Long COVID Conditions – Fatigue 03

Section 3

ROLE OF VAGUS NERVE IN INFLAMMATION

There are two methods by which peripheral inflammation may exacerbate CNS inflammation: leaky regions in the blood-brain barrier and the vagus nerve. The vagus nerve, also known as the tenth cranial nerve, is the autonomic nervous system’s longest nerve. To moderate oxygen demand, this nerve has parasympathetic regulation of various organs involved in breathing, including the lungs, heart, and diaphragm, which might contribute to fatigue.

 

 

Afferents from the vagal nerve tend to transfer pro-inflammatory responses from cells in the peripheral organs to the CNS. From CNS signals, vagal efferents tend to produce anti-inflammatory responses in peripheral tissue. The vagal afferents transmit pro-inflammatory signals from the peritoneum and organs such as the lung, gut, ear, spleen, liver, and lung to trigger inflammatory cytokines in specific centers in the CNS.  From these centers Pro-inflammatory signal from the periphery cause increase pro-inflammatory cytokine production in parts of the brain that impact tiredness and sleep.

 

In contrast, activation of the vagal efferents caused by cholinergic mechanisms in the brain, such as muscarinic acetylcholine receptors dorsal motor nucleus (DMN), may cause anti-inflammatory effects in peripheral tissues. Vagal efferents originating in the brainstem and extending to peripheral organs, may help to reduce inflammation. Vagotomy, which inhibits the vagus nerve, may reveal directional alterations between the periphery and the CNS. Inhibiting   vagal afferents with a vagotomy and administering inflammatory chemicals to the periphery suggest that at low doses, the vagal afferent nerves may be a primary mechanism for translating peripheral inflammation to central inflammation, affecting behavior such as sleep. Vagotomy cannot prevent central inflammation caused by peripheral inflammation as a result of high concentrations of inflammatory stimuli which suggests that the blood-brain barrier is ineffective and also involved in CNS inflammation.

 

In individuals with rheumatoid arthritis, vagal nerve stimulation is utilized as an alternate treatment to decrease TNF.  Vagal nerve stimulation may help those with inflammatory bowel disease. The effects of this anti-inflammatory medication are due in part to the stimulation of cholinergic neurons, which causes peripheral inflammation to be suppressed, which subsequently reduces CNS inflammation. In fact, vagal nerve stimulation decreased daily drowsiness, improved tiredness, and lowered whole blood cell levels of TNF-, IFN-, IL-6, and IL-1 in people with Sjörgen’s syndrome.

 

NEUROVASCULAR

Cerebral blood flow is a critical component in supplying nutrients and oxygen to cells in the central nervous system The neurovasculature also eliminates waste products like as carbon dioxide and signaling chemicals, as well as providing enough energy reserves. Cellular and performance problems may result from a decline in blood supply in a region around neurons in the CNS.  Multiple sclerosis, type 1 diabetes, Alzheimer’s disease, and celiac disease are all linked to hypoperfusion. Neural activity is synchronized with localized cerebral blood flow, which is known as neurovascular coupling.  Increases in the production of vasoactive chemicals are linked to increased brain activity, which may affect vascular hemodynamics directly or indirectly.

 

 

Sleep, and Autoimmune and Related Disorders Endothelial cells, smooth muscle, astrocytes, neurons, and pericytes make up the neurovascular unit at the level of the cerebral microvasculature, which includes arterioles and capillaries, and it is influenced by microglia and perivascular macrophages. Changes in metabolism and inflammation may also affect astrocyte end-feet, affecting cerebral blood flow (CBF). The neurovascular unit regulates blood flow throughout the brain and is influenced by the surrounding cells’ energy demands as well as the vasoconstrictive and vasodilative substances secreted by these cells, such as catecholamines and dopamine.

 

Monoamines released by neurons have both vasodilative and vasoconstrictive properties, which can influence blood flow. Pro-inflammatory molecules tend to be vasodilative, reduce vascular resistance, and increase cerebral CBF, whereas monoamines released by neurons have both vasodilative and vasoconstrictive properties, which can influence blood flow. Vasoconstrictive drugs usually raise vascular resistance and lower CBF.

 

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Long COVID Conditions – Fatigue 02

Section 2

SLEEP AND CIRCADIAN RHYTHMS

Sleep and circadian rhythm abnormalities seem to have a bidirectional link with autoimmune illness. Chronic sleeplessness is linked to a higher risk of acquiring an autoimmune illness . Narcolepsy, a sleep condition, may possibly have an immunological component, according to evidence. Sleep disturbances are common in people with autoimmune diseases. Sleep apnea is more common in people with rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, Sjörgen’s syndrome, pemphigus, and systemic sclerosis. Rapid-eye movement (REM) sleep behavior disorder is more common in people with multiple sclerosis.

 

 

Autoimmune illnesses such as multiple sclerosis, psoriasis, and rheumatoid arthritis are linked to an increased incidence of restless legs syndrome. Non-restorative sleep is also used in the clinical diagnosis of chronic fatigue syndrome/myalgic encephalomyelitis, implying a link between poor sleep and exhaustion.  In addition, sleep may be affected by the secondary effects of autoimmune illness or sleep disorder pathology.

Individuals with autoimmune illness, for example, suffer from persistent discomfort. Sleep disturbances are reported by up to 88 percent of those with chronic pain. Conversely, it has been found that up to 50% of those who have insomnia also have increased pain which might lead to exhaustion. Sleepiness is described as the inability to stay awake or the increased incidence or urge to sleep. Sleep disturbances and sleep disorders are linked to drowsiness.

In addition to causing exhaustion, sleepiness may affect alertness, cognition, mood, and concentration. Many sleep disorders, such as insomnia and sleep apnea, are linked to problems with alertness, cognition, mood, motivation, and attention. Sleepiness may be caused by staying up for long periods of time or by the fragmented sleep that many health disorders, such as sleep apnea and autoimmune illnesses, cause on a regular basis.

Evidence shows that sleep loss has a dose-dependent effect, with more sleep loss correlated with increased tiredness and lower performance. Nonetheless, drowsiness varies with time of day, which might affect an individual’s capacity to sleep or the usefulness of naps in avoiding sleepiness-related impairments in functional activities like cognition. Individuals who suffer from tiredness often go through phases when their exhaustion is at its worst. Furthermore, some people with multiple sclerosis are more fatigued in the morning, while others are more fatigued in the evening.

 

 

Prior sleep or circadian variables are probable contributors to these time-of-day changes, albeit this is speculation. Increased amounts of inflammatory chemicals have been linked to sleep problems such as sleep apnea, insomnia, and REM sleep behavior disorder. Because inflammation may cause tiredness, it’s possible that neuroinflammation associated with disrupted sleep or sleep loss might increase fatigue in autoimmune disease patients.

