My spreadsheet of #COVID19 studies showing longer-term damage to the body has grown to 100 studies. Here's a link and a thread of some of the most interesting. The conclusion is that COVID can attack many parts of the body, remain present in the body, increase risks of serious cardiovascular, brain, lung and immune system disorders, and increase risk of death and disability. Stop taking it so lightly!

https://docs.google.com/spreadsheets/d/12VbMkvqUF9eSggJsdsFEjKs5x0ABxQJi5tvfzJIDd3U/edit?usp=sharing

COVID-19/SARS-CoV-2 Studies

Google Docs
SYMPTOMS 6-12 MONTHS AFTER MILD INFECTION: This study suggests a considerable burden of self-reported post-acute symptom clusters and possible sequelae, notably fatigue and neurocognitive impairment, six to 12 months after acute SARS-CoV-2 infection, even among young and middle aged adults after mild infection, with a substantial impact on general health and working capacity. https://www.bmj.com/content/379/bmj-2022-071050 (2/31)
Post-acute sequelae of covid-19 six to 12 months after infection: population based study

Objectives To describe symptoms and symptom clusters of post-covid syndrome six to 12 months after acute infection, describe risk factors, and examine the association of symptom clusters with general health and working capacity. Design Population based, cross sectional study Setting Adults aged 18-65 years with confirmed SARS-CoV-2 infection between October 2020 and March 2021 notified to health authorities in four geographically defined regions in southern Germany. Participants 50 457 patients were invited to participate in the study, of whom 12 053 (24%) responded and 11 710 (58.8% (n=6881) female; mean age 44.1 years; 3.6% (412/11 602) previously admitted with covid-19; mean follow-up time 8.5 months) could be included in the analyses. Main outcome measures Symptom frequencies (six to 12 months after versus before acute infection), symptom severity and clustering, risk factors, and associations with general health recovery and working capacity. Results The symptom clusters fatigue (37.2% (4213/11 312), 95% confidence interval 36.4% to 38.1%) and neurocognitive impairment (31.3% (3561/11 361), 30.5% to 32.2%) contributed most to reduced health recovery and working capacity, but chest symptoms, anxiety/depression, headache/dizziness, and pain syndromes were also prevalent and relevant for working capacity, with some differences according to sex and age. Considering new symptoms with at least moderate impairment of daily life and ≤80% recovered general health or working capacity, the overall estimate for post-covid syndrome was 28.5% (3289/11 536, 27.7% to 29.3%) among participants or at least 6.5% (3289/50 457) in the infected adult population (assuming that all non-responders had completely recovered). The true value is likely to be between these estimates. Conclusions Despite the limitation of a low response rate and possible selection and recall biases, this study suggests a considerable burden of self-reported post-acute symptom clusters and possible sequelae, notably fatigue and neurocognitive impairment, six to 12 months after acute SARS-CoV-2 infection, even among young and middle aged adults after mild infection, with a substantial impact on general health and working capacity. Trial registration German registry of clinical studies DRKS 00027012. Data from EPILOC phase 1 are available for research purposes upon request from the corresponding author at [email protected].

The BMJ
COVID REINFECTION MULTIPLIES RISK OF DEATH AND SIDE EFFECTS SIX MONTHS POST INFECTION: Compared to no reinfection, reinfection contributed additional risks of death (hazard ratio (HR) = 2.17) (2.17x the risk) hospitalization (HR = 3.32) and sequelae including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental health, musculoskeletal and neurological disorders. The risks persisted in the postacute phase at 6 months. https://www.nature.com/articles/s41591-022-02051-3 (3/31)
Acute and postacute sequelae associated with SARS-CoV-2 reinfection - Nature Medicine

A new analysis using US Department of Veterans Affairs databases showed that reinfection is associated with increased risk of all-cause mortality, hospitalization and a wide range of long COVID complications in individuals who have had SARS-CoV-2 compared to those with no reinfection.

