COVID related information

I personally think it's related to a novel lineage that has hit Mumbai. This condition has been associated with Covid in the past. Important for them to identify the cause.

New XBB.1.16 lineage proposed in MH, India carrying a unique S:E554K and S:V551I combo. Huge changes in SD1 are alarming because they can enhance fusion capabilities found in the S2 domain. github.com/cov-lineages/p…

Thanks to @siamosolocani for spotting this one.

COVID reinfection

covid immunity

FYI about the neurological effects of COVID-19,

"The CNS(central nervous system)-related manifestations [caused by SARS-CoV-2 infection] include headache and dizziness, meningitis and encephalitis, encephalopathy, acute cerebrovascular disease and ischemic stroke, ADEM (acute disseminated encephalomyelitis), ANE (acute necrotizing encephalopathy), seizure and myelitis.

Headache and dizziness are the most observable minor signs shown by 40% of the COVID- 19 patients.. It is due to the decrease function of ACE2 and increased blood pressure in COVID-19 patients. Other reasons are hypoxia and cytokine storm which is developed by increase in the level of cytokines and chemokines, mainly IL-6 and TNF-alpha..

the presence of SARS-CoV-2 [was observed] in the CSF (cerebrospinal fluid) of COVID-19 patients confirmed with the viral encephalitis.. the patient who have meningitis or encephalitis are tested COVID-19 positive because SARS-CoV-2 RNA and proteins are found in their brain tissue and CSF.. these complications are caused by the virus itself by infecting and damaging the brain directly.

Severe COVID-19 patients develop encephalopathy over hours to days with some common symptoms like systemic inflammation, sepsis, hypoxia, cytokine storm and renal failure which is diagnosed by increase in the level of IL-2, IL-7, GCSF, IL-6, and TNF-alpha1.. many patients who died of COVID-19 show hypoxic encephalopathy.. The risk of encephalopathy is soaring in case of COVID-19."

Is your brain fine?

journals.lww.com/md-journal/ful…

From a meta analysis on the reactivation of herpesviruses,

"Evidence from observational studies showed the possible relation between COVID-19 (mostly mRNA based) vaccine administration and VZV (varicella-zoster virus) & HSV (herpes simplex virus) reactivation.. 

the rate of VZV reactivation among those who received the COVID-19 vaccine was 14 persons per 1000 vaccinations.. HSV reactivation showed the rate of 16 persons per 1000 vaccinations.. Most cases reported their disease after the first dose of the vaccine.. Many patients reported having comorbidities, of which hypertension, diabetes mellitus, dyslipidemia, chicken pox, and atrial fibrillation were common.

link.springer.com/article/10.118…

"Pyroptotic immune cell-secreted pro-inflammatory cytokines might worse lymphopenia via the direct killing of lymphocytes, contributing to the dysfunction of adaptive immunity in COVID-19, and it is very well correlated with COVID-19 immunopathogenesis..

Even when SARS-CoVs can hardly replicate in lymphocytes due to rapid apoptosis or pyroptosis, and even when only a few times pyroptosis happens, virions from inside the lymphocyte can release intact outside, ready to infect another T-cells.

This casuistic is a very clear picture of the strategy for viral persistence. The natural evolution of SARS-CoVs, in addition to spread-out more effectively by air, is to reduce the response capacity of the immune system to persist longer in the host, causing Acquired Immune Deficiency Syndrome."

SARS-CoVs cause AIDS..

sciencedirect.com/science/articl…

"..the incidence of herpes zoster continues to rise, potentially leading to devastating consequences when ocular complications occur..

There are case reports of retinal disease because of varicella reactivation after SARS-CoV-2 vaccination, ischemic optic neuropathy occurring during herpes zoster ophthalmicus, VZV(varicella-zoster virus)-induced orbital apex syndrome, and immune-mediated ocular complications in patients with prior neuro-ophthalmic manifestations of VZV.