Dysregulated homeostatic cytokine expression in autoimmune illness leads to sleep abnormalities in autoimmune disease patients. Furthermore, it’s possible that sleep deprivation, which raises pro-inflammatory cytokines, exacerbates sleep problems in those with autoimmune diseases.

 

STRESS

The hypothalamic-pituitary-adrenal (HPA) axis is involved in hormonal responses to stress that control exhaustion. It includes interactions between the hypothalamus and pituitary glands. When compared to the normal population, those with autoimmune diseases are said to have higher stress levels. Stress seems to be able to control brain inflammation in autoimmune illnesses like multiple sclerosis. When the sympathetic nervous system is activated, noradrenaline is released from nerve terminals and adrenaline is released from the adrenal medulla. These catecholamines may raise blood pressure and heart rate.

Adrenaline receptors are expressed by microglia, macrophages, and astrocytes in the central nervous system. Complement-induced innate immunological responses change adrenaline receptors. Several autoimmune and related illnesses, including Sjögren’s syndrome, rheumatoid arthritis, and systemic lupus erythematosus, have been linked to dysregulated complement. Noradrenaline seems to suppress activated microglia in a selective manner.

 

 

Furthermore, when noradrenaline is combined with ATP, it reduces the baseline rate while increasing ATP-induced process extension and migration of microglia in vitro, suggesting that purinergic and adrenergic activation have a link. Beta-adrenergic receptors also have an anti-inflammatory effect on astrocytes, lowering the expression of TNF-related genes such as IL-6, CXCL2, CXCL3, VCAM1, and ICAM1. Stress causes the production of corticotrophin-releasing hormone (CRH) in the hypothalamus. CRH stimulates the pituitary to generate adrenocorticotropic hormone (ACTH), which boosts the production of glucocorticoids from the adrenal cortex. Anti-inflammatory properties of glucocorticoids are achieved in part through suppressing IL-1, IL-6, and IFN-, as well as cyclooxygenases and prostaglandins.

However, cytokines and ACTH and glucocorticoids have a connection in which IL-1, IL-6, and TNF-can activate the pituitary adrenal axis to raise blood levels of ACTH and glucocorticoids inhibiting pro-inflammatory molecules. Glucocorticoids, on the other hand, may have a pro-inflammatory effect on the immune system. Sleep deprivation may also raise cortisol levels, a glucocorticoid. As a result, the consequences of stress, sleep, and exhaustion are all intertwined. Chronic stress, such as that experienced by people with chronic illnesses, may lower glucocorticoid sensitivity, promoting inflammatory signaling. DHEA has the ability to operate as both a positive and negative allosteric modulator of the NMDA and GABA A receptors. In autoimmune diseases such as multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel disease, DHEA levels are reported to be lower. Anxiety, sadness, sleep, and exhaustion are all affected by serotonin.

Serotonin, dopamine, and noradrenaline are all released in response to IL-1. Noradrenaline is an excitatory neurotransmitter that binds to alpha- and beta-adrenergic receptors. are linked to noradrenaline. Low levels of noradrenaline are linked to anxiety, depression, exhaustion, and a lack of drive. Neurons that produce noradrenaline are present in limited parts of the brain. Noradrenaline levels stay relatively stable throughout wakefulness but are increased when a stimulus is required such as wakefulness, attention.

Dopamine is an excitatory neurotransmitter. Motivation, interest, and drive are all affected by dopamine. Low levels of dopamine are seen in those who have trouble finishing activities, have poor attention, have little energy, and are unmotivated. As a result, dopamine imbalance leads to exhaustion, with insufficient dopamine causing fatigue.

Histamine is an excitatory neurotransmitter that binds to four G protein-coupled receptors: histamine 1, histamine 2, histamine 3, and histamine 4.  Sleep/wake cycles, emotions, behavior, and exhaustion are all affected by histamine. Microglia are known to be activated by histamine, resulting in the production of pro-inflammatory cytokines such as IL-6 and TNF- alpha.  In chronic inflammatory disorders, including autoimmune diseases like multiple sclerosis, histamine is also activated.

 

 

Histamine causes vasodilation and may cause blood pressure changes. Histamine may also cause the release of nitric oxide, a powerful vasodilator. Histaminergic neurons may be found in all parts of the brain, including the cortex and the brainstem. Histaminergic receptors, on the other hand, are located on cells throughout the brain. When you’re awake, neurons fire fast, and when you’re sleeping, they don’t. Drowsiness is caused by medicines that target the histamine 1 receptor, and over-the-counter antihistamines are linked to increased sleepiness

Glutamate is a primary excitatory neurotransmitter generated by metabolism and present throughout the Central Nervous System. Glutamate binds N-methyl-D-aspartate (NMDA) receptors, which increase calcium membrane permeability. Low glutamate levels may cause fatigue and impaired brain function. To protect neurons from excitotoxicity, extracellular glutamate concentrations function within a narrow physiological range involving its release and absorption. Ketamine is a strong NMDA receptor antagonist with anti-fatigue properties, according to current studies.

Acetylcholine is an excitatory neurotransmitter made from choline and acetyl-CoA by the enzyme choline acetyltransferase. Acetylcholinesterase is an enzyme that breaks down acetylcholine to acetate and choline. Acetylcholine binds to both nicotinic and muscarinic acetylcholine receptors in the brain.

Acetylcholine is involved in both central and peripheral nervous system (CNS) and peripheral nervous system (PNS) functions, including the neuromuscular junction. Sleep and wakefulness, arousal, cognition, memory, and tiredness are all regulated by acetylcholine.

Long COVID Conditions – Fatigue 01

Section 1 

Long COVID Conditions – Fatigue may be defined as tiredness that does not go away with rest. Fatigue is characterized by moments of exhaustion. Fatigue prevents you from doing your daily tasks. Fatigue is multifaceted, making it difficult to comprehend the origin of its symptoms. Symptoms vary, but exhaustion may make even basic actions like walking across the room, preparing a meal difficult.

 

 

The specific mechanics of fatigue remain a mystery, maybe as a result of its wide definition. Fatigue is a multifactorial condition. It can be caused by some or many different causes. Here we discuss the possible mechanisms of fatigue.

 

Autoimmune:

In the United States of America over 20 million have an autoimmune disorder. There are more than 100 autoimmune disorders that we know. There are many more that are being discovered. The prevalence of many autoimmune diseases is on the rise as well.

The chief complaint amongst patients with autoimmune disorder is significant fatigue. 75% of them find the fatigue as severe, debilitating, and hindered them from doing routine daily duties. Fatigue, in turn leads to a variety of problems such as mood disturbances, social isolation, and inability to work. Consequently, fatigue may have a negative impact on one’s health and put a financial strain on the person, family, and community.

 

 

The kind of fatigue experienced by people with autoimmune illness varies. These variations are likely connected to the tissues, organs, cell types, brain locations, and molecular and physiological pathways that are impacted by the disease. Fatigue in autoimmune disorders may be caused by a variety of mechanisms. Several physiological processes, including oxygen and nutrient supply, metabolism, and daytime drowsiness, have been linked to exhaustion. Many of the variables that modify tiredness also affect inflammation, and vice versa.

