Cancer patients treated with immunotherapy can safely receive mRNA COVID-19 vaccines

 New research published in the October 2022 issue of JNCCN—Journal of the National Comprehensive Cancer Network confirms the safety of mRNA vaccines in people with cancer undergoing immunotherapy treatment. The researchers analyzed the frequency of side effects (also referred to as immune-related adverse events, or irAEs) in 408 patients receiving immune checkpoint inhibitor (ICI) therapy between January 16 and March 27, 2021. They found no increase in type, frequency, or severity of side effects from those receiving both immunotherapy and the vaccine at the same time.

“We see no evidence to suggest that taking the COVID-19 vaccine increases the risk of immune-related adverse events in newly or previously ICI-treated patients. Also, the vaccine will not disrupt treatment or lead to early discontinuation,” said senior author Mini Kamboj, MD, Chief Medical Epidemiologist, Infection Control at Memorial Sloan Kettering Cancer Center (MSK). “Vaccines continue to offer strong protection from severe COVID-19 for all variants, and patients are highly encouraged to stay up-to-date on their COVID-19 vaccination.”

This research supports NCCN’s recommendations for COVID-19 vaccination in people with cancer. The current guidance acknowledges that there is an acceptable safety profile for COVID-19 vaccination in people being treated with immunotherapy, while also calling for more data. The newly-published study in JNCCN can help answer that call. The frequently-updated, evidence-based, expert consensus recommendations can be found at NCCN.org/covid-19.

The JNCCN article cites a previous study[1] that found approximately one-fifth of patients receiving ICI treatment were reluctant to get vaccinated against COVID-19 due to fear of added side effects.

“The main catalyst for this study was vaccine hesitancy among patients on immunotherapy and the uncertainty among treating clinicians on how to address these concerns,” explained lead author Adam Widman, MD, also with MSK. “This was surprising, since there is overwhelming evidence of higher risk for COVID-19-infection related complications in patients actively receiving cancer treatment. We felt it was essential to share our experience and encourage vaccine uptake in this vulnerable population.”

“It is encouraging that patients treated with immunotherapy who were also vaccinated for COVID-19 did not experience immune checkpoint toxicity at a greater rate than those patients who received immunotherapy and were unvaccinated,” commented Bryan J. Schneider, MD, University of Michigan Rogel Cancer Center, who is Vice-Chair of the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Panel for Management of Immunotherapy-Related Toxicity, and was not involved in this research. “The worry that side effects would increase during immune checkpoint therapy may have led patients or providers away from routine vaccination; however, recent reviews have not supported this concern. Patients should receive mRNA-based vaccines per institutional guidelines. This recommendation is also reflected in the NCCN Guidelines for Management of Immunotherapy-Related Toxicities.”

The NCCN Guidelines for Management of Immunotherapy-Related Toxicities, versions of these guidelines for patients and caregivers, as well as a one-page infographic to help patients and caregivers recognize irAEs are all available for free at NCCN.org.

To read the entire study, visit JNCCN.org. Complimentary access to “Immune-Related Adverse Events Among COIVD-19-Vaccinated Patients with Cancer Receiving Immune Checkpoint Blockade” is available until January 10, 2023.

https://www.eurekalert.org/news-releases/968056

New islet transplant method leads to insulin independence

 More than half of the most seriously affected type 1 diabetes patients achieved years of insulin independence after they received a new method of islet cell transplantation, according to a paper published in Diabetes Care on the long-term outcomes of two Phase 3 clinical trials.

In addition to finding that many patients didn't need insulin to maintain their blood sugar for up to eight years, the authors, co-led by Michael Rickels, MD, the Willard and Rhoda Ware Professor in Diabetes and Metabolic Diseases in the Perelman School of Medicine at the University of Pennsylvania, also reported that the new approach necessitated fewer transplants than typical and was exceedingly safe.

"These data are important in showing that in the long run, islet transplantation has efficacy, including among those who have had kidney transplants," said Rickels. "Yes, most type 1 diabetes patients are improved tremendously with current insulin delivery systems. But for those having the most difficulty controlling their blood sugar, and those whose diabetes has already been complicated by needing a kidney transplant, the outcomes we saw in this study are what we've been hoping to achieve for more than 20 years."

Two cohorts of patients were analyzed: Those who received just islet transplantation (48) and those who received islets after kidney transplantation (24). Of those observed all the way through to what was defined as the "long-term" endpoint (up to eight years for islet-only, and seven for those who also had kidney transplants), more than half had surviving islet grafts. Additionally, of the 75 percent who initially were able to come off insulin therapy, more than half maintained total insulin independence, meaning they needed no additional insulin injections throughout the years of follow-up.

