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Biology Covid-19 human body

Omicron XE variant symptoms, severity, treatment. cases so far

Mumbai is the first city to report a case of omicron XE variant, In the U.K., the XE variant was discovered and is a mutation of B.1 and B.2 strains of Omicron. The WHO is currently tracking the XE mutation as part of the Omicron variant. Micron symptoms can include fever, sore throat, scratchy throat, cough and cold, skin irritation and discoloration, gastrointestinal distress, and a dry cough.

Omicron XE Variant

It was detected in the United Kingdom in January 2022 that the new variant XE of COVID-19 was identified. The WHO considers it ten times more contagious than the BA.2 variant. India’s COVID-19 XE variant has recently been updated

Once again, there has been an increase in the Coronavirus outbreak. There has been a fourth wave of Coronavirus in Asia and Europe during the past few weeks. There has been a sudden increase in new cases suspected to be caused by the corona subvariant omicron BA.2. Researchers have found a new corona XE variant in this hour of crisis.

Omicron XE Variant Symptoms

According to the organization, it is difficult to say whether it is fatal given the current situation, but knowing the signs and symptoms will help one avoid contracting the infection. Here are some symptoms of this new variant of the Coronavirus.

This variant is currently being studied. It is common for such a condition to cause early symptoms like fever, sore throat, cough, mucus and cold, and stomach problems. Additionally, the new variant can be even more dangerous for those already ill.

Since it is a mutation of the original Omicron, the vaccine may affect the new variant. The omicron effect in India was different from that in the second wave because of the large number of vaccinations during the third wave.

Omicron XE Variant Severity

Doctor Allison Arwady, Commissioner of Chicago’s Department of Public Health, said Tuesday that omicron “is likely to spread rapidly” and even more rapidly than the delta variant responsible for most of the latest outbreaks in the U.S.

It’s probably three times as contagious as the delta variant. Director Rochelle Walensky said Omicron has a two-day doubling time shorter than delta, indicating higher transmissibility. According to a study released Tuesday, the variant of the virus that is causing a surge in infections in South Africa is better at evading vaccines and causing less severe illness.

However, the data also shows that although the number of cases is increasing, hospitalizations are not rising as fast, which leads scientists to believe that the risk of hospitalization due to the virus is lower than that related to delta or earlier variants. A study adjusted for vaccination status found that admitted adults diagnosed with COVID-19 were 29% fewer than those diagnosed with the wave in mid-2020.

Omicron XE Variant Cases so Far

It is not the vaccine but reaching those at risk that has been the challenge.

Upon being asked if an Omicron vaccine was required, Mahamud said it was too early to tell but stated that a global approach should be taken and that manufacturers should not have the sole decision-making authority.

If you go ahead with Omicron, then a new antigen may emerge that is more immunoevasive or transmissible,” he said. A WHO technical group had recently met to discuss vaccine composition.

In his view, the most effective way to reduce the impact of this variant would be for the WHO to have 70% of each country’s population vaccinated by July, rather than offering third and fourth doses in some nations.

As the number of cases due to Omicron has risen, some countries, including the United States, have shortened quarantine periods for healthy people and allowed them to return to work or school earlier.

According to Mahamud, leaders should decide how strong the local epidemic is. Countries with high numbers of cases may need to omit isolation periods to maintain essential services.

Some places have shut mainly it out, so maintaining the entire 14-day quarantine period might be the best option. You should invest heavily in keeping your numbers very low if your numbers are tiny.