Neuroinflammation (inflammation of the nerves) seems to be a major contributor to fatigue. Because inflammation plays such a big role in fatigue, it’s possible that inflammatory pathways and the resulting physiological changes controlled by inflammation are treatment targets for fatigue in autoimmune disease patients.

 

INFLAMMATION

Autoimmune disorders are linked to increased pro-inflammatory signals in the peripheral and central nervous systems. The location of the increased inflammation varies depending on the kind of autoimmune illness and how far the disease has progressed. Non-autoimmune illness and associated problems with elevated inflammation in the periphery and/or CNS, sleep disturbances, stroke, and traumatic brain injury are all linked to fatigue.  Non-inflammatory factors such as hydration status, pain, pharmaceutical interactions, muscle/exercise, hypothyroidism, radiation therapy lung function, and cardiovascular characteristics such as blood pressure, heart rate, cardiac output, and stroke volume are all known to affect fatigue Many of the non-inflammatory factors that cause tiredness are influenced by or modified by inflammatory processes.

 

 

Inflammatory mediators have been shown to alter a variety of factors that lead to exhaustion, including motivation, drowsiness, cognition, anxiety, depression, and stress. Cytokines are tiny protein molecules that play a role in cell signaling and enable cells to interact through autocrine, paracrine, and endocrine pathways. Immune responses, inflammation, cell development and maturation, and normal physiological processes are all influenced by cytokines. Nucleated cell types such as lymphocytes and macrophages, as well as microglia, astrocytes, and neurons in the CNS, release inflammatory cytokines. The role of cytokines in the genesis of tiredness is implicated by the inflammatory pathways involved. Tumor necrosis, interleukin (IL)-1 beta (IL-1)

T helper cells and macrophages, in particular, increase the production of cytokines such as IL-1, TNF-, IL-6, IL-12, IL-23, and IFN- during autoimmune illness.  As a result, therapies that target components of lymphocyte regulation systems may help people with autoimmune disorders such Sjögren’s syndrome, rheumatoid arthritis, and inflammatory bowel disease. T-cell activities are linked with macrophage activity and macrophages have a role in the pathophysiology of autoimmune disorders. Furthermore, the overall degree of localized cytokine secretion, as well as its sustained increase or attenuation, might cause overexpression or downregulation of related receptors, modulating downstream processes of cytokine synthesis.

The expression of cytokines changes during the day and in response to local activity, and they govern normal physiological activities such as mood, cognition, and sleep. As a result, it’s probable that dysregulation of inflammatory cytokines and their receptors in autoimmune illness causes cytokine homeostasis to be disrupted, contributing to fatigue. Inflammation in the peripheral nervous system may lead to inflammation in the central nervous system (CNS) and illness behaviors, which are behaviors linked to various elements of exhaustion.

Long Covid Part – 2

To Calculate Mortality, Many Methods are Utilized.

 

The Covid 19 Pandemic- 3 – Testing volume, healthcare system quality, treatment choices, government reaction, duration since the first epidemic, and demographic factors, such as age, sex, and general health, all impact these statistics, which vary by area and by time. In countries like Belgium, fatalities from suspected cases, even those without a test, are included, resulting in an increase in the number of cases.

Within a particular time frame, the death-to-case ratio is calculated by dividing the number of deaths linked to COVID-19 by the number of diagnosed cases. According to figures from Johns Hopkins University, the worldwide death-to-case ratio was 1.97 percent as of December 11th, 2021 (5,299,935 fatalities for 269,441,881 cases). Depending on the area, the number changes.

 

Official death tolls have been criticized for underreporting the true death toll, since comparisons of mortality rates before and after the pandemic reveal an increase in fatalities that cannot be explained only by COVID 19 Pandemic deaths.

 

The Economist estimated 9.5 to 18.6 million COVID-19 fatalities globally, whereas the Institute for Health Metrics and Evaluation estimated over 10.3 million.

 

Reporting

 

The WHO assigned two codes for COVID-19, according to the US Centers for Disease Control and Prevention (CDC) on March 24, 2020: U07.1 for laboratory confirmation and U07.2 for clinical or epidemiological diagnosis when laboratory confirmation is equivocal or unavailable.

“Because laboratory test results are not typically reported on death certificates in the United States,” according to the CDC, “[the National Center for Health Statistics (NCHS)] is not planning to implement U07.2 for mortality statistics,” and U07.1 would be used “if the death certificate reports terms such as ‘probable COVID-19’ or ‘likely COVID-19’.” While the “underlying cause” “depends on what and where conditions are documented on the death certificate, the standards for coding and selection of the cause of death are projected to result in COVID 19 Pandemic being the underlying cause more frequently than not,” according to the CDC.

 

The WHO “does not discriminate” between SARS-CoV-2 and COVID-19 infection, according to the report.

 

 

The percentage of people who die from infection (IFR)

 

The infection fatality ratio (IFR), which is defined as the total number of fatalities related to the illness divided by the total number of infected persons, is a critical parameter in appraising a disease (including asymptomatic and undiagnosed infections).

 

To emphasize that this statistic is stated in percentage points, epidemiologists sometimes refer to it as the ‘infection fatality rate’ (not as a decimal). This statistic is known as the ‘infection fatality risk’ in other published investigations.

A research analysis published in Nature in November 2020 revealed a median range of 0.24 percent to 1.49 percent for population-weighted IFRs in different nations, excluding fatalities in aged care institutions.

 

In comparison to older individuals, children and younger adults had substantially lower IFRs (e.g., 0.002 percent at age 10 and 0.01 percent at age 25). (0.4 percent at age 55, 1.4 percent at age 65, 4.6 percent at age 75, and 15 percent at age 85). Across age groups, these rates differ by a factor of 10,000. [83] A fatal COVID-19 infection is two orders of magnitude more probable for middle-aged individuals than the annualized risk of a fatal vehicle collision, and significantly more hazardous than seasonal influenza.

 

According to this research, the majority of the disparities were due to age-related variations in the population and infection patterns particular to each age group.

 

The proportion of cases that die (CFR)

 

The case fatality ratio (CFR), which is the ratio of fatalities to diagnoses, is another statistic used to estimate mortality rate. Since the time between development of symptoms and death, and because testing is limited to symptomatic people, this statistic may be deceptive (and particularly on those manifesting more severe symptoms).  “At this early stage of the pandemic, most estimates of fatality rates have been based on cases found via surveillance and estimated using basic methodologies, giving rise to highly varying CFR estimates by country – from less than 0.1 percent to over 25 percent,” WHO, August 4, 2020.

