Top Tweets for #MildMyAss

🔴 Long COVID did not appear out of nowhere. For more than a century, medicine has described people who did not fully recover after infections. Different names. Different pathogens. Different eras. But often the same pattern: infection → partial recovery → persistent fatigue, pain, cognitive symptoms, sleep disruption, dysautonomia, gut symptoms or inflammatory disease Long COVID is new in scale. But post-infectious illness is not new. (1/62) 🧵

COVID-19 may leave a footprint not only in the lungs, heart and brain—but also in the skeleton. ➡️ A new review brings together emerging evidence that SARS-CoV-2 may disrupt bone remodeling, osteoimmune signaling, bone microarchitecture and mechanical strength through a combination of inflammation, oxidative stress, endothelial dysfunction and ACE2/RAS disturbance. 1/

You know what frightens me... even mild SARS-CoV-2 infections can trigger direct myocardial injury, lasting endothelial damage, persistent inflammation, and a prothrombotic state. This raises the long-term risk of heart attack, heart failure, stroke, arrhythmias, and clots—often by around 1.5–2× (and higher in severe cases) for years afterward. Each reinfection can compound this cumulative cardiovascular burden, heightening Long COVID risks and making every exposure a potential step closer to accelerated or lifelong heart disease vulnerability, though vaccination can lower the risks but does not erase them! #AvoidSars2 #AvoidReinfections

🤔 Long COVID isn't AIDS—but it is rapid-onset "AIDS-like": the same NK-cell exhaustion, chronic immune dysregulation, mucosal collapse, and failed coordination as in HIV, just without the retrovirus and on fast-forward!😷 ZDENEK: A "Post-acute immune dysregulation syndrome (PAIDS)" may be a fitting new label! 🤔🧵👇

Prevalence and Symptoms of Post-COVID-19 Syndrome in Active-Duty Military Personnel 🚨The ALARMING USA army news today: Over 42% of active-duty military personnel who contracted COVID-19 developed long-lasting post-COVID syndrome—dominated by pulmonary, neurological, and fatigue issues—threatening their fitness, readiness, and the military’s ability to respond to threats. ➡️A large retrospective study analysed electronic health records from the U.S. Military Health System (2019–2024), identifying post-COVID-19 syndrome in 42.8% of 650,173 COVID-19 cases among active-duty personnel. The cohort was predominantly male (74.1%), young (mean age 31.3 years), and enlisted (83.3%). ➡️Findings: 1. Prevalence: - Post-COVID-19 syndrome identified in 42.8% of 650,173 COVID-19 cases, - “In our sample of 650,173 COVID cases among active-duty military personnel, a total of 278,278 were identified as having post-COVID-19 syndrome (42.8%).” 2. Demographics: - Predominantly male (74.1%), - Young population (mean age 31.3 years), - Mostly enlisted ranks (83.3%), 3. Most common persistent symptoms: - Pulmonary issues: 22.4% (median duration 670 days), - Neurological problems: 14.6% (median 576 days), - Fatigue: 13.5% (median 667 days), - Digestive issues: 12.5%, - Fever: 11.5%, - Cognitive symptoms: only 3.7% but longest persistence (median 710 days), 4. Sex differences: - Females → higher odds of neurological (OR 1.645) and digestive symptoms, - Females → lower odds of pulmonary (OR 0.851) and cognitive symptoms, 5. Comorbidity impact: - Obesity → triples odds of pulmonary symptoms, - Anxiety → quadruples odds of cognitive symptoms, - Other comorbidities significantly amplify risk across domains, 6. Military-specific patterns: - Rank differences: warrant officers showed higher fatigue and pulmonary odds, - Service branch differences: Air Force personnel had elevated pulmonary symptoms (possible environmental exposure link), 7. Comparison to civilians: - Military pattern differs: pulmonary and neurological issues more prominent than the fatigue-dominant profile typical in civilian populations, ➡️‼️So, post-COVID-19 syndrome affects over 40% of young, fit active-duty service members post-C19, and poses a serious long-term threat to military medical readiness and operational capability. #REINFECTIONS ➡️‼️And AGAIN: Long COVID strikes millions worldwide, often with persistent pulmonary, neurological, and fatigue symptoms lasting months to years, severely impairing daily function, work productivity, and overall quality of life in a substantial portion of those infected. #LONGCOVIDAWARENESSMONTH #AVOIDREINFECTIONS #AVOIDSARS2 https://t.co/nGbJez1QiZ

