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One thing we know for sure about SARS-CoV-2, the virus that causes COVID-19, is that it keeps changing. Since the start of the pandemic, we have seen several notable variants, including Alpha, Beta, Delta, and Omicron. New variants are a normal part of how viruses evolve, but keeping an eye on each emerging one is crucial to make sure people, both in the U.S. and around the world are prepared.
This is particularly important if a variant spreads faster, causes more severe illness, resists vaccines, or combines all these factors compared with the original virus.
The World Health Organization (WHO) uses letters from the Greek alphabet to name new coronavirus variants, beginning with Alpha, which first appeared in 2020. While COVID no longer sparks the same widespread fear, the virus continues to evolve.
Since 2020, countless variants have appeared, each carrying different levels of risk in different countries. Below, we take a chronological look at these variants, how dangerous they have been, and how they have been mutating across regions.
Variants and strains are not the same. A variant occurs when the virus changes slightly (mutates) from the original version, often due to an error in its genetic code during replication. A variant is like a new version of the virus. A strain, however, is when the virus accumulates enough variants that it behaves differently, for example, becoming far more transmissible than the original. All strains are variants, but not every variant counts as a strain, as noted by NHS.
By the end of 2020, the original L strain of COVID had undergone several mutations, including the S, V, and G strains. The first widely reported variant, B.1.1.7, known as Alpha, appeared in the U.K. in September 2020. Alpha triggered a global surge of infections before vaccines were available and was deadlier than the original virus. Common symptoms included loss of taste or smell, fever, dry cough, shortness of breath, headache, sore throat, congestion, nausea, vomiting, and diarrhea. Pfizer, Moderna, and Johnson & Johnson vaccines remained effective against Alpha.
Soon after Alpha, the Beta variant (B.1.351) emerged in South Africa and spread to other countries. According to CDC estimates, Beta was roughly 50% more transmissible than the original virus, though it only accounted for a small share of U.S. cases. Pfizer, Moderna, and J&J vaccines were still effective against Beta.
The Gamma variant, P.1, appeared in Brazil in November 2020. It caused relatively few cases in the U.S., though CDC data in fall 2021 suggested it could sometimes cause breakthrough infections among fully vaccinated people. Gamma did not seem as contagious as Alpha or Delta.
Delta (B.1.617.2) surged in spring 2021, first dominating in India and spreading to over 130 countries, resulting in severe waves worldwide. It caused more serious illness and hospitalizations among the unvaccinated than previous variants.
Even as U.S. vaccination efforts were underway, Delta could evade some vaccine-induced immunity, leading to breakthrough infections, as per CDC. More than 70% of cases were reported in fully vaccinated individuals, prompting booster campaigns. Headache, sore throat, runny nose, and fever were the most common symptoms.
Delta AY.4.2, known as Delta Plus, was an offshoot of Delta rather than a standalone variant. It had two spike protein mutations that helped it infect cells more efficiently, making it about 10–20% more transmissible. Delta Plus caused a surge in the U.K. but did not take hold in the U.S.
Omicron And Its Subvariants
Omicron and its subvariants have been the dominant strains in the U.S. for nearly two years. The original Omicron (BA.1) no longer circulates widely, but its subvariants now drive most infections. Omicron was first detected in Botswana and South Africa in November 2021 and quickly spread globally. By December, it caused U.S. daily cases to exceed a million.
In 2022, several subvariants emerged, and in 2023, EG.5 (nicknamed “Eris”) became dominant, with BA.2.86 (“Pirola”) also under observation. Omicron subvariants spread very efficiently, partly due to over 30 mutations on the spike protein that increase their ability to infect human cells. Early data suggested the original Omicron caused less severe illness than earlier variants, but high case numbers could still strain hospitals.
Vaccines remain protective against severe disease, though breakthrough infections can occur. The CDC recommends staying up to date with boosters, including the updated 2023 fall shot designed to target EG.5 and BA.2.86.
Nimbus and Stratus are informal names for Omicron subvariants being monitored in 2025. Nimbus (NB.1.8.1) appeared in China early in 2025. Highly transmissible, it spread across Asia, Europe, and the U.S., causing symptoms like a razor-like sore throat, fatigue, mild cough, and congestion.
Stratus (XFG) first appeared in Canada and became dominant in Europe and the U.K. It shows enhanced immune evasion and causes a hoarse or raspy voice in some patients.
“Frankenstein” is a nickname for hybrid variants formed when someone is infected with two COVID strains simultaneously. Stratus itself is a Frankenstein-type variant. These combination of viruses circulate like any other, but their mixed genetics can make them more transmissible or better at evading immune defenses.