Islet cells are located in the pancreas and are critical to keeping blood sugar in check by producing the hormone insulin. But the islets of those with type 1 diabetes are destroyed by the immune system and don't make insulin. A form of cell replacement therapy—which exists elsewhere in the world (such as in Australia, Canada, the United Kingdom, and many parts of Europe) but is still considered experimental in the United States—is islet cell transplantation, which takes normal-functioning cells from the pancreases of deceased donors and introduces them via a small catheter to patients whose own islets no longer work.

Rickels; Ali Naji, MD, Ph.D., the J. William White Professor of Surgical Research; and the multi-institution Clinical Islet Transplantation Consortium have been working since 2004 to establish optimized and standardized methods for islet isolation and transplantation, and to demonstrate its safety and efficacy as a novel cell therapy for the treatment of type I diabetes.

Their approach has included T-cell depletion to induce immunosuppression combined with anti-inflammatory, anti-coagulation, and early intensive insulin therapies to prevent the transplanted islets from being damaged or stressed before a new blood supply from the liver is established, making the process of islet engraftment and survival more efficient.

This new approach was performed with 72 patients who volunteered, all of whom had type I diabetes and "impaired awareness hypoglycemia," which meant that they had incidents of severely low blood sugar that occurred when they weren't aware of it, which can result in a seizure or loss of consciousness. A group had also had previously undergone kidney transplantation as a result of their diabetes. Essentially, these patients were among the most critically affected by the disease.

When it came to measuring the safety of the process, important because of the severity of disease in the patient population, the researchers found that there were 104 "serious adverse events"—which effectively meant hospitalization for anything that could range from dehydration to an infection—for the total patient population in the study after receiving islets. While their study didn't allow for a control group who didn't receive islet transplantation to compare directly, Rickels said the number of adverse events was much lower than could be expected for a similar patient population.

"These are the most seriously affected patients, and you'd be expecting to see some hospitalizations in a population managed on immunosuppression therapy," Rickels said. "It's important to note that none of the adverse events were related to the actual islet product. Also, kidney function remained stable during long-term follow-up in both cohorts, in fact improving in those who had kidney transplants. Overall, this is a much less invasive procedure that opens itself up to significantly fewer complications than what many of these patients would otherwise require, a pancreas transplant, which involves major abdominal surgery."

A particularly impactful finding, Rickels said, was that this study showed their method was achieving success while using fewer donor pancreases.

"Currently, around the world, there's an expectation of two-to-three donor pancreases being needed," Rickels said. "Here, it's one, maybe two. It's a much more efficient protocol, and opens up access for more islet transplantation as a hoped-for alternative to pancreas transplants."

Rickels and colleagues plan to submit their data as part of a biologic license application to the Food and Drug Administration (FDA) to make their islet transplantation technique an approved treatment for patients like those in the trials.

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Explore further

Cell research offers diabetes treatment hope

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More information: Michael R. Rickels et al, Long-term Outcomes With Islet-Alone and Islet-After-Kidney Transplantation for Type 1 Diabetes in the Clinical Islet Transplantation Consortium: The CIT-08 Study, Diabetes Care (2022). DOI: 10.2337/dc21-2688

https://medicalxpress.com/news/2022-10-islet-transplant-method-insulin-independence.html

Targeting enzyme could alleviate muscle wasting for cancer patients

 Targeting a specific enzyme in the muscle could help cancer patients preserve muscle mass and potentially prolong their survival, according to research from UTHealth Houston.

A study led by Yi-Ping Li, PhD, professor in the Department of Integrative Biology and Pharmacology with McGovern Medical School at UTHealth Houston, found that an enzyme known as UBR2 plays a critical role in cancer-induced muscle wasting, also called cancer cachexia.

The results were published today in the scientific journal PNAS.

"The findings will fill a key gap in understanding how cancer causes muscle mass and function loss," said Li, senior author of the study and a faculty member with The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences.

Cancer cachexia is a complication developed in the late stages of cancer in roughly 60% of all cancer patients. Cachexia patients waste away by losing body weight, primarily due to progressive loss of muscle mass, causing respiratory and heart failure. Approximately 30% of all cancer patients die of cachexia, making the complication a major determinant of cancer survival.

Historically, there has been no treatment of cancer cachexia due to poor understanding of its origins. Therefore, a key focus of Li's lab over the past two decades has been to decipher the molecular mechanisms through which cancer causes cachexia.

Building upon a series of discoveries in mice, his lab recently identified the role of the enzyme UBR2. This is the key enzyme in muscle that seeks out subtypes of the contractile protein myosin heavy chain, a critical component for sustaining muscle contraction, for destruction in response to cancer.