⚠️ SARS-CoV-2 (the virus causing COVID-19) is not classified as a classic oncovirus like HPV, EBV, or HBV, which directly cause ~15% of cancers through well-established mechanisms. However, extensive reviews and studies (including molecular, in vitro, observational, and epidemiological data up to 2026) indicate that SARS-CoV-2 infection can **elevate cancer risk or accelerate progression** in susceptible individuals, particularly through long-term effects like Long COVID, chronic inflammation, and immune changes. Key supporting evidence includes: - Reviews synthesizing molecular pathways (e.g., Ogarek et al., 2023 in *Frontiers in Molecular Biosciences*; Tyagi et al., 2025 in *Biochimica et Biophysica Acta*; Jaiswal et al., 2024). - In vitro studies showing direct effects on cancer cell lines (breast, colorectal, prostate). - Epidemiological signals, such as significantly elevated risks of HPV-related cancers (cervical +67%, anal +92%, etc.) post-infection in large matched cohorts. - Observational data on rapid cancer progression, recurrence, or reactivation of dormant tumors after infection. - Mechanisms overlapping with known oncogenic processes (inflammation, hypoxia, oxidative stress). **Note**: These are primarily mechanistic/hypothetical or associative findings (not proven direct causation in large randomized studies). Some reports note potential oncolytic (anti-cancer) effects in rare cases, but the net evidence leans toward increased risk, especially for lung, colorectal, and virus-associated cancers due to high ACE2/TMPRSS2 expression. Antiviral treatments or vaccines are not the focus here—the query concerns the virus itself. Here are the **5 primary ways** SARS-CoV-2 increases cancer chances, synthesized from all major studies/reviews examined: 1. **Chronic inflammation and cytokine storm** SARS-CoV-2 triggers massive release of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IFN-γ, VEGF, etc.), creating a persistent “cytokine storm” and low-grade chronic inflammation. This activates NF-κB and IL-6/JAK/STAT3 pathways, promoting DNA damage, angiogenesis, cell survival/proliferation, invasion, metastasis, and a tumor-favorable microenvironment (e.g., shifting macrophages to pro-tumor M2 phenotype). It also reawakens dormant cancer cells via inflammatory signals. **Evidence**: Central mechanism in nearly every review; directly linked to tumor progression in lung/colorectal cancers; cytokine levels mirror those driving oncogenesis. 2. **Immune dysregulation, lymphopenia, and impaired surveillance** The virus causes profound lymphopenia (depletion of CD4+/CD8+ T cells and NK cells), T-cell exhaustion, overexpression of inhibitory receptors (e.g., NKG2A), and suppression of type I interferons. This weakens anti-tumor immunity, allowing pre-cancerous or dormant cells to escape detection, proliferate, and metastasize. It also disrupts dendritic cells, neutrophils (NETs), and overall adaptive responses. **Evidence**: Documented in severe COVID-19 and post-infection; explains reactivation of latent tumors and synergy with oncogenic viruses (e.g., higher HPV-related carcinoma in situ/cancer rates); parallels cancer immune evasion. 3. **Oxidative stress and genomic instability** Infection downregulates ACE2, leading to angiotensin II accumulation, reactive oxygen species (ROS) overproduction, and oxidative damage to DNA, proteins, and lipids. This causes mutations, epigenetic changes (e.g., altered DNA methylation, miRNA dysregulation, HDAC interactions), and impaired DNA repair—hallmarks of carcinogenesis. **Evidence**: Repeatedly highlighted; ROS links directly to cancer initiation/progression; observed in COVID-19 survivors and tied to genomic instability in multiple pathways. 1/2