The book of covid

This cohort study investigates the association of SARS-CoV-2 infection with risk of incident diabetes among individuals in Canada.

The objective of the current investigation was to examine associations between symptomatic COVID-19 history, neurocognitive function, and psychiatric …

A study illustrates how SARS-CoV-2 can damage your immune response.

The failure to recognise the ongoing severity of COVID-19 is creating a reality gap that is being filled by groups peddling misinformation.

Millions of COVID-19 pediatric survivors are facing the risk of long COVID after recovery from acute COVID-19. The primary objective of this study was to systematically review the available literature and determine the pooled prevalence of, and risk factors ...

Many antibody drugs are no longer effective against COVID-19 due to the rapid evolution of the virus and its many subvariants, writes Syra Madad. The US government desperately needs to continue to invest in more covid therapeutics to keep up with the evolving nature of the virus.

Structural changes in the brain may explain the persistent fatigue and neuropsychiatric complications tied to long covid.

COVID-19-associated vascular disease complications are primarily associated with endothelial dysfunction; however, the consequences of disease on vascular structure and function, particularly in the long term (7 weeks post-infection), remain unexplored. Individual pre- and post-infection changes in arterial stiffness as well as central and systemic hemodynamic parameters were measured in patients diagnosed with mild COVID-19. As part of in-laboratory observational studies, baseline measurements were taken up to two years before, whereas the post-infection measurements were made 2–3 months after the onset of COVID-19. We used the same measurement protocol throughout the study as well as linear and mixed-effects regression models to analyze the data. Patients (N = 32) were predominantly healthy and young (mean age ± SD: 36.6 ± 12.6). We found that various parameters of arterial stiffness and central hemodynamics—cfPWV, AIx@HR75, and cDBP as well as DBP and MAP—responded to a mild COVID-19 disease. The magnitude of these responses was dependent on the time since the onset of COVID-19 as well as age (pregression_models ≤ 0.013). In fact, mixed-effects models predicted a clinically significant progression of vascular impairment within the period of 2–3 months following infection (change in cfPWV by +1.4 m/s, +15% in AIx@HR75, approximately +8 mmHg in DBP, cDBP, and MAP). The results point toward the existence of a widespread and long-lasting pathological process in the vasculature following mild COVID-19 disease, with heterogeneous individual responses, some of which may be triggered by an autoimmune response to COVID-19.

Coronavirus disease 2019 (COVID-19) is associated with adverse impacts in the cardiovascular system, but the mechanisms driving this response remain unclear. In this study, we conducted “pseudoviral infection” of SARS-CoV-2 subunits to evaluate their toxic effects in cardiomyocytes (CMs), that were derived from human induced pluripotent stem cells (hiPSCs).

A study that used wastewater signals to identify cases of covid-19 found that even a small increase in the proportion of people wearing masks at elementary schools in one California county significantly reduced the chance of a case.

A recent study found 59% of people with long covid had damage to at least one organ a year after their initial symptoms.

A February 2023 pandemic decision is being based on reported cases, even though we severely curtailed our ability to ensure that this number reflects the actual amount of cases.

Autopsy studies show that the virus can persist in some people for many months even though they have no symptoms and test negative for the virus. Brains donated by people who died of covid-19 also show widespread problems in the cells lining the blood vessels and exaggerated clotting, supporting the idea of covid-19 as a blood flow disorder that brings on brain disease.

We alerted the World Health Organization (WHO) about the potential significance of the airborne transmission of SARS-CoV-2 and the urgent need to control it, but our concerns were dismissed. Here we describe how this happened and the consequences.

Our data demonstrate that the human thymus is a target of SARS-CoV-2 and thymic function is altered following infection. These findings expand our current knowledge of the effects of SARS-CoV-2 infection on T-cell homeostasis and suggest that monitoring thymic activity may be a useful marker to pred …

Vaccinated subjects (n = 259,821) did not show an increased risk of all-cause death, non-covid death, or any PVR-SAEs, as compared to the unvaccinated (n = 56,494). These results were consistent across genders, age-classes, vaccine types, and SARS-CoV-2 infection status and did not vary in Cox models adjusting for age, gender, SARS-CoV-2 infection, and selected comorbidities.

We report nine patients suffering with long covid for 101 to 547 days. All exhibited significant perturbations of their immune systems, but only one was known to be immunodeficient prior to the studies directed at evaluating them for possible treatment. Neurological and cardiac symptoms were most common.

Covid increases your risk of heart attack, stroke, cardiac arrest, and more. But while anti-vaxxers falsely claim these deaths as MRNA shot complications, the Biden admin is silent.

It caused substantially more deaths in CYP annually than any vaccine-preventable disease historically in the recent period before vaccines became available. Various factors, including underreporting and not accounting for covid-19’s role as a contributing cause of death from other diseases, mean that these estimates may understate the true mortality burden of covid-19.

More than a million people have called out sick for the past three years, and CDC says long covid probably a contributor too.

As rich people plough money into ventilation to protect themselves, those with long Covid are treated as an embarrassment.

SARS-CoV-2 infection is clinically heterogeneous, ranging from asymptomatic to deadly. A few patients with covid-19 appear to recover from acute viral infection but nevertheless progress in their disease and eventually die, despite persistent negativity at molecular tests for SARS-CoV-2 RNA.

Covid-19 infection, including long-covid, is associated with increased short- and long-term risks of CVD and mortality. Ongoing monitoring of signs and symptoms of developing these cardiovascular complications post diagnosis and up till at least a year post recovery may benefit infected patients, especially those with severe disease.

At least 75% of the children who acquired covid-19 showed no symptoms. This suggests they unknowingly had virus in their noses but may have been spreading it to others. Schools ranked the highest as public sources of exposure compared with health clinics and grocery stores.

Colin Furness debunks the popular theory and explains how covid may be weakening our immune systems in the long run.

Corporate media’s overarching message is that it’s “time to move on,” and radicals holding on to precautions are impeding economic recovery.

At the 6-month follow-up period, the risk of various autoimmune diseases is substantially higher in covid-19 individuals than in non-covid controls after accounting for competing risk of death. Given the large sample size and relative moderate intensity of the effects, this study should be replicated in other independent dataset from different countries to objectively examine the role of SARS-CoV-2 infection in triggering or causing autoimmune diseases.

How covid actively suppresses and evades your immune system [Part 2]. Part 2 looks at how mild and moderate #covid infection reprograms white #blood cells (#monocytes) to reduce #innate #immune functions and how it evades the mucus layer in our #nose.

How #covid actively suppresses and evades your #immune system [Part 1]. This thread highlights multiple methods that the virus uses to help keep #reinfecting people including #MHC-I and #interferon #suppression, #evasion of Natural Killer (NK) cells, and reprogramming of #monocytes.

Long covid is an often debilitating illness that occurs in at least 10% of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. More than 200 symptoms have been identified with impacts on multiple organ systems.