Cancer causes an increase of UBR2 in muscle, and blocking the increase of or removing UBR2 spares mice from tumor-caused muscle mass and function loss. By examining the muscle of cancer patients, researchers obtained evidence that UBR2 is increased, which is associated with loss of the specific subtype of myosin heavy chain preferentially lost in cachexia.

Li said this discovery is significant for the future of cancer cachexia therapy.

"We have learned in animal studies that muscle wasting in cancer hosts can be ameliorated by blocking UBR2 increase through repurposing some existing drugs," he said. "Based on the findings, we plan to conduct clinical trials for the therapy of cancer cachexia."

Song Gao, PhD, former postdoctoral research fellow with McGovern Medical School, was the first author of the study. Co-authors with the Department of Integrative Biology and Pharmacology at McGovern Medical School included Yong Zhou, PhD, assistant professor, as well as former faculty members Guohua Zhang, PhD; Zicheng Zhang, MD, PhD; James Z. Zhu; and Li Li, PhD.

Other co-authors were George G. Rodney Jr., PhD, and Reem S. Abo-Zahrah, PhD, both with Baylor College of Medicine in Houston; Lindsey Anderson, PhD, and Jose M. Garcia, MD, PhD, both with VA Puget Sound Health Care System in Seattle; and Yong Tae Kwon, PhD, with Seoul National University in South Korea.

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Story Source:

Materials provided by University of Texas Health Science Center at Houston. Original written by Caitie Barkley. Note: Content may be edited for style and length.

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Journal Reference:

1. Song Gao, Guohua Zhang, Zicheng Zhang, James Z. Zhu, Li Li, Yong Zhou, George G. Rodney, Reem S. Abo-Zahrah, Lindsey Anderson, Jose M. Garcia, Yong Tae Kwon, Yi-Ping Li. UBR2 targets myosin heavy chain IIb and IIx for degradation: Molecular mechanism essential for cancer-induced muscle wasting. Proceedings of the National Academy of Sciences, 2022; 119 (43) DOI: 10.1073/pnas.2200215119

https://www.sciencedaily.com/releases/2022/10/221017161116.htm

Brain discovery holds key to boosting body's ability to fight Alzheimer's, MS

 UVA Health researchers have discovered a molecule in the brain responsible for orchestrating the immune system's responses to Alzheimer's disease and multiple sclerosis (MS), potentially allowing doctors to supercharge the body's ability to fight those and other devastating neurological diseases.

The molecule the researchers identified, called a kinase, is crucial to both removing plaque buildup associated with Alzheimer's and preventing the debris buildup that causes MS, the researchers found. It does this, the researchers showed, by directing the activity of brain cleaners called microglia. These immune cells were once largely ignored by scientists but have, in recent years, proved vital players in brain health.

UVA's important new findings could one day let doctors augment the activity of microglia to treat or protect patients from Alzheimer's, MS and other neurodegenerative diseases, the researchers report.

"Unfortunately, medical doctors do not currently possess effective treatments to target the root causes of most neurodegenerative diseases, such as Alzheimer's, Parkinson's or ALS [amyotrophic lateral sclerosis, commonly called Lou Gehrig's disease]. In our studies, we have discovered a master controller of the cell type and processes that are required to protect the brain from these disorders," said senior researcher John Lukens, PhD, of the University of Virginia School of Medicine and its Center for Brain Immunology and Glia (BIG), as well as the Carter Immunology Center and the UVA Brain Institute. "Our work further shows that targeting this novel pathway provides a potent strategy to eliminate the toxic culprits that cause memory loss and impaired motor control in neurodegenerative disease."

Toxic Brain Buildup

Many neurodegenerative diseases, including Alzheimer's and MS, are thought to be caused by the brain's inability to cleanse itself of toxic buildup. Recent advances in neuroscience research have shed light on the importance of microglia in removing harmful debris from the brain, but UVA's new discovery offers practical insights into how this cleaning process occurs -- and the dire consequences when it doesn't.

Using a mouse model of Alzheimer's disease, the UVA researchers found that a lack of the molecule they identified, spleen tyrosine kinase, triggered plaque buildup in the brain and caused the mice to suffer memory loss -- like the symptoms seen in humans with Alzheimer's. Further, the neuroscientists were able to reduce the plaque buildup by activating this molecule and microglia in the brain, suggesting a potential treatment approach for human patients, though that would require significantly more research and testing.

"Our work has described a critical element of microglial function during Alzheimer's disease and MS," said researcher Hannah Ennerfelt, the first author of a new scientific paper outlining the findings. "Understanding the underlying biology of these cells during neurodegeneration may allow for scientists and doctors to develop increasingly informed and effective therapeutic interventions."

