen, Mst Shamima Khatun, Calder R. Ellsworth, Mohammad Islamuddin, Jefferson Evangelista, Skye M. Minor, Nadia Golden, Kevin J. Zwezdaryk, Nicholas J. Maness, Robert V. Blair, Jay K. Kolls, Derek A. Pociask, Tracy Fischer, and Xuebin Qin. *Frontiers in Immunology*  \n**DOI:10.3389\/fimmu.2026.1755141**\n***\n**Abstract**\n\n**Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice**\n\n**Introduction:**\n\nSARS-CoV-2 and, to a lesser extent, influenza A can lead to long-term complications in the respiratory and nervous systems. However, the mechanisms driving post-viral sequelae remain poorly understood.\n\n**Methods:**\n\nTo address this gap, we longitudinally characterized C57BL\/6 mice infected with sublethal doses of mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). Lung and brain tissues were analyzed at 14-, 21-, and 28-days post-infection (DPI) using histological analysis and bulk-RNA sequencing.\n\n**Results:**\n\nIn the lungs, both infections caused prolonged inflammation and fibrosis. MA30-infected lungs showed persistent upregulation of inflammation, coagulation, complement, as well as fibrotic, and extracellular matrix (ECM) remodeling pathways at 21 DPI, alongside downregulation of epithelial junction and metabolic program pathways.\n\nIn contrast, PR8-infected lungs exhibited a strong acute interferon response and chronic upregulation of basal epithelial markers (e.g., *Krt5*, *Krt14*), consistent with epithelial regeneration. Notably, only PR8-infected mice displayed KRT5+ progenitor cell migration into damaged lung regions, indicating divergence in repair mechanisms.\n\nNeither MA30-infected, nor PR8-infected mice had detectable brain infection. However, MA30 mice, but not PR8-infected mice exhibited an elevated frequency of microhemorrhages at early timepoints and marked neuroinflammation at all timepoints. Transcriptomic profiling of MA30-infected brains showed enrichment for up-regulation of ECM remodeling, vascular dysfunction, IL6-signaling pathways along with a virus-specific disruption of the hypothalamic–pituitary axis with MA30 infection not seen in PR8-infected brains.\n\nThese included genes linked to neuroinflammation, sensory processing disruption, and microvascular injury, mirroring clinical features of Long COVID.\n\n**Discussion:**\n\nTogether, these findings establish distinct tissue-specific trajectories of long-term pathology following SARS-CoV-2 and influenza infection and provide a foundation for dissecting the mechanisms of post-viral lung and brain disease.\n\nTags\n\n[brain fog](https:\/\/neurosciencenews.com\/neuroscience-terms\/brain-fog\/)[dopamine](https:\/\/neurosciencenews.com\/neuroscience-terms\/dopamine\/)[influenza](https:\/\/neurosciencenews.com\/neuroscience-terms\/influenza\/)[long COVID](https:\/\/neurosciencenews.com\/neuroscience-terms\/long-covid\/)[neuroinflammation](https:\/\/neurosciencenews.com\/neuroscience-terms\/neuroinflammation\/)[Neurology](https:\/\/neurosciencenews.com\/neuroscience-terms\/neurology\/)[Neuroscience](https:\/\/neurosciencenews.com\/neuroscience-terms\/neuroscience\/)[serotonin](https:\/\/neurosciencenews.com\/neuroscience-terms\/serotonin\/)[Tulane University](https:\/\/neurosciencenews.com\/neuroscience-terms\/tulane-university\/)\n\n[Share](https:\/\/www.facebook.com\/sharer\/sharer.php?u=https%3A%2F%2Fneurosciencenews.com%2Fcovid-flu-brain-fog-inflammation-30192%2F)[Tweet](https:\/\/twitter.com\/intent\/tweet?via=neurosciencenew&text=COVID-19%20Uniquely%20Rewires%20the%20Brain%20Compared%20to%20the%20Flu%20-%20https%3A%2F%2Fneurosciencenews.com%2Fcovid-flu-brain-fog-inflammation-30192%2F)[Share](https:\/\/www.linkedin.com\/shareArticle?url=https%3A%2F%2Fneurosciencenews.com%2Fcovid-flu-brain-fog-inflammation-30192%2F)[Share](https:\/\/share.flipboard.com\/bookmarklet\/popout?v=2&title=COVID-19%20Uniquely%20Rewires%20the%20Brain%20Compared%20to%20the%20Flu&url=https%3A%2F%2Fneurosciencenews.com%2Fcovid-flu-brain-fog-inflammation-30192%2F)[Submit](https:\/\/reddit.com\/submit?url=https%3A%2F%2Fneurosciencenews.com%2Fcovid-flu-brain-fog-inflammation-30192%2F)[Email](https:\/\/neurosciencenews.com\/cdn-cgi\/l\/email-protection#b788d5d8d3ce8adfc3c3c7c49284f69285f19285f1d9d2c2c5d8c4d4ded2d9d4d2d9d2c0c499d4d8da9285f1d4d8c1ded39ad1dbc29ad5c5d6ded99ad1d8d09aded9d1dbd6dadad6c3ded8d99a8487868e859285f1)\n\n[![](https:\/\/secure.gravatar.com\/avatar\/e214cbb17f634803396f5a2cb3007667dcec7222e76385144040a0c8a9da3591?s=60&d=blank&r=g)](https:\/\/neurosciencenews.com\/author\/neurosciencenew\/)\n\n[Neuroscience News](https:\/\/neurosciencenews.com\/author\/neurosciencenew\/)\n\nNeuroscience News posts science research news from labs, universities, hospitals and news departments around the world. 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Subscribe\nNeuroscience News Daily Emails\n\nGo to Appearance \\> Customize \\> Subscribe Pop-up to set this up.","attrs_readable_markdown":"**Summary:** While both the flu and COVID-19 are respiratory viruses that can leave lasting lung damage, only COVID-19 appears to leave a persistent, inflammatory footprint on the brain. New research reveals that SARS-CoV-2 causes small blood vessel injury and ongoing brain inflammation even after the virus is cleared.\n\nThis study found that COVID-19 specifically disrupts serotonin and dopamine signaling—neurotransmitters critical for mood, cognition, and energy. These findings provide a biological explanation for why “brain fog” and fatigue are hallmark symptoms of Long COVID, but are rarely seen after the seasonal flu.