Pradeep Chopra, MD

The Long Covid Treatment Center

102 Smithfield ave.

Pawtucket, RI 02860

Email; [email protected]

Covid 19 Symptoms And Signs

COVID-19 Symptoms Vary, Ranging From Moderate Symptoms to Severe Sickness.

 

Headache, loss of smell and taste, nasal congestion and runny nose, cough, muscular discomfort, sore throat, fever, diarrhea, and breathing problems are all common symptoms. People with the same virus may have a variety of symptoms, which may vary over time. A respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and exhaustion; and a digestive symptom cluster with stomach discomfort, vomiting, and diarrhea have all been discovered.COVID-19 is linked to loss of taste and smell in persons who have never had ear, nose, or throat problems, and it has been documented in as many as 88 percent of instances.

Only 81 percent of those who display symptoms have mild to moderate symptoms (up to mild pneumonia), whereas 14 percent develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging), and 5% develop critical symptoms (respiratory failure, shock, or multiorgan dysfunction).

 

At least a third of those who are infected with the virus never show any signs or symptoms.  Asymptomatic carriers are less likely to get tested and hence transmit the illness. Other infected persons may develop symptoms later, referred to as “pre-symptomatic,” or have extremely weak symptoms, and can transfer the virus to others.

 

There is a lag between when a person gets sick and when the first symptoms occur, as is usual with infections. COVID-19 has a four to five day median delay. Symptoms appear in the majority of sick persons two to seven days after exposure, and virtually everyone has at least one symptom by 12 days.

 

The majority of patients recover from the disease’s acute phase. However, some individuals – more than half of a cohort of home-isolated young adults – continue to suffer a variety of consequences, including as weariness, for months after recovery, a condition known as chronic COVID; long-term organ damage has also been documented. Long-term research are being conducted to learn more about the disease’s long-term impact.

 

Transmission

 

COVID-19 Transmission is the main article.

 

The pulmonary route of COVID-19 transmission, which includes bigger droplets and aerosols.

When individuals inhale droplets and minute airborne particles (that create an aerosol) that infected persons exhale while they breathe, speak, cough, sneeze, or sing, the illness is mostly spread via the respiratory route.

When infected persons are physically near, they are more likely to transfer COVID-19. Infection may, however, spread across greater distances, especially indoors.

Infectivity might appear 1-3 days before symptoms appear.

Even if they are asymptomatic or pre-symptomatic, infected people may transmit the illness.

In most cases, the peak viral load in upper respiratory tract samples comes close to the beginning of symptoms and then diminishes after the first week. According to current research, viral shedding and infectiousness may last up to 10 days after symptom start in people with mild to moderate COVID-19, and up to 20 days in those with severe COVID-19, including immunocompromised people.

 

Infectious particles vary in size from small aerosols that float in the air for a long time to bigger droplets that float or fall to the ground.

 

Furthermore, COVID-19 research has reshaped our knowledge of how respiratory viruses are spread. The biggest droplets of respiratory fluid do not go far and may infect mucous membranes of the eyes, nose, and mouth if breathed or landed on them. When individuals are physically near, aerosols are at their peak concentration, making viral transmission simpler. However, airborne transmission may occur over longer distances, especially in poorly ventilated areas; tiny particles can stay suspended in the air for minutes to hours in certain situations.

Only 10 to 20% of persons are responsible for the disease’s propagation, therefore the number of people affected by a single sick person fluctuates.

It spreads in clusters, with infections linked to an index case or a specific geographic place. In many of these cases, superspreading episodes occur, in which a single individual infects a large number of others.

 

Coronavirus 2 causes severe acute respiratory syndrome (SARS).

 

SARSCoV2 is a virus that belongs to the coronavirus family of viruses.

 

It has a single linear RNA segment and is a positive-sense single-stranded RNA (+ssRNA) virus. Humans, other mammals, including cattle and companion animals, and avian species are all infected by coronaviruses. Human coronaviruses may cause illnesses ranging from the common cold to more serious infections like Middle East respiratory syndrome (MERS, which has a 34% death rate). After 229E, NL63, OC43, HKU1, MERS-CoV, and the original SARS-CoV, SARS-CoV-2 is the sixth known coronavirus to infect humans.

 

Data on viral genomic sequences may reveal if viruses that are isolated in time and location are likely to be epidemiologically connected.

 

It is feasible to recreate a phylogenetic tree of a virus family’s mutation history with a sufficient number of sequenced genomes. Five genomes of SARSCoV2 had been identified from Wuhan and reported by the Chinese Center for Disease Control and Prevention (CCDC) and other institutes by 12 January 2020; by 30 January 2020, the number of genomes had climbed to 42. The samples were found to be “strongly linked with at most seven alterations relative to a common ancestor” in a phylogenetic study, hinting that the first human infection happened around November or December 2019. At the outset of the pandemic, the structure of the phylogenetic tree revealed strong similarities between human isolates. As of August 21, 2021, 3,422 SARSCoV2 genomes from 19 strains have been publicly released from all continents except Antarctica.

 

COVID-19 testing for further details

 

A nasopharyngeal swab is shown for COVID-19 testing.

 

Nucleic acid assays, which identify the presence of viral RNA fragments, are the main techniques of testing for the presence of SARS-CoV-2.

 

The usefulness of these tests to assess the length of infectivity of patients is restricted since they detect RNA but not infectious virus. The test is usually performed on respiratory samples acquired using a nasopharyngeal swab, although it may also be performed on a nasal swab or a sputum sample. The results are usually ready in a matter of hours. The World Health Organization (WHO) has released various illness testing procedures.

CT scans of the chest may be useful in diagnosing COVID-19 in people who have a strong clinical suspicion of infection, but they are not suggested for regular screening.

 

Early infection is characterized by bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and posterior distribution. As the illness advances, subpleural dominance, crazy paving (lobular septal thickening with varying alveolar filling), and consolidation may emerge. Asymmetric peripheral ground-glass opacities without pleural effusions are common imaging findings on chest radiographs and computed tomography (CT) of persons who are symptomatic.

 

Prevention

 

Additional information is available at: COVID-19 pandemic prevention, COVID-19 pandemic face masks, and COVID-19 pandemic social distancing methods. Pathogens may spread rapidly without pandemic containment measures like social separation, immunization, and face masks. This graph depicts how early implementation of containment measures protects a larger portion of the population.

Getting vaccinated, staying at home, wearing a mask in public, avoiding crowded places, keeping a safe distance from others, ventilating indoor spaces, managing potential exposure durations,washing hands with soap and water frequently and for at least twenty seconds, practicing good respiratory hygiene, and avoiding touching the eyes, nose, or mouth with unwashed hands are all preventive measures to reduce the risk of infection.

 

The CDC advises those who have been diagnosed with COVID-19 or suspect they may be infected to stay at home except for medical care, call ahead before visiting a healthcare provider, wear a face mask before entering the healthcare provider’s office and when in any room or vehicle with another person, cover coughs and sneezes with tissues, wash hands frequently with soap and water, and avoid sharing personal household items.