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Biology Covid-19 human body

Post covid-19 syndrome

Long Covid-19
• Fever (83-99%)
• Cough (59-82%)
• Fatigue (44-70%)
• Anorexia (20-84%)
• SOB (31-40%)
• Myalgia (11-35%)
• Others: anosmia, loss of taste, GI, headache
Who gets Long Covid-19?
• Factors that appear to be associated with a greater risk of suffering from
“Long COVID-19” appear to be:
• Increasing age
• Excess weight/ obesity
• DM-2 ,COPD,CKD
• Patients on immunosuppression medication ,organ transplant recipients
• Multiple symptoms at presentation
Fever
• May be treated symptomatically with Paracetamol or non-steroidal antiinflammatory drugs.
• Monitoring functional status in post-acute coivd-19 patients is not yet an
exact science.
Chest Pain
Chest pain is common in post-acute covid-19 syndrome approximate
incidence 12 to 44 %. The clinical priority is to separate musculoskeletal
and other non-specific chest pain from serious cardiovascular conditions.
Cardiopulmonary complications include myocarditis, pericarditis, myocardial
infarction, dysrhythmias, and pulmonary embolus; they may present
several weeks after acute covid-19. They are commoner in patients with
pre-existing cardiovascular disease
Cough
• chronic cough as one that persists beyond eight weeks. Up to that time,
and unless there are signs of super-infection or other complications such
as painful pleural inflammation, cough seems to be best managed with
simple breathing control exercises and medication where indicated.
Thromboembolism
• Covid-19 is an inflammatory and hypercoagulable state, with an increased
risk of thromboembolic events.
• Many hospitalized patients receive prophylactic anticoagulation.
thromboprophylaxis.
• If the patient has been diagnosed with a thrombotic episode,
anticoagulation and further investigation and monitoring should follow
standard guidelines.
Neurological Sequelae
• Ischemic stroke, seizures, encephalitis, and cranial neuropathies have
been described after covid-19, but these all seem to be rare.
• A patient suspected of these serious complications should be referred to a
higher centre.
• Common non-specific neurological symptoms, which seem to co-occur
with fatigue and breathlessness, include headaches, dizziness, and
cognitive blunting (“brain fog”).
Breathlessness
• A degree of breathlessness is common after acute covid-19. Severe
breathlessness, which is rare in patients who were not Hospitalised,may
require urgent referral. Breathlessness tends to improve with breathing
exercises .
• Pulse Oximeters may be extremely useful for assessing and monitoring
respiratory symptoms after covid-19.
• An exertional desaturation test should be performed as part of baseline
assessment for patients whose resting pulse oximeter reading is 96% or
above but whose symptoms suggest exertional desaturation (such as lightheadedness or severe breathlessness on exercise).
• Typically, oxygen saturation (pulse oxymeter) would be a daily reading
taken on a clean, warm finger without nail polish, after resting for 20
minutes; the device should be left to stabilize and the highest reading
obtained should be recorded.
Fatigue
• The profound and prolonged nature of fatigue in some post-acute covid-19patients shares features with chronic fatigue syndrome described after otherserious infections including SARS, MERS, and community acquired pneumonia.
• We found no published research evidence on the efficacy of eitherpharmacological or non-pharmacological interventions on fatigue after covid-19.
• Patient resources on fatigue management and guidance for clinicians on returnto exercise and graded return to performance for athletes in covid-19 arecurrently all based on indirect evidence.
Fatigue Management
which may include:
• Energy management – 3 P’s: plan, priorities and pace,
• Anxiety- Re-assure normal for fatigue after viral infection
• Routine Gentle activity within self assessed limitation Physical activity
advice
• Rest and Sleep
• Hydration and nutrition
• Pain

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Covid-19 human body

Antibody From Recovered COVID-19 Patients Found To Substantially Reduce Severity of Disease

Study found that an antibody, P36-5D2, demonstrated a substantial decrease in infectious virus load in the lungs and brain, and reduced lung disease in laboratory models.

In a study jointly conducted by the Bio-Safety Level 3 (BSL-3) Core Facility at the NUS Yong Loo Lin School of Medicine (NUS Medicine) and Beijing Tsinghua University, an antibody was found to be capable of neutralizing major SARS-CoV-2 variants of concern.