\n\n**Key Facts**\n\n- **Vascular Injury:** COVID-19, but not the flu, causes tiny areas of bleeding and inflammation in the brain’s small blood vessels, even in mild cases.\n- **Neurotransmitter Disruption:** SARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, which explains the persistent cognitive and mood changes in Long COVID.\n- **Lung Repair Failure:** While both viruses cause lung scarring (collagen buildup), the lungs switch into “repair mode” after the flu. Following COVID-19, this natural healing response is largely missing.\n- **Absence of Virus:** Strikingly, the brain inflammation occurred despite the fact that no actual virus was detected in the brain tissue, suggesting the damage is caused by the body’s overactive immune response.\n- **Subchronic Effects:** The study focused on the “subchronic” phase—weeks after the initial infection—to specifically map out the transition from acute illness to long-term symptoms.\n\n**Source:** Tulane University\n\n**Even a mild case of COVID-19 or the flu can impact the body long after the fever and cough fade, according to new Tulane University research that may help explain why some people struggle to feel fully recovered weeks or months later.**\n\nTulane researchers found that while both viruses can leave lasting lung damage, only SARS-CoV-2 infection caused persistent brain inflammation and small blood vessel injury, even after the virus was no longer detectable.\n\n![This shows a brain surrounded by the COVID virus](https:\/\/neurosciencenews.com\/files\/2026\/02\/covid-flu-brain-neuroscience.jpg)\n\nNew evidence suggests that Long COVID’s neurological symptoms are driven by persistent vascular inflammation and the disruption of key neurotransmitter pathways that are unaffected by influenza. Credit: Neuroscience News\n\nThe findings, published in *Frontiers in Immunology*, help explain why long COVID often includes neurological symptoms such as brain fog, fatigue and mood changes, while influenza is more commonly associated with respiratory complications.\n\n“Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” said Dr. Xuebin Qin, lead author and professor of microbiology and immunology at the Tulane National Biomedical Research Center.\n\nTo separate effects common to severe respiratory infections from those unique to COVID-19, researchers used a mouse model to examine lung and brain tissue after infection had cleared.\n\nIn the lungs, both viruses left behind a similar picture: immune cells that failed to fully stand down and increased buildup of collagen, a protein associated with scarring. Those changes can stiffen lung tissue and make breathing feel more labored — a possible biological explanation for why some people report lingering shortness of breath after respiratory infections.\n\nBut when the researchers looked more closely, they found a key difference. After the flu, the lungs appeared to switch into repair mode, sending specialized cells into damaged areas to help rebuild the lining of the airways. That repair response was largely missing after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing process.\n\nThe most striking differences appeared in the brain.\n\nAlthough neither virus was found in brain tissue, mice that had COVID-19 showed signs of persistent brain inflammation weeks later, along with tiny areas of bleeding. Gene expression analysis revealed ongoing inflammatory signaling and disruption of pathways involved in serotonin and dopamine regulation, systems closely tied to mood, cognition and energy levels. These persistent changes were largely absent in influenza-infected animals.\n\n“In both infections, we observed lasting lung injury,” Qin said. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.”\n\nThis study was supported by an American Heart Association award Qin received as part of a national effort to understand the long-term cardiovascular and cerebrovascular effects of COVID-19. The findings shed new light on how vascular and immune changes may contribute to persistent neurological symptoms.\n\nBy defining these biological changes, the research offers a clearer foundation for monitoring patients and developing treatments aimed at preventing lasting damage. As lingering symptoms continue to complicate recovery for some, understanding what is driving them is essential to reducing long-term health consequences.\n\n**Funding:** This research was supported by the American Heart Association Long COVID Impact Project (AHA962950), the National Institutes of Health, including P51OD011104-62 and R01HL165265, and institutional funding.\n\n### Key Questions Answered:\n**Q: Why does COVID feel so different from the flu during recovery?**\n\n**A:** This study shows that while both can scar your lungs, only COVID-19 effectively “sets fire” to your brain’s communication lines. By damaging small blood vessels and disrupting serotonin and dopamine, COVID creates a biological environment for depression, fatigue, and “fog” that the flu simply doesn’t.\n\n**Q: If the virus isn’t in my brain, how is it causing damage?**\n\n**A:** It’s an immune “echo.” Even after the virus is gone, your body’s inflammatory signals stay turned on in the brain. This ongoing inflammation causes small leaks in blood vessels and messes with the chemicals that help you think and feel happy.