 

Vaccines

 

COVID-19 vaccine is the main topic of this essay.

 

See also COVID-19 Vaccine Development History and COVID-19 Vaccine Deployment.

A COVID19 vaccine is a vaccine designed to confer acquired immunity against the virus that causes coronavirus illness 2019 (COVID19), the severe acute respiratory syndrome coronavirus 2 (SARSCoV2). Prior to the COVID19 pandemic, there was a well-established body of information regarding the structure and function of coronaviruses that cause illnesses like SARS and Middle East respiratory syndrome (MERS). The development of multiple vaccine platforms was hastened as a result of this information in early 2020.

SARS-CoV-2 vaccinations were developed with the goal of avoiding symptomatic, frequently severe sickness. SARS-CoV-2 genetic sequence data was exchanged via GISAID on January 10, 2020, and the global pharmaceutical sector declared a strong commitment to address COVID19 on March 19, 2020. The COVID19 vaccinations have been extensively credited with lowering the severity and fatality rates associated with COVID19.

 

Many nations have devised staggered distribution programs that prioritize people who are most at risk of difficulties, such as the elderly, as well as those who are most at risk of exposure and transmission, such as healthcare personnel.

 

The European Union authorized the Pfizer BioNTech vaccine on December 21, 2020. On December 27, 2020, vaccinations started to be delivered. The Moderna vaccine received approval on January 6, 2021, while the AstraZeneca vaccine received approval on January 29, 2021.

 

On February 4, 2020, US Secretary of Health and Human Services Alex Azar issued a notice of declaration under the Public Readiness and Emergency Preparedness Act for medical countermeasures against COVID-19, stating that the declaration covers “any vaccine, used to treat, diagnose, cure, prevent, or mitigate COVID-19, or the transmission of SARS-CoV-2 or a virus mutating therefrom,” and that the declaration precludes “liability claims alleging negligence by a manufacturer in creating a

 

[156] According to a research published on the 8th of December, the AstraZeneca vaccine is roughly 70% effective. [157]

 

More than 4.6 billion doses of COVID-19 vaccination has been delivered in over 190 countries as of mid-August 2021. The vaccination developed by Oxford-AstraZeneca was the most commonly utilized. [158]

 

Treatment

 

COVID-19 treatment and management is the main article.

 

COVID-19 does not have a particular, effective therapy or cure.

 

[160] Supportive care, which includes treatment to ease symptoms, fluid therapy, oxygen support, and prone posture if required, as well as drugs or devices to assist other afflicted essential organs, is the cornerstone of COVID-19 management. [161]

 

Invasive ventilation is being given to a severely unwell patient at the intensive care unit of the University of So Paulo’s Heart Institute. A bridge ventilator is being utilized to automatically trigger a bag valve mask due to a scarcity of mechanical ventilators.

The majority of COVID-19 instances are minor. To treat symptoms (fever,[162] body pains, cough), supportive therapy involves medicines such as paracetamol or NSAIDs, as well as enough oral fluid intake and relaxation. [160] [163] A balanced diet and good personal cleanliness are also encouraged. [164] Those who are unwell should remain at home, according to the CDC. [165]

 

Severe instances may need hospitalization. The glucocorticoid dexamethasone is indicated for patients with low oxygen levels because it may minimize the risk of mortality. [166] To maintain breathing, noninvasive ventilation and, eventually, admission to an intensive care unit for mechanical ventilation may be necessary. [167] To treat respiratory failure, extracorporeal membrane oxygenation (ECMO) has been employed. [168] [169]

 

Clinical studies are now underway for a number of investigational medicines.

 

[159] Others that have been deemed to be successful, such as hydroxychloroquine and lopinavir/ritonavir, as well as so-called early therapy, are not advised by US or European health officials. [159] [170] [171] In high-risk situations, two monoclonal antibody-based treatments are available for early usage. [171] The antiviral remdesivir is available with varying restrictions in the United States, Canada, Australia, and a few other countries; however, it is not recommended for use with mechanical ventilation, and the World Health Organization (WHO) discourages its use altogether due to limited evidence of its efficacy. [159]

 

Variants

 

SARS-CoV-2 Variants (Main article)

 

WHO has designated some variations as variants of concern (VoC) or variants of interest (VoI) (VoI). They both had the D614G mutation, which is more contagious: [17

 

Prognosis

 

COVID-19 has a range of severity. The illness may have a moderate course with little or no symptoms, similar to other upper respiratory infections like the common cold. Symptoms are severe enough to need hospitalization in 3–4 percent of patients (7.4% for those over 65). [177] Mild instances usually recover in two weeks, whereas severe or critical illnesses might take three to six weeks to recover from. The interval between the beginning of symptoms and death has varied from two to eight weeks in individuals who have died.

[178] The median duration between the beginning of symptoms and death was twelve days, according to the Italian IstitutoSuperiore di Sanità, with seven people being hospitalized. People admitted to an ICU, on the other hand, spent an average of 10 days in the hospital before dying. [179] On arrival to the hospital, a prolonged prothrombin time and high C-reactive protein levels are linked to a severe course of COVID-19 and a transfer to the ICU. [180] [181]

 

Strategies

 

COVID-19 Public Health Mitigation is the main article.

 

Many governments tried to restrict or halt the spread of COVID-19 by advocating, requiring, or forbidding behavioural modifications, while others largely concentrated on delivering information. The measures varied from public warnings to complete lockdowns. Containment and mitigation are two strategies for controlling an epidemic. They may be pursued in any order or at the same time. [182]

 

Delaying and decreasing the peak strain on healthcare (flattening the curve) as well as reducing total instances and health effect are among the mitigating goals.

 

[184] Furthermore, boosting healthcare capacity (raising the line) over time, such as by increasing bed count, employees, and equipment, helps to fulfill rising demand. [185]

 

Masks (like as those worn by Taiwanese President Tsai Ing-wen) are recommended by the CDC and WHO to help prevent the transmission of SARS-CoV-2.

 

Containment

 

Containment is the process of preventing an epidemic from spreading to the wider public. Individuals that are infected are isolated while they are contagious. People they’ve come into touch with are contacted and isolated for long enough to confirm they’re not sick or infectious. Rt is reduced to less than 1 after successful containment or suppression. [186]

Screening is the first step in the containment process. Screening involves looking for symptoms in order to identify sick people who may subsequently be isolated and/or treated. [187]

 

Mitigation

 

If containment fails, efforts will shift to mitigation, which involves taking steps to prevent the spread of the virus and reduce its impact on the healthcare system and society.

 

The term “flattening the epidemic curve” refers to the process of delaying and reducing the peak of an epidemic.