In India, the Ministry of Health and Family Welfare reports 30,440 cases from January to September 2025, though many go unreported due to self-treatment at home. Meanwhile, cases have been rising in the U.S. and U.K.
For the week ending September 27, 6.7% of Americans tested positive, slightly down from 7.9% the previous week. COVID accounted for 0.8% of U.S. deaths and 0.7% of ER visits during the same period.
SARS-CoV-2 continues to evolve. Healthy, vaccinated adults face lower risk of severe disease than during the Delta wave, but older adults and immunocompromised people should remain cautious. Public-health authorities in India and worldwide are actively monitoring variants and will highlight any that significantly change risk.
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Orforglipron, a new daily pill, may be more effective than existing oral treatments for weight loss and blood sugar control than semaglutide, according to a recent clinical trial.
Semaglutide belongs to a group of drugs known as GLP-1 medications, known to mimic a natural hormone that helps regulate appetite, slow digestion, and control blood sugar. The drug is commonly sold under the brand names Wegovy and Ozempic.
Despite being highly effective, semaglutide usually needs to be injected and requires refrigeration, which can make it inconvenient and harder to access for some patients. Additionally, the drug also carries a high price point.
However, in a 52-week trial involving people with Type 2 Diabetes, orforglipron was found to lower average blood sugar levels more than oral semaglutide and also led to greater weight loss.
Participants taking orforglipron lost around up to eight kilograms on average, compared to about five kilograms with semaglutide. Morever, orforglipron is a once-daily pill that does not require injections or cold storage.
But the study also found that orforglipron caused more side effects, particularly digestive issues like nausea and diarrhea. Yet scientists believe it may still be a better alternative to semaglutide as its easier and cheaper to produce than peptide-based drugs like semaglutide.
They also noticed that the drug absorbed more efficiently by the body and does not require strict timing around meals, unlike current oral versions of semaglutide.
READ MORE: Alkem Laboratories Launches Cheapest Semaglutide Injection In India
The first thing to remember here is that Ozempic is a brand-name medicine that contains semaglutide as its active ingredient. Semglutide is the synthetic version of GLP-1—a natural hormone produced in the intestines that regulates blood sugar, appetite, and digestion. Now, every time you eat, your body produces various hormones, including GLP-1. These are called Post nutrition hormones, and help you absorb the energy you just consumed.
GLP-1 travels to your pancreas, prompting it to produce insulin. It also travels to the hypothalamus in your brain, which gives you the feeling of being full or satiated. Ozempic imitates this hormone, thereby, silencing the food chatter in the brain. Interestingly, for some people this food chatter is really quiet ( people with low appetite) and for others it is an outbrurst, (people who generally binge eat.) So with Ozempic, silencing this self-talk in the brain, people tend to lose their appetite and eventually weight.
However, it is important to note that losing weight includes not just fat but muscle as well. Losing too much muscle can lead to reduced strength and a shorter life span. Notably, records show that most people who start taking them stop it at 12 weeks; therefore, it is important for some but not for others.
As reiterated by doctors and health care experts, Ozempic is a drug that is tasked to help diabetic patients manage their blood sugar levels and weight. However, recent research has shown its effectiveness in mitigating various addictions like alcohol and drugs by inhibiting hormones. But what people ignore are its side effects, which include:
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People with blood type B, either positive or negative, are 28 percent more likely to develop Type 2 diabetes, according to a 2024 BMC Medicine study.
Human blood is categorized into eight main groups based on the sugars and proteins, or lack thereof, present on the surface of your red blood cells.
A, B, and AB types are based on the presence of antigens, sugar molecules that can trigger an immune response. O-type blood has no A or B antigens. Meanwhile, Rhesus (Rh) factors are proteins that determine blood compatibility and give your blood its positive or negative designation.
According to a group of Chinese researchers, who conducted a thorough umbrella review of 270 studies, the strongest link between a blood group and Type 2 diabetes was between those with a B blood group.
The researchers also didn't examine what might drive this increased risk. A 2025 study suggests that the gut microbiome may be involved; however, further investigation is needed.
However, the results do suggest that there's a real, tangible association between blood type and Type 2 diabetes – one that people can factor into how they think about their own risk.
Type 2 diabetes (T2D) occurs when blood sugar (glucose) remains consistently high. Normal blood sugar levels fall between 70 and 99 milligrams per deciliter (mg/dL). If undiagnosed, Type 2 diabetes often shows levels of 126 mg/dL or more.