Nature
COVID MULTIPLIES RISKS OF CARDIOVASCULAR AND PULMONARY CONDITIONS: The incidence of hospitalisation within 89 days of onset of COVID‐19 was higher than during the baseline period for several conditions, including myocarditis and pericarditis (IRR, 14.8), thrombocytopenia (IRR, 7.4), pulmonary embolism (IRR, 6.4), acute myocardial infarction (IRR, 3.9), and cerebral infarction (IRR, 2.3). https://www.mja.com.au/journal/2022/218/1/associations-between-covid-19-and-hospitalisation-respiratory-and-non (4/31)
Associations between COVID‐19 and hospitalisation with respiratory and non‐respiratory conditions: a record linkage study

SARS-CoV-2 infection is associated with higher incidence of hospitalisation with several respiratory and non-respiratory conditions

HEART ATTACK RISKS POST-COVID: The risk of acute myocardial infarction was 93% higher in COVID-19 recovered patients compared to the general population. https://www.internationaljournalofcardiology.com/article/S0167-5273(22)01914-3/fulltext (5/31)
COVID AGES THE BRAIN: COVID-19 is associated with molecular signatures of brain aging and emphasize the value of neurological follow-up in recovered individuals... Aging-associated and cognitive decline-associated gene expression changes observed in individuals with COVID-19 may lead to increased rates of cognitive decline. https://www.nature.com/articles/s43587-022-00321-w (6/31)
Severe COVID-19 is associated with molecular signatures of aging in the human brain - Nature Aging

Mavrikaki et al. show that severe COVID-19 is associated with molecular signatures of aging and low cognitive performance in the human frontal cortex; and emphasize the value of neurological follow-up in recovered individuals.

Nature
COVID PRESENT IN LUNGS 359 DAYS POST INFECTION AND CAUSES ONGOING VASCULAR DAMAGE: The fact that in our data we find the level of vascular derangement higher in post-acute than in acute COVID-19 suggests that vascular remodeling is a continuously acting process during post-acute COVID disease. We find evidence of viral presence in the lung up to 359 days after the acute phase of disease, including in patients with negative nasopharyngeal swab tests. https://www.medrxiv.org/content/10.1101/2022.11.28.22282811v1 (7/31)
POORER MENTAL HEALTH POST COVID: The risk of incident mental health disorders was consistently higher in the covid-19 group. The covid-19 group showed an increased risk of incident anxiety disorders (hazard ratio 1.35) (35% IGHER), depressive disorders (1.39); and stress and adjustment disorders (1.38). https://www.bmj.com/content/376/bmj-2021-068993 (8/31)
Risks of mental health outcomes in people with covid-19: cohort study