 

[183] This reduces the danger of overburdening health-care systems and gives researchers more time to create vaccinations and therapies. [183]

 

Interventions that aren’t pharmacological

 

Personal actions such as hand hygiene, wearing face masks, and self-quarantine; community measures aimed at reducing interpersonal contacts such as closing workplaces and schools and canceling mass gathering events; community engagement to encourage acceptance and participation in such interventions; and environmental measures such as surface cleaning are all non-pharmaceutical interventions that may help manage the outbreak.

 

[188] Many of these steps have been criticized as hygiene theater, such as scrubbing surfaces. [189]

 

Additional measures

 

Attempts have been made in several jurisdictions to take more harsh measures, such as quarantining whole communities and imposing stringent travel limits.

 

[190] The most severe restrictions have been imposed by China and Australia. The most stringent travel restrictions were imposed by New Zealand. South Korea used widespread screening and localized quarantines, as well as issuing notifications about infected people’s travels. Singapore gave financial assistance, isolated those who did not comply, and fined those who did not. Taiwan expanded face mask manufacture and penalized medical supply hoarding. [191]

 

Tracing of contacts

 

See also: COVID-19 pandemic mitigation software use and development and COVID-19 pandemic mitigation public health information technology.

 

Contact tracing is a method of trying to discover recent contacts of newly infected people in order to test them for infection.

[192] Traditionally, infectees are asked to provide a list of contacts, which are subsequently contacted by phone or in person.

 

Another method is to gather location data from mobile devices in order to identify persons who have had considerable interaction with infectees, albeit this has raised privacy issues.

 

[193] Google and Apple unveiled a privacy-preserving contact tracking endeavor on April 10, 2020. [194] [195] Palantir Technologies first supplied COVID-19 tracking services in Europe and the United States. [196]

 

Health-care services

 

Additional information: Flattening the curve, a list of nations organized by hospital beds, and COVID-19 pandemic shortages

 

In Brazil, there is a makeshift hospital for COVID-19 patients.

 

The WHO describes increasing capacity and tailoring healthcare to the requirements of COVID-19 patients as a crucial outbreak response strategy.

 

[197] The ECDC and the WHO’s European Regional Office issued guidelines for hospitals and primary healthcare services to shift resources at multiple levels, such as focusing laboratory services on COVID-19 testing, canceling elective procedures, separating and isolating COVID-19 patients, and increasing intensive care capabilities by training personnel and adding ventilators and beds. [197] [198] Telehealth has exploded as a result of the epidemic. [199]

 

Manufacturing on the fly

 

Some manufacturers have begun 3D printing nasal swabs and ventilator components due to capacity constraints in conventional supply chains.

 

[201] For example, after reverse-engineering and printing one hundred required ventilator valves overnight, an Italian startup got legal threats for suspected patent infringement.

 

[202] NASA claimed creating a ventilator in 37 days on April 23, 2020, which is now being tested. [203] [204] Individuals and groups of makers generated and shared open source ideas, as well as gadgets that were made using locally found materials, sewing, and 3D printing. Face shields, protective robes, and masks in the millions were produced. Shoe coverings, surgical caps, motorized air-purifying respirators, and hand sanitizer were among the other improvised medical equipment. Ear savers, non-invasive ventilation helmets, and ventilator splitters are examples of novel equipment. [205]

 

Immunity of the herd

 

Several specialists raised worry in July 2021 that obtaining herd immunity may not be attainable at this time since the Delta variation is transferred among persons who have received existing immunizations.

[206] The CDC released data demonstrating that persons who had been vaccinated may transmit the Delta form, something experts thought was impossible with other versions. As a result, the WHO and the CDC recommend those who have been vaccinated to continue taking precautions including social distance and wearing masks inside. [207]

 

History

 

COVID-19 pandemic timeline (main article)

 

Additional information: Pandemic prevention and forecasts, as well as preparations for the COVID-19 pandemic

 

2019 In this essay, we’ll look at the timeline for the COVID-19 pandemic in 2019.

 

Aerial image of the market, which seems to be under development.

 

After being shut down, the Huanan Seafood Wholesale Market reopened in March 2020.

 

Desc-i.svg

 

Confirmed instances per million persons are shown on an interactive timeline map.

 

(may not work on mobile devices; drag circle to adjust)

 

The epidemic was detected in Wuhan in November 2019, despite the fact that the virus’s specific origin is still unclear. Many early instances of COVID-19 were connected to visitors to Wuhan’s Huanan Seafood Wholesale Market, although it’s probable that human-to-human transmission occurred before then. [26] [27] According to a retrospective investigation, the number of COVID-19 cases in Hubei rapidly climbed beginning in December 2019, reaching 60 by December 20 and at least 266 by December 31. [208]

 

A bronchoalveolar lavage fluid (BAL) sample from an unresolved clinical case was delivered to sequencing firm Vision Medicals on December 24, 2019.

 

[209] The findings of the test were reported to the Wuhan Central Hospital and the China CDC (CCDC) on the 27th and 28th of December, indicating the presence of a new coronavirus. [209] [210] On the 26th of December, a pneumonia cluster of unknown origin was discovered and treated by Doctor Zhang Jixian at Hubei Provincial Hospital. On December 27, he notified the Wuhan Jianghan CDC. [211]

 

On December 30, 2019, a test report from business CapitalBioMedlab mailed to Wuhan Central Hospital showed an erroneous positive result for SARS, prompting Wuhan Central Hospital physicians to notify their colleagues and hospital officials. Eight of those physicians were eventually warned by the police for spreading false rumors, including Li Wenliang (who was also penalized on 3 January)[212], while another doctor, Ai Fen, was reprimanded by her supervisors. [213] The Wuhan Municipal Health Commission (WMHC) issued an alert to medical institutes that evening about “the treatment of pneumonia of unknown etiology.” [214] The following day, WMHC issued the first public disclosure of an unidentified cause pneumonia epidemic, confirming 27 cases[215][216][217]—enough to warrant an inquiry. [218]

 

The WHO office in China was notified on December 31st of instances of pneumonia with an unknown etiology in Wuhan.

 

[215] At the beginning of January 2020, an investigation was begun. [218]

 

Early occurrences, according to official Chinese sources, were largely related to the Huanan Seafood Wholesale Market, which also sold live animals.

 

[220] CCDC director George Gao said in May 2020 that animal samples gathered from the market had tested negative, suggesting that the market was not the cause of the first epidemic. [221] WHO released its assessment in March 2021, saying that transmission via an animal host was the most plausible scenario, while bats and the food supply chain were not ruled out. [2] [25]

 

2020 COVID-19 pandemic

 

COVID-19 pandemic timelines by month for 2020: January, February, March, April, May, June, July, August, September, October, November, and December

 

On March 20, 2020, Chinese physicians in Huanggang, Hubei.

 

Chinese officials reported 44 instances of “pneumonia of unknown etiology” to WHO between December 31, 2019 and January 3, 2020.