\n\n**Q: Can the lung damage be reversed?**\n\n**A:** The research found that after the flu, the body sends in a “repair crew” to fix the airway lining. After COVID, that crew never shows up. This suggests we may need specific treatments to jumpstart the healing process in Long COVID patients.\n### Editorial Notes:\n- This article was edited by a Neuroscience News editor.\n- Journal paper reviewed in full.\n- Additional context added by our staff.\n## About this COVID-19 and neurology research news\n**Author:** [Andrew Yawn](https:\/\/neurosciencenews.com\/cdn-cgi\/l\/email-protection#9bfae2faecf5dbefeef7faf5feb5feffee)  \n**Source:** [Tulane University](https:\/\/tulane.edu\/)  \n**Contact:** Andrew Yawn – Tulane University  \n**Image:** The image is credited to Neuroscience News\n\n**Original Research:** Open access.  \n“[Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice](https:\/\/dx.doi.org\/10.3389\/fimmu.2026.1755141)” by Joshua Currey, Chenxiao Wang, Meredith G. Mayer, Yilin Chen, Ana Karina Nisperuza Vidal, Michaela J. Allen, Mst Shamima Khatun, Calder R. Ellsworth, Mohammad Islamuddin, Jefferson Evangelista, Skye M. Minor, Nadia Golden, Kevin J. Zwezdaryk, Nicholas J. Maness, Robert V. Blair, Jay K. Kolls, Derek A. Pociask, Tracy Fischer, and Xuebin Qin. *Frontiers in Immunology*  \n**DOI:10.3389\/fimmu.2026.1755141**\n***\n**Abstract**\n\n**Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice**\n\n**Introduction:**\n\nSARS-CoV-2 and, to a lesser extent, influenza A can lead to long-term complications in the respiratory and nervous systems. However, the mechanisms driving post-viral sequelae remain poorly understood.\n\n**Methods:**\n\nTo address this gap, we longitudinally characterized C57BL\/6 mice infected with sublethal doses of mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). Lung and brain tissues were analyzed at 14-, 21-, and 28-days post-infection (DPI) using histological analysis and bulk-RNA sequencing.\n\n**Results:**\n\nIn the lungs, both infections caused prolonged inflammation and fibrosis. MA30-infected lungs showed persistent upregulation of inflammation, coagulation, complement, as well as fibrotic, and extracellular matrix (ECM) remodeling pathways at 21 DPI, alongside downregulation of epithelial junction and metabolic program pathways.\n\nIn contrast, PR8-infected lungs exhibited a strong acute interferon response and chronic upregulation of basal epithelial markers (e.g., *Krt5*, *Krt14*), consistent with epithelial regeneration. Notably, only PR8-infected mice displayed KRT5+ progenitor cell migration into damaged lung regions, indicating divergence in repair mechanisms.\n\nNeither MA30-infected, nor PR8-infected mice had detectable brain infection. However, MA30 mice, but not PR8-infected mice exhibited an elevated frequency of microhemorrhages at early timepoints and marked neuroinflammation at all timepoints. Transcriptomic profiling of MA30-infected brains showed enrichment for up-regulation of ECM remodeling, vascular dysfunction, IL6-signaling pathways along with a virus-specific disruption of the hypothalamic–pituitary axis with MA30 infection not seen in PR8-infected brains.\n\nThese included genes linked to neuroinflammation, sensory processing disruption, and microvascular injury, mirroring clinical features of Long COVID.\n\n**Discussion:**\n\nTogether, these findings establish distinct tissue-specific trajectories of long-term pathology following SARS-CoV-2 and influenza infection and provide a foundation for dissecting the mechanisms of post-viral lung and brain disease.","meta_canonical":null}

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Meta Title	COVID-19 Uniquely Rewires the Brain Compared to the Flu - Neuroscience News
Meta Description	Researchers discover that COVID-19 uniquely causes brain inflammation and disrupts serotonin/dopamine pathways, explaining "brain fog" in Long COVID.
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Boilerpipe Text	Summary: While both the flu and COVID-19 are respiratory viruses that can leave lasting lung damage, only COVID-19 appears to leave a persistent, inflammatory footprint on the brain. New research reveals that SARS-CoV-2 causes small blood vessel injury and ongoing brain inflammation even after the virus is cleared. This study found that COVID-19 specifically disrupts serotonin and dopamine signaling—neurotransmitters critical for mood, cognition, and energy. These findings provide a biological explanation for why “brain fog” and fatigue are hallmark symptoms of Long COVID, but are rarely seen after the seasonal flu. Key Facts Vascular Injury: COVID-19, but not the flu, causes tiny areas of bleeding and inflammation in the brain’s small blood vessels, even in mild cases. Neurotransmitter Disruption: SARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, which explains the persistent cognitive and mood changes in Long COVID. Lung Repair Failure: While both viruses cause lung scarring (collagen buildup), the lungs switch into “repair mode” after the flu. Following COVID-19, this natural healing response is largely missing. Absence of Virus: Strikingly, the brain inflammation occurred despite the fact that no actual virus was detected in the brain tissue, suggesting the damage is caused by the body’s overactive immune response. Subchronic Effects: The study focused on the “subchronic” phase—weeks after the initial infection—to specifically map out the transition from acute illness to long-term symptoms. Source: Tulane University Even a mild case of COVID-19 or the flu can impact the body long after the fever and cough fade, according to new Tulane University research that may help explain why some people struggle to feel fully recovered weeks or months later. Tulane researchers found that while both viruses can leave lasting lung damage, only SARS-CoV-2 infection caused persistent brain inflammation and small blood vessel injury, even after the virus was no longer detectable. New evidence suggests that Long COVID’s neurological symptoms are driven by persistent vascular inflammation and the disruption of key neurotransmitter pathways that are unaffected by influenza. Credit: Neuroscience News The findings, published in Frontiers in Immunology , help explain why long COVID often includes neurological symptoms such as brain fog, fatigue and mood changes, while influenza is more commonly associated with respiratory complications. “Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” said Dr. Xuebin Qin, lead author and professor of microbiology and immunology at the Tulane National Biomedical Research Center. To separate effects common to severe respiratory infections from those unique to COVID-19, researchers used a mouse model to examine lung and brain tissue after infection had cleared. In the lungs, both viruses left behind a similar picture: immune cells that failed to fully stand down and increased buildup of collagen, a protein associated with scarring. Those changes can stiffen lung tissue and make breathing feel more labored — a possible biological explanation for why some people report lingering shortness of breath after respiratory infections. But when the researchers looked more closely, they found a key difference. After the flu, the lungs appeared to switch into repair mode, sending specialized cells into damaged areas to help rebuild the lining of the airways. That repair response was largely missing after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing process. The most striking differences appeared in the brain. Although neither virus was found in brain tissue, mice that had COVID-19 showed signs of persistent brain inflammation weeks later, along with tiny areas of bleeding. Gene expression analysis revealed ongoing inflammatory signaling and disruption of pathways involved in serotonin and dopamine regulation, systems closely tied to mood, cognition and energy levels. These persistent changes were largely absent in influenza-infected animals. “In both infections, we observed lasting lung injury,” Qin said. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.” This study was supported by an American Heart Association award Qin received as part of a national effort to understand the long-term cardiovascular and cerebrovascular effects of COVID-19. The findings shed new light on how vascular and immune changes may contribute to persistent neurological symptoms. By defining these biological changes, the research offers a clearer foundation for monitoring patients and developing treatments aimed at preventing lasting damage. As lingering symptoms continue to complicate recovery for some, understanding what is driving them is essential to reducing long-term health consequences. Funding: This research was supported by the American Heart Association Long COVID Impact Project (AHA962950), the National Institutes of Health, including P51OD011104-62 and R01HL165265, and institutional funding. Key Questions Answered: Q: Why does COVID feel so different from the flu during recovery? A: This study shows that while both can scar your lungs, only COVID-19 effectively “sets fire” to your brain’s communication lines. By damaging small blood vessels and disrupting serotonin and dopamine, COVID creates a biological environment for depression, fatigue, and “fog” that the flu simply doesn’t. Q: If the virus isn’t in my brain, how is it causing damage? A: It’s an immune “echo.” Even after the virus is gone, your body’s inflammatory signals stay turned on in the brain. This ongoing inflammation causes small leaks in blood vessels and messes with the chemicals that help you think and feel happy. Q: Can the lung damage be reversed? A: The research found that after the flu, the body sends in a “repair crew” to fix the airway lining. After COVID, that crew never shows up. This suggests we may need specific treatments to jumpstart the healing process in Long COVID patients. Editorial Notes: This article was edited by a Neuroscience News editor. Journal paper reviewed in full. Additional context added by our staff. About this COVID-19 and neurology research news Author: Andrew Yawn Source: Tulane University Contact: Andrew Yawn – Tulane University Image: The image is credited to Neuroscience News Original Research: Open access. “ Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice ” by Joshua Currey, Chenxiao Wang, Meredith G. Mayer, Yilin Chen, Ana Karina Nisperuza Vidal, Michaela J. Allen, Mst Shamima Khatun, Calder R. Ellsworth, Mohammad Islamuddin, Jefferson Evangelista, Skye M. Minor, Nadia Golden, Kevin J. Zwezdaryk, Nicholas J. Maness, Robert V. Blair, Jay K. Kolls, Derek A. Pociask, Tracy Fischer, and Xuebin Qin. Frontiers in Immunology DOI:10.3389/fimmu.2026.1755141 Abstract Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice Introduction: SARS-CoV-2 and, to a lesser extent, influenza A can lead to long-term complications in the respiratory and nervous systems. However, the mechanisms driving post-viral sequelae remain poorly understood. Methods: To address this gap, we longitudinally characterized C57BL/6 mice infected with sublethal doses of mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). Lung and brain tissues were analyzed at 14-, 21-, and 28-days post-infection (DPI) using histological analysis and bulk-RNA sequencing. Results: In the lungs, both infections caused prolonged inflammation and fibrosis. MA30-infected lungs showed persistent upregulation of inflammation, coagulation, complement, as well as fibrotic, and extracellular matrix (ECM) remodeling pathways at 21 DPI, alongside downregulation of epithelial junction and metabolic program pathways. In contrast, PR8-infected lungs exhibited a strong acute interferon response and chronic upregulation of basal epithelial markers (e.g., Krt5 , Krt14 ), consistent with epithelial regeneration. Notably, only PR8-infected mice displayed KRT5+ progenitor cell migration into damaged lung regions, indicating divergence in repair mechanisms. Neither MA30-infected, nor PR8-infected mice had detectable brain infection. However, MA30 mice, but not PR8-infected mice exhibited an elevated frequency of microhemorrhages at early timepoints and marked neuroinflammation at all timepoints. Transcriptomic profiling of MA30-infected brains showed enrichment for up-regulation of ECM remodeling, vascular dysfunction, IL6-signaling pathways along with a virus-specific disruption of the hypothalamic–pituitary axis with MA30 infection not seen in PR8-infected brains. These included genes linked to neuroinflammation, sensory processing disruption, and microvascular injury, mirroring clinical features of Long COVID. Discussion: Together, these findings establish distinct tissue-specific trajectories of long-term pathology following SARS-CoV-2 and influenza infection and provide a foundation for dissecting the mechanisms of post-viral lung and brain disease.
Markdown	[![Neuroscience News logo for mobile.](https://neurosciencenews.com/files/2020/07/Neuroscience-News_AZ_RevNewest-scaled-e1596228355273-1.jpg)](https://neurosciencenews.com/) [![Neuroscience News Logo](https://neurosciencenews.com/files/2020/07/Neuroscience-News_AZ_RevNewest-scaled-e1596228355273.jpg)](https://neurosciencenews.com/) # COVID-19 Uniquely Rewires the Brain Compared to the Flu [Featured](https://neurosciencenews.com/neuroscience-topics/featured/)[Neurology](https://neurosciencenews.com/neuroscience-topics/neurology/)[Neuroscience](https://neurosciencenews.com/neuroscience-topics/neuroscience/) · February 25, 2026 Summary: While both the flu and COVID-19 are respiratory viruses that can leave lasting lung damage, only COVID-19 appears to leave a persistent, inflammatory footprint on the brain. New research reveals that SARS-CoV-2 causes small blood vessel injury and ongoing brain inflammation even after the virus is cleared. This study found that COVID-19 specifically disrupts serotonin and dopamine signaling—neurotransmitters critical for mood, cognition, and energy. These findings provide a biological explanation for why “brain fog” and fatigue are hallmark symptoms of Long COVID, but are rarely seen after the seasonal flu. Key Facts - Vascular Injury: COVID-19, but not the flu, causes tiny areas of bleeding and inflammation in the brain’s small blood vessels, even in mild cases. - Neurotransmitter Disruption: SARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, which explains the persistent cognitive and mood changes in Long COVID. - Lung Repair Failure: While both viruses cause lung scarring (collagen buildup), the lungs switch into “repair mode” after the flu. Following COVID-19, this natural healing response is largely missing. - Absence of Virus: Strikingly, the brain inflammation occurred despite the fact that no actual virus was detected in the brain tissue, suggesting the damage is caused by the body’s overactive immune response. - Subchronic Effects: The study focused on the “subchronic” phase—weeks after the initial infection—to specifically map out the transition from acute illness to long-term symptoms. Source: Tulane University Even a mild case of COVID-19 or the flu can impact the body long after the fever and cough fade, according to new Tulane University research that may help explain why some people struggle to feel fully recovered weeks or months later. Tulane researchers found that while both viruses can leave lasting lung damage, only SARS-CoV-2 infection caused persistent brain inflammation and small blood vessel injury, even after the virus was no longer detectable. ![This shows a brain surrounded by the COVID virus](https://neurosciencenews.com/files/2026/02/covid-flu-brain-neuroscience.jpg) New evidence suggests that Long COVID’s neurological symptoms are driven by persistent vascular inflammation and the disruption of key neurotransmitter pathways that are unaffected by influenza. Credit: Neuroscience News The findings, published in Frontiers in Immunology, help explain why long COVID often includes neurological symptoms such as brain fog, fatigue and mood changes, while influenza is more commonly associated with respiratory complications. “Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” said