Objective To estimate the risks of incident mental health disorders in survivors of the acute phase of covid-19. Design Cohort study. Setting US Department of Veterans Affairs. Participants Cohort comprising 153 848 people who survived the first 30 days of SARS-CoV-2 infection, and two control groups: a contemporary group (n=5 637 840) with no evidence of SARS-CoV-2, and a historical control group (n=5 859 251) that predated the covid-19 pandemic. Main outcomes measures Risks of prespecified incident mental health outcomes, calculated as hazard ratio and absolute risk difference per 1000 people at one year, with corresponding 95% confidence intervals. Predefined covariates and algorithmically selected high dimensional covariates were used to balance the covid-19 and control groups through inverse weighting. Results The covid-19 group showed an increased risk of incident anxiety disorders (hazard ratio 1.35 (95% confidence interval 1.30 to 1.39); risk difference 11.06 (95% confidence interval 9.64 to 12.53) per 1000 people at one year), depressive disorders (1.39 (1.34 to 1.43); 15.12 (13.38 to 16.91) per 1000 people at one year), stress and adjustment disorders (1.38 (1.34 to 1.43); 13.29 (11.71 to 14.92) per 1000 people at one year), and use of antidepressants (1.55 (1.50 to 1.60); 21.59 (19.63 to 23.60) per 1000 people at one year) and benzodiazepines (1.65 (1.58 to 1.72); 10.46 (9.37 to 11.61) per 1000 people at one year). The risk of incident opioid prescriptions also increased (1.76 (1.71 to 1.81); 35.90 (33.61 to 38.25) per 1000 people at one year), opioid use disorders (1.34 (1.21 to 1.48); 0.96 (0.59 to 1.37) per 1000 people at one year), and other (non-opioid) substance use disorders (1.20 (1.15 to 1.26); 4.34 (3.22 to 5.51) per 1000 people at one year). The covid-19 group also showed an increased risk of incident neurocognitive decline (1.80 (1.72 to 1.89); 10.75 (9.65 to 11.91) per 1000 people at one year) and sleep disorders (1.41 (1.38 to 1.45); 23.80 (21.65 to 26.00) per 1000 people at one year). The risk of any incident mental health diagnosis or prescription was increased (1.60 (1.55 to 1.66); 64.38 (58.90 to 70.01) per 1000 people at one year). The risks of examined outcomes were increased even among people who were not admitted to hospital and were highest among those who were admitted to hospital during the acute phase of covid-19. Results were consistent with those in the historical control group. The risk of incident mental health disorders was consistently higher in the covid-19 group in comparisons of people with covid-19 not admitted to hospital versus those not admitted to hospital for seasonal influenza, admitted to hospital with covid-19 versus admitted to hospital with seasonal influenza, and admitted to hospital with covid-19 versus admitted to hospital for any other cause. Conclusions The findings suggest that people who survive the acute phase of covid-19 are at increased risk of an array of incident mental health disorders. Tackling mental health disorders among survivors of covid-19 should be a priority. All data are available through the US Department of Veterans Affairs.

The BMJ
CARDIOVASCULAR RISKS EVEN IN MILD COVID INFECTION: Individuals with COVID-19 are at increased risk of incident cardiovascular disease spanning several categories. These risks and burdens were evident even among individuals who were not hospitalized during the acute phase of the infection and increased in a graded fashion according to the care setting during the acute phase (non-hospitalized, hospitalized and admitted to intensive care). https://www.nature.com/articles/s41591-022-01689-3 (9/31)
Long-term cardiovascular outcomes of COVID-19 - Nature Medicine

Individuals with COVID-19 are at increased long-term risk for a wide range of cardiovascular disorders, even for individuals who were not hospitalized during the acute phase of the infection.

Nature
HIGHER RISK OF RSV INFECTION IN KIDS POST COVID: Among RSV-infected children in 2022, 19.2% had prior documented COVID-19 infection, significantly higher than the 9.7% among uninfected children. https://www.medrxiv.org/content/10.1101/2022.11.29.22282887v1 (10/31)
DIABETES RISK RISES POST COVID: SARS-CoV-2 is associated with higher risk of incident diabetes in men but not in women. SARS-CoV-2 was associated with higher risk of incident diabetes, compared with no positive tests, among men (120 days, odds ratio [OR] 2.56; all time, 1.95) but not women (120 days, 1.21; all time, 1.04). https://pubmed.ncbi.nlm.nih.gov/35085391/ (11/31)
The Incidence of Diabetes Among 2,777,768 Veterans With and Without Recent SARS-CoV-2 Infection - PubMed

SARS-CoV-2 is associated with higher risk of incident diabetes in men but not in women even after greater surveillance related to hospitalization is accounted for.

PubMed
INCREASED CANCER RISKS EVEN WITH MILD INFECTION: The primary MR analyses results suggested that the reported SARS-CoV-2 infection (odds ratio (OR) = 1.165), hospitalized COVID-19 (OR 1.145), and critically ill COVID-19 (OR 1.075) had a significant positive correlation with the risk of endometrial cancer. https://www.journalofinfection.com/article/S0163-4453(22)00261-4/fulltext (12/31)
LASTING LUNG DYSFUNCTION 360 DAYS POST COVID: Both ventilated and perfused lung parenchyma (V/Q match) was reduced from 81±6.1% in healthy controls to 62±19% (P =.006) in the recovered group and 60±20% (P=.003) in the long COVID group. V/Q match was lower in post COVID patients with infection less than 180 days (63±20%), 180 to 360 days (63±18%) and 360 days ago (41±12%) as compared with the never-infected healthy controls (81±6.1%). https://pubs.rsna.org/doi/10.1148/radiol.221250 (13/31)
Pulmonary Dysfunction after Pediatric COVID-19