Early diagnosis and treatment are important for better visual outcomes."

journals.lww.com/co-ophthalmolo…

"Direct effects of a COVID-19 infection, such as acute respiratory distress syndrome, can result in cardiac arrest if not rapidly treated. Cardiac arrest might also occur due to thromboembolism, direct cardiac injury, myocarditis, vascular inflammation, and arrhythmias. COVID-19 is prothrombotic and patients are at higher risk of myocardial infarction, stroke and pulmonary embolism, and acute heart failure than uninfected people, all of which can lead to SCA (sudden cardiac arrest).. [In addtion] indirect effects of the pandemic might have had a considerable contribution to the increase in out-of-hospital cardiac arrest incidence.."

Note that your heart can be suddenly arrested even if you did nothing wrong.

sciencedirect.com/science/articl…

As to 39 COVID-19 patients hospitalized with elevated muscle enzymes in Italy,

"15 patients presented also rhabdomyolysis. The most common symptoms were: asthenia, fever, arthomyalgia, lipothymia and syncope.. All patients were affected by omicron SARS-CoV-2 variants. 4 patients died (2 due to rhabdomyolysis and 2 due to sepsis).."

I'm afraid that those who survived rhabdomyolysis would present muscular dystrophy.

preprints.org/manuscript/202…

"Up to one-third of individuals who survive acute COVID-19 infection will develop symptoms persisting longer than 6 weeks, known as long COVID-19 or PASC. Many individuals with PASC experience neurologic symptoms including cognitive impairment, fatigue, autonomic disturbances, myalgia, headache, & other pain syndromes, termed Neuro-PASC (NP).

Most patients with NP experience mild and transient respiratory symptoms of COVID-19 and do not require hospitalization during the acute infection.. databases of confirmed infections underestimate the total number of COVID-19 cases due to the limited access to testing.. 

This suggests that millions of Americans are experiencing the long-term consequences of COVID-19 without having an official diagnosis of acute disease."

I'm afraid that such patients with mysterious neurologic symptoms would significantly increase from now on, owing to the spread of EG.5 (Eris).

nn.neurology.org/content/10/6/e…

"Of the ten metals and metalloids of interest.., elevated serum Zn and Se were associated with reduced COVID-19 severity and mortality.. higher levels of serum Fe were associated with lower levels of cellular damage and symptoms of SARS-CoV-2 infection and with faster recovery from COVID-19. On the other hand, higher serum and urinary Cu and serum Mg levels were associated with higher COVID-19 severity and mortality.."

Some supplement may be effective against COVID-19.

link.springer.com/article/10.100…

"We discovered that SARS-CoV-2 infection leads to a prolonged alteration of the gene expression profile of circulating T, B and NK cells and monocytes. Some of the genes affected were..implying a pro-inflammatory status. The altered transcriptional profile was detected in COVID-19 patients for at least 2 months after the onset of the disease symptoms..

SARS-CoV-2 infection causes a prolonged increase in the pro-inflammatory transcriptional status that could predispose post-acute patients to the development of long-term health consequences, including autoimmune disease, reactivation of other viruses and disruption of the host immune system-microbiome ecosystem."

SARS-CoV-2 can distrupt the microbiome ecosystem, like humans can disrupt the global ecosystem.

genomemedicine.biomedcentral.com/articles/10.11…

"Even though Omicron caused less severe disease than Delta, the incidence of neurological manifestations is similar. More than 30% of patients experienced 'brain fog', delirium, stroke, and cognitive impairment, and over half of these patients presented abnormal neuroimaging outcomes.. 

The most frequent imaging features (affecting >60% of patients) include ischemic infarcts, intracerebral hemorrhages, perfusion abnormalities, and leptomeningeal enhancement. Hypometabolism in the pons, cerebellum, bilateral insula, bilateral medial lobes, and prefrontal cortex indicates brain function dysregulation in COVID patients. The high incidence of cerebrovascular events such as ischemic stroke and intracerebral hemorrhage, indicates potential endothelial injury and coagulation dysfunction. Other investigations have also reported hypoxic alterations in the cerebellum and cerebrum, metabolic alterations of astrocytes, microglial activation, neuro-axonal damage, and neuronal loss.."

Memorizing all these symptoms would be difficult for a damaged brain.

link.springer.com/article/10.100…