Dr. Xuebin Qin, lead author and professor of microbiology and immunology at the Tulane National Biomedical Research Center. To separate effects common to severe respiratory infections from those unique to COVID-19, researchers used a mouse model to examine lung and brain tissue after infection had cleared. In the lungs, both viruses left behind a similar picture: immune cells that failed to fully stand down and increased buildup of collagen, a protein associated with scarring. Those changes can stiffen lung tissue and make breathing feel more labored — a possible biological explanation for why some people report lingering shortness of breath after respiratory infections. But when the researchers looked more closely, they found a key difference. After the flu, the lungs appeared to switch into repair mode, sending specialized cells into damaged areas to help rebuild the lining of the airways. That repair response was largely missing after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing process. The most striking differences appeared in the brain. Although neither virus was found in brain tissue, mice that had COVID-19 showed signs of persistent brain inflammation weeks later, along with tiny areas of bleeding. Gene expression analysis revealed ongoing inflammatory signaling and disruption of pathways involved in serotonin and dopamine regulation, systems closely tied to mood, cognition and energy levels. These persistent changes were largely absent in influenza-infected animals. “In both infections, we observed lasting lung injury,” Qin said. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.” This study was supported by an American Heart Association award Qin received as part of a national effort to understand the long-term cardiovascular and cerebrovascular effects of COVID-19. The findings shed new light on how vascular and immune changes may contribute to persistent neurological symptoms. By defining these biological changes, the research offers a clearer foundation for monitoring patients and developing treatments aimed at preventing lasting damage. As lingering symptoms continue to complicate recovery for some, understanding what is driving them is essential to reducing long-term health consequences. Funding: This research was supported by the American Heart Association Long COVID Impact Project (AHA962950), the National Institutes of Health, including P51OD011104-62 and R01HL165265, and institutional funding. ### Key Questions Answered: Q: Why does COVID feel so different from the flu during recovery? A: This study shows that while both can scar your lungs, only COVID-19 effectively “sets fire” to your brain’s communication lines. By damaging small blood vessels and disrupting serotonin and dopamine, COVID creates a biological environment for depression, fatigue, and “fog” that the flu simply doesn’t. Q: If the virus isn’t in my brain, how is it causing damage? A: It’s an immune “echo.” Even after the virus is gone, your body’s inflammatory signals stay turned on in the brain. This ongoing inflammation causes small leaks in blood vessels and messes with the chemicals that help you think and feel happy. Q: Can the lung damage be reversed? A: The research found that after the flu, the body sends in a “repair crew” to fix the airway lining. After COVID, that crew never shows up. This suggests we may need specific treatments to jumpstart the healing process in Long COVID patients. ### Editorial Notes: - This article was edited by a Neuroscience News editor. - Journal paper reviewed in full. - Additional context added by our staff. ## About this COVID-19 and neurology research news Author: [Andrew Yawn](https://neurosciencenews.com/cdn-cgi/l/email-protection#9bfae2faecf5dbefeef7faf5feb5feffee) Source: [Tulane University](https://tulane.edu/) Contact: Andrew Yawn – Tulane University Image: The image is credited to Neuroscience News Original Research: Open access. “[Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice](https://dx.doi.org/10.3389/fimmu.2026.1755141)” by Joshua Currey, Chenxiao Wang, Meredith G. Mayer, Yilin Chen, Ana Karina Nisperuza Vidal, Michaela J. Allen, Mst Shamima Khatun, Calder R. Ellsworth, Mohammad Islamuddin, Jefferson Evangelista, Skye M. Minor, Nadia Golden, Kevin J. Zwezdaryk, Nicholas J. Maness, Robert V. Blair, Jay K. Kolls, Derek A. Pociask, Tracy Fischer, and Xuebin Qin. Frontiers in Immunology DOI:10.3389/fimmu.2026.1755141 * Abstract Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice Introduction: SARS-CoV-2 and, to a lesser extent, influenza A can lead to long-term complications in the respiratory and nervous systems. However, the mechanisms driving post-viral sequelae remain poorly understood. Methods: To address this gap, we longitudinally characterized C57BL/6 mice infected with sublethal doses of mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). Lung and brain tissues were analyzed at 14-, 21-, and 28-days post-infection (DPI) using histological analysis and bulk-RNA sequencing. Results:** In the lungs, both infections caused prolonged inflammation and fibrosis. MA30-infected lungs showed persistent upregulation of inflammation, coagulation, complement, as well as fibrotic, and extracellular matrix (ECM) remodeling pathways at 21 DPI, alongside downregulation of epithelial junction and metabolic program pathways. In contrast, PR8-infected lungs exhibited a strong acute