Background Long COVID occurs in lower frequency in children and adolescents than in adults. Morphologic and free-breathing phase-resolved functional low-field MRI may identify persistent pulmonary manifestations after SARS-CoV-2 infection. Purpose To characterize both morphologic and functional changes of lung parenchyma on low-field MRI in children and adolescents with post COVID-19 compared with healthy controls. Materials and Methods Between August and December 2021, a cross-sectional, prospective clinical trial using low-field MRI was performed in children and adolescents from a single academic medical center. The primary outcome was the frequency of morphologic changes on MRI. Secondary outcomes included MRI-derived functional proton ventilation and perfusion parameters. Clinical symptoms, the duration from positive RT-PCR test and serological parameters were compared with imaging results. Nonparametric tests for pairwise and corrected tests for groupwise comparisons were applied to assess differences in healthy controls, recovered participants and with long COVID. Results A total of 54 participants post COVID-19 infection (mean age, 11 years ±3 [SD], 56 males) and 9 healthy controls (mean age, 10 years ±3 [SD], 70 males) were included: 29 (54%) in the COVID-19 group had recovered from infection and 25 (46%) were classified as having long COVID on the day of enrollment. Morphologic abnormality was identified in one recovered participant. Both ventilated and perfused lung parenchyma (V/Q match) was reduced from 81±6.1% in healthy controls to 62±19% (P =.006) in the recovered group and 60±20% (P=.003) in the long COVID group. V/Q match was lower in post COVID patients with infection less than 180 days (63±20%, P=.03), 180 to 360 days (63±18%, P=0.03) and 360 days ago (41±12%, P<.001) as compared with the never-infected healthy controls (81±6.1%). Conclusion Low-field MRI showed persistent pulmonary dysfunction in both children and adolescents recovered from COVID-19 and with long COVID. ClinicalTrials.gov: NCT04990531 See also the editorial by Paltiel.

Radiology
DAMAGE TO MALE REPRODUCTIVE SYSTEM: These perturbations tended to persist over time and were correlated with significant impairments in semen volume, progressive motility, sperm morphology, sperm concentration, and the number of spermatozoa. We provide the direct experimental evidence that the male reproductive system could be targeted and damaged by the COVID-19 infection. https://rep.bioscientifica.com/view/journals/rep/161/3/REP-20-0382.xml (14/31)
COVID-19 and male reproductive function: a prospective, longitudinal cohort study

The existing evidence suggests that the human reproductive system may be potentially vulnerable to COVID-19 infection. However, little is known about the virus–host interaction of COVID-19 in sperm cells. We are the first to address the connection between changes in multiple seminal biomarkers and reproductive function in male patients recovering from COVID-19. In a prospective longitudinal cohort study, seminal ACE2 activity, markers of inflammation and oxidative stress, apoptotic variables, and semen quality parameters were evaluated at 10-day intervals for a maximum follow-up time of 60 days among male patients with laboratory-confirmed COVID-19 (n = 84) and healthy controls (CON; n = 105). At the baseline and the subsequent follow-ups, the COVID-19 group revealed significantly higher levels of seminal plasma ACE2 enzymatic activity, IL-1β, IL-6, IL-8, IL-10, TGF-β, TNF-α, IFN-α, IFN-γ, ROS, caspase-8, caspase-9, and caspase-3 activity as well as lower levels of SOD activity than those in the CON group (P  < 0.05). These perturbations tended to persist over time and were correlated with significant impairments in semen volume, progressive motility, sperm morphology, sperm concentration, and the number of spermatozoa. We provide the direct experimental evidence that the male reproductive system could be targeted and damaged by the COVID-19 infection. These findings go beyond our current understanding of the disease, suggesting that the reproductive function of the patients recovering from the disease should be precisely followed and evaluated to detect and avoid more serious reproductive problems in the future, as they may develop a transient state of male subfertility like those with oligoasthenoteratozoospermia.