As SARS-CoV-2 variants continue to emerge and spread around the world, antibodies and vaccines to confer broad and potent neutralizing activity are urgently needed. The paper titled “A Potent and Protective Human Neutralizing Antibody Against SARS-CoV-2 Variants,” which was first published in Frontiers in Immunology December 2021, explained how the team isolated and characterized monoclonal antibodies from individuals infected with SARS-CoV-2.

In the study, crystal and electron cryo-microscopy structure analyses revealed that P36-5D2, when targeted to a conserved epitope on the receptor-binding domain of the spike protein, withstood three key mutations. These mutations, namely K417N, E484K, and N501Y, are found in variants that escape from many potent neutralizing monoclonal antibodies. A single intraperitoneal injection of P36-5D2 as a prophylactic treatment demonstrated protection of the in vivo models from severe disease in the course of an infection with SARS-CoV-2 Alpha and Beta variants. These models had normal activities and body weight and were devoid of infection-associated death for up to 14 days, and demonstrated a substantial decrease of the infectious virus in the lungs and brain, as well as reduced lung disease.

The effects of P36-5D2 serve as an important reference for the development of antibody therapies against SARS-CoV-2 and its current and emerging variants. The team is conducting further research to study its effects of protection against the infection of the Delta and Omicron variants.

“The discovery of this antibody means we can be more confident in our fight against COVID-19 and its variants. With a strong and established collaboration within NUS Medicine and Beijing Tsinghua University, our scientists would be able to improve our technology to identify antibodies that can potentially treat more unknown variants that may come up in the future,” said Dr. Mok Chee Keng, Head, Science and Service Support Team, BSL-3 Core Facility at NUS Medicine.

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Biology Covid-19 human body

Omicron Not “Same Disease We Were Seeing A Year Ago”: Oxford Scientist

The strain first discovered at the end of November appears to be less severe and even patients who do end up in the hospital spend less time there, John Bell, regius professor of medicine at Oxford, said on BBC Radio 4’s Today program.

The omicron variant that’s taking the world by storm is not “the same disease we were seeing a year ago,” a University of Oxford immunologist said, reinforcing reports about the strain’s milder nature.

The strain first discovered at the end of November appears to be less severe and even patients who do end up in the hospital spend less time there, John Bell, regius professor of medicine at Oxford, said on BBC Radio 4’s Today program. 

“The horrific scenes that we saw a year ago — intensive care units being full, lots of people dying prematurely — that is now history in my view, and I think we should be reassured that that’s likely to continue,” Bell said. 

Bell’s comments came after the U.K. government said it wouldn’t introduce stricter Covid-19 restrictions in England before the end of the year. 

Infections have jumped by more than a quarter of a million in the past week, heaping pressure on Prime Minister Boris Johnson to respond. Health Secretary Sajid Javid late Monday said he’s monitoring the latest data and urged people to be careful, particularly at New Year celebrations. 

Stay Home Stay Safe!!

virus surge
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Biology Covid-19 human body

m-RNA treatment for flu and Covid-19 viruses

With a relatively minor genetic change, a new treatment developed by researchers at the Georgia Institute of Technology and Emory University appears to stop replication of both flu viruses and the virus that causes COVID-19. Best of all, the treatment could be delivered to the lungs via a nebulizer, making it easy for patients to administer themselves at home.

The therapy is based on a type of CRISPR, which normally allows researchers to target and edit specific portions of the genetic code, to target RNA molecules. In this case, the team used mRNA technology to code for a protein called Cas13a that destroys parts of the RNA genetic code that viruses use to replicate in cells in the lungs. It was developed by researchers in Philip Santangelo’s lab in the Wallace H. Coulter Department of Biomedical Engineering.

“In our drug, the only thing you have to change to go from one virus to another is the guide strand—we only have to change one sequence of RNA. That’s it,” Santangelo said. “We went from flu to SARS-CoV-2, the virus that causes COVID-19. They’re incredibly different viruses. And we were able to do that very, very rapidly by just changing a guide.”