interferon response and chronic upregulation of basal epithelial markers (e.g., Krt5, Krt14), consistent with epithelial regeneration. Notably, only PR8-infected mice displayed KRT5+ progenitor cell migration into damaged lung regions, indicating divergence in repair mechanisms. Neither MA30-infected, nor PR8-infected mice had detectable brain infection. However, MA30 mice, but not PR8-infected mice exhibited an elevated frequency of microhemorrhages at early timepoints and marked neuroinflammation at all timepoints. Transcriptomic profiling of MA30-infected brains showed enrichment for up-regulation of ECM remodeling, vascular dysfunction, IL6-signaling pathways along with a virus-specific disruption of the hypothalamic–pituitary axis with MA30 infection not seen in PR8-infected brains. These included genes linked to neuroinflammation, sensory processing disruption, and microvascular injury, mirroring clinical features of Long COVID. Discussion: Together, these findings establish distinct tissue-specific trajectories of long-term pathology following SARS-CoV-2 and influenza infection and provide a foundation for dissecting the mechanisms of post-viral lung and brain disease. 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Readable Markdown	Summary: While both the flu and COVID-19 are respiratory viruses that can leave lasting lung damage, only COVID-19 appears to leave a persistent, inflammatory footprint on the brain. New research reveals that SARS-CoV-2 causes small blood vessel injury and ongoing brain inflammation even after the virus is cleared. This study found that COVID-19 specifically disrupts serotonin and dopamine signaling—neurotransmitters critical for mood, cognition, and energy. These findings provide a biological explanation for why “brain fog” and fatigue are hallmark symptoms of Long COVID, but are rarely seen after the seasonal flu. Key Facts - Vascular Injury: COVID-19, but not the flu, causes tiny areas of bleeding and inflammation in the brain’s small blood vessels, even in mild cases. - Neurotransmitter Disruption: SARS-CoV-2 infection alters gene expression related to serotonin and dopamine regulation, which explains the persistent cognitive and mood changes in Long COVID. - Lung Repair Failure: While both viruses cause lung scarring (collagen buildup), the lungs switch into “repair mode” after the flu. Following COVID-19, this natural healing response is largely missing. - Absence of Virus: Strikingly, the brain inflammation occurred despite the fact that no actual virus was detected in the brain tissue, suggesting the damage is caused by the body’s overactive immune response. - Subchronic Effects: The study focused on the “subchronic” phase—weeks after the initial infection—to specifically map out the transition from acute illness to long-term symptoms. Source: Tulane University Even a mild case of COVID-19 or the flu can impact the body long after the fever and cough fade, according to new Tulane University research that may help explain why some people struggle to feel fully recovered weeks or months later. Tulane researchers found that while both viruses can leave lasting lung damage, only SARS-CoV-2 infection caused persistent brain inflammation and small blood vessel injury, even after the virus was no longer detectable. ![This shows a brain surrounded by the COVID virus](https://neurosciencenews.com/files/2026/02/covid-flu-brain-neuroscience.jpg) New evidence suggests that Long COVID’s neurological symptoms are driven by persistent vascular inflammation and the disruption of key neurotransmitter pathways that are unaffected by influenza. Credit: Neuroscience News The findings, published in Frontiers in Immunology, help explain why long COVID often includes neurological symptoms such as brain fog, fatigue and mood changes, while influenza is more commonly associated with respiratory complications. “Influenza and COVID-19 affect large populations worldwide and carry a significant public health toll, yet the mechanisms behind their long-term effects remain poorly understood,” said Dr. Xuebin Qin, lead author and professor of microbiology and immunology at the Tulane National Biomedical Research Center. To separate effects common to severe respiratory infections from those unique to COVID-19, researchers used a mouse model to examine lung and brain tissue after infection had cleared. In the lungs, both viruses left behind a similar picture: immune cells that failed to fully stand down and increased buildup of collagen, a protein associated with scarring. Those changes can stiffen lung tissue and make breathing feel more labored — a possible biological explanation for why some people report lingering shortness of breath after respiratory infections. But when the researchers looked more closely, they found a key difference. After the flu, the lungs appeared to switch into repair mode, sending specialized cells into damaged areas to help rebuild the lining of the airways. That repair response was largely missing after COVID-19 infection, suggesting the virus may interfere with the lung’s natural healing process. The most striking differences appeared in the brain. Although neither virus was found in brain tissue, mice that had COVID-19 showed signs of persistent brain inflammation weeks later, along with tiny areas of bleeding. Gene expression analysis revealed ongoing inflammatory signaling and disruption of pathways involved in serotonin and dopamine regulation, systems closely tied to mood, cognition and energy levels. These persistent changes were largely absent in influenza-infected animals. “In both infections, we observed lasting lung injury,” Qin said. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.” This study was supported by an American Heart Association award Qin received as part of a national effort to understand the long-term cardiovascular and cerebrovascular effects of COVID-19. The findings shed new light on how vascular and immune changes may contribute to persistent neurological symptoms. By defining these biological changes, the research offers a clearer foundation for monitoring patients and developing treatments aimed at preventing lasting damage. As lingering symptoms continue to complicate recovery for some, understanding what is driving them is essential to reducing long-term health consequences. Funding: This research was supported by the American Heart Association Long COVID Impact Project (AHA962950), the National Institutes of Health, including P51OD011104-62 and R01HL165265, and institutional funding. ### Key Questions Answered: Q: Why does COVID feel so different from the flu during recovery? A: This study shows that while both can scar your lungs, only COVID-19 effectively “sets fire” to your brain’s communication lines. By damaging small blood vessels and disrupting serotonin and dopamine, COVID creates a biological environment for depression, fatigue, and “fog” that the flu simply doesn’t. Q: If the virus isn’t in my brain, how is it causing damage? A: It’s an immune “echo.” Even after the virus is gone, your body’s inflammatory signals stay turned on in the brain. This ongoing inflammation causes small leaks in blood vessels and messes with the chemicals that help you think and feel happy. Q: Can the lung damage be reversed? A: The research found that after the flu, the body sends in a “repair crew” to fix the airway lining. After COVID, that crew never shows up. This suggests we may need specific treatments to jumpstart the healing process in Long COVID patients. ### Editorial Notes: - This article was edited by a Neuroscience News editor. - Journal paper reviewed in full. - Additional context added by our staff. ## About this COVID-19 and neurology research news Author: [Andrew Yawn](https://neurosciencenews.com/cdn-cgi/l/email-protection#9bfae2faecf5dbefeef7faf5feb5feffee) Source: [Tulane University](https://tulane.edu/) Contact: Andrew Yawn – Tulane University Image: The image is credited to Neuroscience News Original Research: Open access. “[Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice](https://dx.doi.org/10.3389/fimmu.2026.1755141)” by Joshua Currey, Chenxiao Wang, Meredith G. Mayer, Yilin Chen, Ana Karina Nisperuza Vidal, Michaela J. Allen, Mst Shamima Khatun, Calder R. Ellsworth, Mohammad Islamuddin, Jefferson Evangelista, Skye M. Minor, Nadia Golden, Kevin J. Zwezdaryk, Nicholas J. Maness, Robert V. Blair, Jay K. Kolls, Derek A. Pociask, Tracy Fischer, and Xuebin Qin. Frontiers in Immunology DOI:10.3389/fimmu.2026.1755141 * Abstract Characterization of Subchronic Lung and Brain Consequences Caused by Mouse-Adapted SARS-CoV-2 and Influenza A Infection of C57BL6 mice Introduction: SARS-CoV-2 and, to a lesser extent, influenza A can lead to long-term complications in the respiratory and nervous systems. However, the mechanisms driving post-viral sequelae remain poorly understood. Methods: To address this gap, we longitudinally characterized C57BL/6 mice infected with sublethal doses of mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8). Lung and brain tissues were analyzed at 14-, 21-, and 28-days post-infection (DPI) using histological analysis and bulk-RNA sequencing. Results:** In the lungs, both infections caused prolonged inflammation and fibrosis. MA30-infected lungs showed persistent upregulation of inflammation, coagulation, complement, as well as fibrotic, and extracellular matrix (ECM) remodeling pathways at 21 DPI, alongside downregulation of epithelial junction and metabolic program pathways. In contrast, PR8-infected lungs exhibited a strong acute interferon response and chronic upregulation of basal epithelial markers (e.g., Krt5, Krt14), consistent with epithelial regeneration. Notably, only PR8-infected mice displayed KRT5+ progenitor cell migration into damaged lung regions, indicating divergence in repair mechanisms. Neither MA30-infected, nor PR8-infected mice had detectable brain infection. However, MA30 mice, but not PR8-infected mice exhibited an elevated frequency of microhemorrhages at early timepoints and marked neuroinflammation at all timepoints. Transcriptomic profiling of MA30-infected brains showed enrichment for up-regulation of ECM remodeling, vascular dysfunction, IL6-signaling pathways along with a virus-specific disruption of the hypothalamic–pituitary axis with MA30 infection not seen in PR8-infected brains. These included genes linked to neuroinflammation, sensory processing disruption, and microvascular injury, mirroring clinical features of Long COVID. Discussion: Together, these findings establish distinct tissue-specific trajectories of long-term pathology following SARS-CoV-2 and influenza infection and provide a foundation for dissecting the mechanisms of post-viral lung and brain disease.
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