rep
DIABETES RISK RISE MONTHS AFTER COVID INFECTION: At 1, 3, and 6 months after infection, risk of diagnosis of Type 1 Daibetes was greater among those infected with SARS-CoV-2 compared with those with non–COVID-19 respiratory infection (1 month: HR, 1.96; 3 months: HR, 2.10; 6 months: HR, 1.83). (That is a 96% increase in risk, a 110% increase, and an 83% increase, respectively.) https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2796649 (15/31)
SARS-CoV-2 Infection and New-Onset Type 1 Diabetes Among Pediatric Patients

This cohort study assesses the association of COVID-19 with new-onset type 1 diabetes among pediatric patients.

IMMUNE SYSTEM DAMAGE: The number of total T cells, CD4+ and CD8+ T cells were dramatically reduced in COVID-19 patients, especially in patients requiring Intensive Care Unit (ICU) care. T cell counts are reduced significantly in COVID-19 patients, and the surviving T cells appear functionally exhausted. https://pubmed.ncbi.nlm.nih.gov/32425950/ (16/31)
Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19) - PubMed

<span><b>Background:</b> The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has posed great threat to human health. T cells play a critical role in antiviral immunity but their numbers and functional state in COVID-19 patients remain</span> …

PubMed
COVID REMAINS IN BRAIN FOR MONTHS EVEN WITH ASYMPTOMATIC COVID; SARS-CoV-2 is widely distributed, even among patients who died with asymptomatic to mild COVID-19, and that virus replication is present in multiple tissues. Further, we detected SARS-CoV-2 RNA in multiple anatomic sites, including regions throughout the brain, for up to 230 days following symptom onset. Our data prove that SARS-CoV-2 causes systemic infection and can persist in the body for months. https://www.researchsquare.com/article/rs-1139035/v1 (17/31)
SARS-CoV-2 infection and persistence throughout the human body and brain

COVID-19 is known to cause multi-organ dysfunction1-3 in acute infection, with prolonged symptoms experienced by some patients, termed Post-Acute Sequelae of SARS-CoV-2 (PASC)4-5. However, the burden of infection outside the respiratory tract and time to viral clearance is n...

LONG-TERM IMMUNE SYSTEM DAMAGE FROM MILD COVID: SARS-CoV-2 infection leaves an inflammatory imprint in the monocyte/ macrophage compartment that drives aberrant macrophage effector functions and eicosanoid metabolism, resulting in long-term immune aberrations in patients recovering from mild COVID-19. https://www.nature.com/articles/s41385-021-00482-8 (18/31)
Mild COVID-19 imprints a long-term inflammatory eicosanoid- and chemokine memory in monocyte-derived macrophages - Mucosal Immunology

Monocyte-derived macrophages (MDM) drive the inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and they are a major source of eicosanoids in airway inflammation. Here we report that MDM from SARS-CoV-2-infected individuals with mild disease show an inflammatory transcriptional and metabolic imprint that lasts for at least 5 months after SARS-CoV-2 infection. MDM from convalescent SARS-CoV-2-infected individuals showed a downregulation of pro-resolving factors and an increased production of pro-inflammatory eicosanoids, particularly 5-lipoxygenase-derived leukotrienes. Leukotriene synthesis was further enhanced by glucocorticoids and remained elevated at 3–5 months, but had returned to baseline at 12 months post SARS-CoV-2 infection. Stimulation with SARS-CoV-2 spike protein or LPS triggered exaggerated prostanoid-, type I IFN-, and chemokine responses in post COVID-19 MDM. Thus, SARS-CoV-2 infection leaves an inflammatory imprint in the monocyte/ macrophage compartment that drives aberrant macrophage effector functions and eicosanoid metabolism, resulting in long-term immune aberrations in patients recovering from mild COVID-19.