The guide strand is a map that basically tells the Cas13a protein where to attach to the viruses’ RNA and begin to destroy it. Working with collaborators at the University of Georgia, Georgia State University, and Kennesaw State University, Santangelo’s team tested its approach against flu in mice and SARS-CoV-2 in hamsters. In both cases, the sick animals recovered.

Their results are reported Feb. 3 in the journal Nature Biotechnology. It’s the first study to show mRNA can be used to express the Cas13a protein and get it to work directly in lung tissue rather than in cells in a dish. It’s also the first to demonstrate the Cas13a protein is effective at stopping replication of SARS-CoV-2.

What’s more, the team’s approach has the potential to work against 99% of flu strains that have circulated over the last century. It also appears it would be effective against the new highly contagious variants of the coronavirus that have begun to circulate.

The key to that broad effectiveness is the sequence of genes the researchers target.

“In flu, we’re attacking the polymerase genes. Those are the enzymes that allow the virus to make more RNA and to replicate,” said Santangelo, the study’s corresponding author.

With help from a collaborator at the Centers for Disease Control and Prevention, they looked at the genetic sequences of prevalent flu strains over the last 100 years and found regions of RNA that are unchanged across nearly all of them.

“We went after those, because they’re far better conserved,” Santangelo said. “We let the biology dictate what our targets would be.”

Likewise, in SARS-CoV-2, the sequences the researchers targeted so far remain unchanged in the new variants.

The approach means the treatment is flexible and adaptable as new viruses emerge, said Daryll Vanover, a research scientist in Santangelo’s lab and the paper’s second author.

“One of the first things that society and the CDC is going to get when a pandemic emerges is the genetic sequence. It’s one of the first tools that the CDC and the surveillance teams are going to use to identify what kind of virus this is and to begin tracking it,” Vanover said. “Once the CDC publishes those sequences—that’s all we need. We can immediately screen across the regions that we’re interested in to target it and knock down the virus.”

Vanover said that can result in lead candidates for clinical trials in a matter of weeks—which is about how long it took them to scan the sequences, design their guide strands, and be ready for testing in this study.

“It’s really quite plug-and-play,” Santangelo said. “If you’re talking about small tweaks versus large tweaks, it’s a big bonus in terms of time. And in pandemics—if we had had a vaccine in a month or two after the pandemic hit, think about what things would look like now. If we had a therapy a month after it hit, what would things look like now? It could make a huge difference, the impact on the economy, the impact on people.”

The project was funded by the Defense Advanced Research Projects Agency’s (DARPA) PReemptive Expression of Protective Alleles and Response Elements (PREPARE) program, with the goal of creating safe, effective, transient, and reversible gene modulators as medical countermeasures that could be adapted and delivered rapidly. That’s why the team decided to try a nebulizer for delivering the treatment, Santangelo said.

“If you’re really trying to think of something that’s going to be a treatment that someone can actually give themselves in their own house, the nebulizer we used is not terribly different from one that you can go buy at a pharmacy,” he said.

The team’s approach also was sped along by their previous work on delivering mRNA to mucosal surfaces like those in the lungs. They knew there was a good chance they could tackle respiratory infections with that approach. They decided to use mRNA to code for the Cas13a protein because it’s an inherently safe technique.

“The mRNA is transient. It doesn’t get into the nucleus, doesn’t affect your DNA,” Santangelo said, “and for these CRISPR proteins, you really don’t want them expressed for long periods of time.”

He and Vanover said additional work remains—especially understanding more about the specific mechanisms that make the treatment effective. It has produced no side effects in the animal models, but they want to take a deeper look at safety as they consider moving closer to a therapy for human patients.

“This project really gave us the opportunity to push our limits in the lab in terms of techniques, in terms of new strategy,” said Chiara Zurla, the team’s project manager and a co-author on the paper. “Especially with the pandemic, we feel an obligation to do as much as we can as well as we can. This first paper is a great example, but many will follow; we’ve done a lot of work, and we have a lot of promising results.”