[222] The Chinese National Health Commission informed WHO on 11 January that the epidemic was linked to market exposures and that China had discovered a new strain of coronavirus, which it had isolated on 7 January. [219]

 

In the beginning, the number of cases doubled every seven and a half days.

 

[223] The virus expanded to other Chinese regions in early and mid-January, aided by the Chinese New Year migration. Wuhan operated as a significant rail junction and transportation center. [224] The virus’ genome was provided through GISAID on January 10th. [225] According to a retrospective research published in March, 6,174 persons had reported symptoms by January 20th,[226], with the possibility that more had been affected. [227] Given the virus’ “pandemic potential,” a study released on January 24 suggested human transmission, urged personal protective equipment for health professionals, and encouraged testing. [39] [228] The first published modeling research, released on January 31, predicted “independent self-sustaining epidemics in major cities throughout the world” and urged for “large-scale public health measures.” [229]

 

On the 30th of January, WHO declared the epidemic a Public Health Emergency of International Concern, citing 7,818 illnesses (PHEIC).

 

[230][231] WHO labeled it a pandemic on March 11th. [232][233]

 

Italy got its first confirmed illnesses on the 31st of January, in two Chinese visitors.

 

[234] Italy surpassed China as the nation with the most recorded fatalities on March 19. [235] The United States has surpassed China and Italy as the nation with the most confirmed illnesses by March 26. [236] According to genomic sequencing, the bulk of confirmed illnesses in New York originated from Europe rather than Asia. [237] Prior samples indicated a person infected on December 27, 2019[238][239] in France, and a person in the United States who died from the sickness on February 6, 2019. [240]

 

In the absence of artificial ventilation, a patient in Ukraine in May 2020 wears a diving mask.

 

In October, the WHO claimed that one out of every 10 people on the planet, or 780 million individuals, may have been infected, with just 35 million illnesses verified.

 

Pfizer revealed trial data for a potential vaccine on November 9th, indicating 90 percent efficacy against severe illness.

 

[242] Novavax submitted an FDA Fast Track application for its vaccine on that day. [243]

 

Public Health England said on December 14 that a variation has been detected in the UK’s southeast, mostly in Kent. Variant of Concern 202012/01 exhibited alterations to the spike protein that might make it more infectious. A total of 1,108 illnesses has been confirmed as of December 13th. [244]

 

2021 COVID-19 pandemic

 

COVID-19 pandemic timelines in 2021, organized by month: January, February, March, April, May, June, July, August, September, October, November, and December

 

VOC-202012/01, a form of SARS-CoV-2 initially detected in the United Kingdom, was discovered in 33 nations on January 2nd.

 

The P.1 variety was originally discovered in Japanese travelers returning from Brazil on January 6th.

 

A WHO-led team of scientists arrived in China on 14 January to investigate the virus’s origins and track out intermediate hosts between the initial reservoir and humans.

In a clinical experiment in South Africa on January 29, it was shown that the Novavax vaccine was only 49% effective against the 501.V2 strain.

 

[249] In a clinical experiment in Brazil, the China COVID-19 vaccine CoronaVac was shown to be 50.4 percent effective. [250]

 

Due to blood clotting issues, notably cerebral venous sinus thrombosis, various nations discontinued using the Oxford-AstraZeneca COVID-19 vaccination on March 12th (CVST).

 

[251] The WHO and the European Medicines Agency found no relation to thrombus on March 20, prompting some nations to restart vaccination. [252]

 

India was the first place where the Delta variety was discovered. The variety was initially discovered in the UK in mid-April, and two months later it had spread to a third wave, causing the authorities to postpone the planned reopening from lockdown in June. [253]

The Covid 19 Pandemic- 2

Variants

 

The Covid 19 Pandemic- 2 – Viruses are continually changing due to mutations, and these changes may occasionally lead to a new viral strain. Some varieties arrive and then go, while others stick around. There will continue to be new versions. In the United States and across the world, the CDC and other public health agencies keep track of all forms of the COVID-19 virus.

The Delta variant of the virus that causes COVID-19 produces more illnesses and spreads more quickly than the initial SARS-CoV-2 strain. COVID-19 vaccines are still the most effective approach to lower your risk of serious disease, hospitalization, and death.

 

Facts to know about variants

 

The virus is predicted to evolve into new strains. The best method to delay the formation of new variations is to take actions to minimize the transmission of illness, including acquiring a COVID-19 vaccination.

 

COVID 19 Pandemic vaccinations lower your chances of being sick, being hospitalized, and dying.

 

Adults aged 18 and over should have a COVID-19 booster shot. Teenagers 16–17 years old who had Pfizer-BioNTech COVID-19 vaccinations may obtain a booster dose if they are at least 6 months post-immunization with Pfizer-BioNTech.

 

Variant Types

 

Scientists keep track of all variants, but some are classified as being watched, of interest, of worry, or of significant relevance. COVID-19 instances may increase if certain variations spread more readily and faster than others. A rise in the number of cases will place a greater demand on healthcare resources, resulting in more hospitalizations and perhaps more fatalities.

These categories are based on how quickly a variation spreads, how severe its symptoms are, how well it responds to therapies, and how effectively immunizations protect against it.

 

Variants of Concern

 

1. 1.1.529, Omicron

South Africa was the first place to be discovered.

Spread: Other varieties, particularly Delta, may spread more readily.

The current severity of disease and mortality linked with this variation is unknown due to the minimal number of instances.

Vaccine: While outbreaks among fully vaccinated persons are to be anticipated, vaccinations are beneficial in reducing serious disease, hospitalization, and death. According to preliminary findings, those who have been completely vaccinated and get the Omicron form may transfer the virus to others. All vaccinations that have been approved or recommended by the FDA are predicted to protect against serious disease, hospitalization, and death. The recent appearance of the Omicron variety stresses the significance of immunization and boosters even more.

 

Therapies: Some monoclonal antibody treatments for Omicron infection may not be as successful.

 

The Delta – B.1.617.2. variant was first discovered in India

 

Spread: This variety spreads more readily than others.

 

Severe disease and death: This variety has the potential to be more severe than the others.

 

Vaccine: While outbreaks among fully vaccinated persons are to be anticipated, vaccinations are beneficial in reducing serious disease, hospitalization, and death. According to preliminary findings, those who have been completely vaccinated and get the Delta form may transfer the virus to others. All vaccinations that have been approved by the FDA or that have been authorized by the FDA are effective in preventing serious disease, hospitalization, and death.

 

Therapies: FDA-approved monoclonal antibody treatments are effective against almost all variants now circulating in the United States.

 

Deaths

 

COVID 19 Pandemic was responsible for around 5.29 million fatalities as of 11 December 2021. People who died after testing positive for COVID-19 are referred to as official COVID-19 fatalities. People who die without undergoing a test may be missed by such tallies. Deaths of persons with underlying illnesses, on the other hand, may result in an overcount. Excess mortality is seen in several nations when figures for all-cause fatalities are compared to multi-year averages. Deaths as a result of healthcare capacity and priority limits are among them.