Nature
ERECTILE DYSFUNCTION RISKS RISE POST COVID: We found that COVID-19 diagnosis was significantly associated with ED (odds ratio 1.20) (20% higher risk). https://pubmed.ncbi.nlm.nih.gov/34931145/#affiliation-2 (19/31)
COVID-19 Infection Is Associated With New Onset Erectile Dysfunction: Insights From a National Registry - PubMed

There is an increased chance of new onset erectile dysfunction post-COVID-19 infection.<b>Chu KY, Nackeeran S, Horodyski L, et al. COVID-19 Infection Is Associated With New Onset Erectile Dysfunction: Insights From a National Registry. Sex Med 2022;10:100478.</b>

PubMed
LONG-TERM IMMUNE SYSTEM DAMAGE: Persisting reduction of all DC (dendritic cells) subpopulations was accompanied by an expansion of proliferating Lineage−HLADR+ cells lacking DC markers. Long-lasting depletion and functional impairment of DCs and monocytes may have consequences for susceptibility to secondary infections and therapy of COVID-19 patients. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009742 (20/31)
Impaired function and delayed regeneration of dendritic cells in COVID-19

Author summary Dendritic cells (DCs) recognize viral infections and trigger innate and adaptive antiviral immunity. COVID-19 severity is greatly influenced by the host immune response and modulation of DC generation and function after SARS-CoV-2 infection could play an important role in this disease. This study identifies a long-lasting reduction of DCs in the blood of COVID-19 patients and a functional impairment of these cells. Downregulation of costimulatory molecule CD86 and upregulation of inhibitory molecule PD-L1 in conventional DCs correlated with disease severity and were accompanied by a reduced ability to stimulate T cells. A higher frequency of CD163+ CD14+ cells in the DC3 subpopulation correlated with systemic inflammation suggesting that these cells may play a role in inflammatory responses of COVID-19 patients. Depletion and functional impairment of DCs beyond the acute phase of the disease may have consequences for susceptibility to secondary infections and clinical management of COVID-19 patients.

INCREASED MORBIDITY IN ALL GROUPS POST COVID: We observed significant new onset morbidity in children, adolescents, and adults across 13 prespecified diagnosis/symptom complexes, following COVID-19 infection. These findings expand the existing available evidence on post-COVID-19 conditions in younger age groups and confirm previous findings in adults. https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1004122 (21/31)
Post-COVID-19-associated morbidity in children, adolescents, and adults: A matched cohort study including more than 157,000 individuals with COVID-19 in Germany

In a matched cohort study from Germany, including more than 157,000 individuals with COVID-19, Dr. Martin Roessler and colleagues investigate post COVID-19 associated morbidity in children, adolescents, and adults.

BRAIN AND COGNITIVE DAMAGE POST COVID IN MILD COVID: We identified a greater reduction in grey matter thickness and a greater reduction in global brain size in the SARS-CoV-2 cases. The participants who were infected with SARS-CoV-2 also showed on average a greater cognitive decline between the two time points. Importantly, these imaging and cognitive longitudinal effects were still observed after excluding the 15 patients who had been hospitalised. https://www.nature.com/articles/s41586-022-04569-5 (22/31)
SARS-CoV-2 is associated with changes in brain structure in UK Biobank - Nature

After infection with SARS-CoV-2, individuals show a greater reduction in grey matter thickness and tissue contrast in the orbitofrontal cortex and parahippocampal gyrus; greater changes in markers of tissue damage in regions that are functionally connected to the primary olfactory cortex; and a greater reduction in global brain size.

Nature
@augieray Yet people act like it is not that serious.
@augieray
Makes sense to me. It was about 6-7 months after I was positive with the Delta variant that I experienced bouts of utter fatigue while at work and would head home early
And at times I’ll forget the names of basic things I’m trying to talk about. Fatigue isn’t as much of a problem anymore tho, thankfully. 14 months past positive test
@PapaPear Hope you stay healthy in the new year!