T2D happens because the pancreas doesn’t produce enough insulin, the body can’t use insulin effectively, or a combination of both. This differs from Type 1 diabetes, which arises when the immune system attacks the pancreas, leaving the body unable to produce insulin at all.
Type 2 diabetes is widespread. Over 37 million people in the US have diabetes (around 1 in 10), with 90–95 percent of cases being T2D. Globally, it affects roughly 6.3 percent of the population. While it’s most common in adults over 45, younger adults and even children can develop it.
The American Diabetes Association recommends the following ranges for adults with type 1 or type 2 diabetes and children with type 2 diabetes:
Recommended Blood Sugar Range
Fasting (before eating): 80 to 130 mg/dL
1 to 2 hours after meal: Lower than 180 mg/dL
T2D has complex causes, but genes play a significant role. If one biological parent has T2D, your lifetime risk is around 40 percent, and if both parents do, it rises to 70%. Scientists have identified over 150 DNA variations linked to T2D risk, some increase the chance of insulin resistance or reduced insulin production, while others influence obesity risk. These genetic factors interact with lifestyle and health habits to determine overall risk.
Doctors use several blood tests to confirm T2D:
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Scientists have found a new potential way to treat Alzheimer’s disease and it's already approved by the US Food and Drug Administration.
Researchers at the the Indiana University School of Medicine have found that removing or reducing a specific brain cell enzyme, known as IDOL, can significantly lower the buildup of amyloid plaques while also helping the brain resist further damage.
As of now, Lecanemab and Donanemab drugs can help achieve this as they work by clearing these plaques from the brain and can help slow the progression of symptoms.
However, the researchers' new theory focuses on preventing plaque buildup in the first place, while also improving how brain cells communicate and process fats.
The scientists claim that enzymes such as IDOL are easier to target with drugs due to their well-defined structures, allowing them to design treatments that are more precise and potentially have fewer side effects.
Kim, the P. Michael Conneally Professor of Medical and Molecular Genetics: "What makes this exciting is that we now have a specific target that could lead to a new type of treatment.
"We believe that IDOL will provide us with an alternative strategy to treat Alzheimer’s disease. Targeting enzymes in drug development offers key advantages due to their well-defined active sites or ‘pockets’ where drugs can attach and block their activity. This precision means we can design molecules that hit the right target with minimal side effects."
Kim notes that the team now plans to explore several approaches to target IDOL as part of new Alzheimer’s treatments including testing the safety and effectiveness of potential compounds in preclinical models.
The researchers will also study whether blocking IDOL can help preserve synaptic connections and reduce tau pathology, another key feature of the disease.
READ MORE: The One Critical Thing You Should Do To Prevent Alzheimer's Disease
Alzheimer's disease is one of the most common forms of dementia and mostly affects adults over the age of 65.
About 8.8 million Indians aged 60 and above are estimated to be living with Alzheimer's disease. Over seven million people in the US 65 and older live with the condition and over 100,00 die from it annually.
Alzheimer's disease is believed to be caused by the development of toxic amyloid and beta proteins in the brain, which can accumulate in the brain and damage cells responsible for memory.
Amyloid protein molecules stick together in brain cells, forming clumps called plaques. At the same time, tau proteins twist together in fiber-like strands called tangles. The plaques and tangles block the brain's neurons from sending electrical and chemical signals back and forth.
Over time, this disruption causes permanent damage in the brain that leads to Alzheimer's disease and dementia, causing patients to lose their ability to speak, care for themselves or even respond to the world around them.
While there is no clear cause of Alzheimer's disease, experts believe it can develop due to genetic mutations and lifestyle choices, such as physical inactivity, unhealthy diet and social isolation.
Early symptoms of Alzheimer's disease include forgetting recent events or conversations. Over time, Alzheimer's disease leads to serious memory loss and affects a person's ability to do everyday tasks.
There is no cure for this progressive brain disorder and in advanced stages, loss of brain function can cause dehydration, poor nutrition or infection. These complications can result in death.
The US Food and Drug Administration has approved the use of a blood test which can help diagnose Alzheimer’s disease in adults aged 55 and above.
The blood test, known as Lumipulse, can detect amyloid plaques associated with Alzheimer’s disease and has proven to be a “less invasive option” that “reduces reliance on PET scans and increases diagnosis accessibility.”
FDA Commissioner Martin A. Makary said of the landmark decision, "Alzheimer’s disease impacts too many people, more than breast cancer and prostate cancer combined.
"Knowing that 10 percent of people aged 65 and older have Alzheimer's, and that by 2050 that number is expected to double, I am hopeful that new medical products such as this one will help patients."
It remains unclear when this test will be available for commercial use across the world.
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