On January 9, 2020, Wuhan recorded the first verified fatality. The first fatality outside of China happened on February 1, 2020, in the Philippines, while the first death outside of Asia occurred on February 6, 2020, in the United States.

 

The duration between the beginning of symptoms and mortality is generally between 6 and 41days, with the average being about 14. The elderly (65 years and older) and those with underlying illnesses are the people who are most at risk from COVID-19. Obesity, diabetic problems, mental disorders, and the overall number of ailments are the most significant risk factors for serious illness.

 

Long Covid Part – 1

The Covid 19 Pandemic- 1 – The COVID-19 pandemic, also known as the coronavirus pandemic, is a worldwide coronavirus disease. The 2019 (COVID-19) pandemic caused by the coronavirus 2 that causes severe acute respiratory syndrome (SARS-CoV-2). The new virus was initially discovered in December 2019 in the Chinese city of Wuhan; a lockdown in Wuhan and other towns in Hubei’s surrounding region failed to control the spread.

On January 30, 2020, the World Health Organization (WHO) declared a Public Health Emergency of International Concern, and on March 11, 2020, a pandemic. The Alpha, Beta, Gamma, Delta, and Omicron forms of the virus are among the first to appear. More than 269 million illnesses and 5.29 million fatalities have been confirmed as of December 11, 2021, making it the worst pandemic in history.

The symptoms of COVID-19 may vary from non-existent to life-threatening. Patients who are older or have specific underlying medical issues are more prone to have severe sickness. COVID-19 is an airborne virus that is disseminated by minute particles contaminating the air. Infection is more likely to spread among individuals who are close together, although it may also spread across greater distances, especially indoors in poorly ventilated places. Transmission may also happen via contaminated surfaces or fluids;however this is unusual. Infected people may be infectious for up to 20 days and transmit the virus even if they don’t show any symptoms.

 

Vaccines Have Been Licensed For Use in Several Nations.

Vaccination efforts for the general public started in December 2020. Social distance, wearing face masks in public, ventilation/air-filtering, covering one’s mouth while sneezing or coughing, hand washing, sanitizing surfaces, and quarantining people who have been exposed or are symptomatic are all advised preventative measures. Treatments are aimed at alleviating symptoms, however antiviral medicines are being developed. Travel restrictions, lockdowns, company closures, workplace hazard precautions, testing processes, and tracking infected contacts are all examples of government involvement.

Panic purchasing, supply chain disruptions, and food shortages all contributed to widespread supply shortages. As a consequence of the near-global lockdowns, pollution emissions dropped to levels never seen before. Many educational institutions and public locations were closed in part or whole, and many activities were canceled or rescheduled. Political tensions grew as misinformation spread via social media and the mainstream media. The epidemic has brought up concerns of racial and regional discrimination, health fairness, and finding a balance between public health and individual rights.

 

Etymology

There are various names for the pandemic. Despite the presence of previous human coronaviruses that have produced epidemics and outbreaks, it is often referred to as “the coronavirus pandemic”

The virus and illness were dubbed “coronavirus,” “Wuhan coronavirus,” “the coronavirus epidemic,” and “Wuhan coronavirus outbreak”, with the sickness dubbed “Wuhan pneumonia” during the first outbreak in Wuhan.

The World Health Organization recommended that it be called 2019-nCoVand 2019-nCoV acute respiratory diseaseas interim names for the virus and disease in January 2020, in accordance with 2015 guidance and international guidelines against using geographical locations (e.g. Wuhan, China), animal species, or groups of people in disease and virus names, in part to avoid social stigma.

On February 11, 2020, the WHO announced the official designations COVID-19 pandemic and SARS-CoV-2. Co is for corona, VI for virus, D for disease, and 19 for the day the epidemic was initially discovered, according to Tedros Adhanom (31 December 2019). In public communications, the WHO also refers to “the COVID-19 virus” and “the virus that causes COVID-19.”

Virus variants are also referred to by a variety of names. Initially, they were given names based on the locations where the variations were discovered (e.g. Delta variant was known as the Indian variant). The variant’s PANGO lineage was represented in a more systematic naming method (e.g., Omicron’s lineage is B.1.1.529). The WHO implemented a policy of utilizing Greek letters for variations of concern and variants of interest by the end of May 2021.

 

Background

 

The first reported epidemic began in November 2019 in Wuhan, Hubei, China, despite the fact that the virus’s specific origin is still unclear. Many early cases of COVID-19 have been connected to visitors to Wuhan’s Huanan Seafood Wholesale Market. However, human-to-human transmission may have been occurring prior to this. SARS-CoV-2 is a recently found virus with strong ties to bat coronaviruses, pangolin coronaviruses, and SARS-CoV.

The virus is most likely zoonotic, meaning it came from bats or a closely related species, according to the scientific consensus.

Regardless, the topic has sparked a lot of debate. The origins debate exacerbated global tensions, particularly between the US and China.

On December 1st, 2019, the first known infected individual became unwell. That individual had no apparent ties to the subsequent wet market cluster. On the other hand, an earlier instance on November 17th may have happened. The market was connected to two-thirds of the first case cluster. The index case was most likely infected between mid-October and mid-November 2019, according to a molecular clock study.

The number of persons who have been tested for COVID-19 and whose results have been verified positive according to official procedures is referred to as the official case count.

Early on, several nations had formal regulations prohibiting the testing of people who only showed minor symptoms. According to an examination of the epidemic up to the 23rd of January, 86 percent of COVID-19 infections had gone undetected, and these infections were the cause of 79 percent of recorded cases. According to many additional studies, the overall number of infections is much higher than the number of cases recorded.

On April 9, 2020, early findings revealed that 15% of a population sample in Gangelt, Germany, tested positive for antibodies. Gangelt is at the heart of a large infection cluster.

Positive COVID-19 antibody tests were identified in pregnant women in New York City and blood donors in the Netherlands, indicating that there were more infections than reported. Seroprevalence estimations are cautious since some studies demonstrate that people with mild symptoms don’t have detectable antibodies.

In early 2020, an examination of cases by age among China revealed that instances in people under the age of 20 accounted for a small percentage of all cases. It was unclear if this was due to the fact that young individuals were less likely to be infected or to exhibit symptoms and be tested, or both. Children and adults were equally likely to be infected, according to a retrospective cohort research in China.

The basic reproduction number (R0) for COVID-19 was first estimated to be between 1.4 and 2.5 in January, however a further investigation suggested it may be about 5.7. (with a 95 percent confidence interval of 3.8 to 8.9). R0 is not to be confused with the effective reproduction number (often referred to as R), which takes into consideration mitigation measures and herd immunity and might vary between populations/circumstances.

Pradeep Chopra, MD

The Long Covid Treatment Center

102 Smithfield ave.

Pawtucket, RI 02860

Email; [email protected]