A lack of the molecule in a mouse model of MS, meanwhile, led to the buildup of damaged myelin, a protective coating on nerve cells. When myelin is damaged, the cells cannot transmit messages properly, causing MS symptoms such as mobility problems and muscle spasms. The UVA researchers conclude in a new scientific paper that the molecule they identified, abbreviated as SYK, is "critically involved" in the crucial removal of myelin debris. "If boosting SYK activity in microglia can decrease the amount of myelin debris in MS lesions, developing new drugs to target SYK could stop the progression of MS and help to reverse the damage," said Elizabeth L. Frost, PhD, a critical researcher on the project. "This is an especially promising option given that most of the currently available drugs for MS treatment dampen adaptive immunity. These immunosuppressive drugs lead to susceptibility to infection and higher risk of potentially fatal side effects like progressive multifocal leukoencephalopathy. Additionally, some forms of MS do not have a strong involvement of the immune system, and therefore there are currently very limited treatment options for those patients."

"Targeting SYK in microglia," she noted, "would circumvent multiple limitations of present-day therapeutics for MS."

Based on their promising results, the researchers report that targeting the molecule to stimulate the brain's immune activity could offer a way to treat not just Alzheimer's and MS but a "spectrum" of neurodegenerative diseases.

"These findings are especially exciting because they point to a treatment avenue in which we could alter the behavior of these native brain cells, microglia, to behave in a more neuroprotective way," said researcher Coco Holliday, a UVA undergraduate working in the Lukens lab. "It could potentially be applied to a variety of different neurological diseases that all share the problem of a buildup of toxic waste in the brain. It's been a very exciting project to be a part of."

The researchers have published their findings in the scientific journal Cell. The team consisted of Ennerfelt,Frost, Daniel A. Shapiro, Holliday, Kristine E. Zengeler, Gabrielle Voithofer, Ashley C. Bolte, Catherine R. Lammert, Joshua A. Kulas, Tyler K. Ulland and Lukens. The researchers reported no financial interests in the work.

The research was supported by the National Institutes of Health's National Institute of Aging, grantRF1AG071996-01; the National Institute of Neurological Disorders and Stroke, grant R01NS106383; the Alzheimer's Association, grant ADSF-21-816651; the Cure Alzheimer's Fund; The Owens Family Foundation; and several training grants.

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Story Source:

Materials provided by University of Virginia Health System. Note: Content may be edited for style and length.

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Journal Reference:

1. Hannah Ennerfelt, Elizabeth L. Frost, Daniel A. Shapiro, Coco Holliday, Kristine E. Zengeler, Gabrielle Voithofer, Ashley C. Bolte, Catherine R. Lammert, Joshua A. Kulas, Tyler K. Ulland, John R. Lukens. SYK coordinates neuroprotective microglial responses in neurodegenerative disease. Cell, 2022; DOI: 10.1016/j.cell.2022.09.030

https://www.sciencedaily.com/releases/2022/10/221017142440.htm

Metabolism, not genes, may offer more insight into risk of some diseases

 Our ancestry can be detected not only in our genes, but also in our metabolism, a new Yale-led study has found.

In an analysis of the metabolic profiles of healthy American babies, researchers found surprising differences among ethnic groups which may help make screening for inherited metabolic disorders, cystic fibrosis, or hypothyroidism much more accurate than traditional genetic disease screens.

"We don't want to miss a baby who is potentially sick, and we don't want to put families through the burdens and concerns that can stem from a false-positive test," said Curt Scharfe, associate professor of genetics at Yale School of Medicine and senior author of the study published in the journal Molecular Genetics and Metabolism.

For the study, Scharfe and colleagues analyzed data collected from more than 400,000 babies, representing 17 self-reported ethnic groups, who were part of California's newborn screening program. Specifically, they wanted to know if these ethnic differences could be detected in metabolites, molecules that provide energy by breaking down food or body tissue such as fat, found in the blood of the infants.

The question was not only of academic interest but of concern to pediatricians. For instance, it is known that babies of African heritage are more likely to have elevated blood biomarkers indicating cystic fibrosis than babies born to white parents, even though babies born to white parents are far more likely to eventually develop the disease. Researchers hope that using ancestry to interpret these differences in marker levels might offer more accurate ways to assess risks than traditional genetic tests.

People of African heritage are also known to have greater genetic diversity than those from ethnic groups because they are descendants of the world's oldest ancestral population. Modern humans emigrated from Africa to regions across the planet; other ethnic groups are descendants of these original migrants, and have enough variation in their DNA to make them genetically identifiable.

But metabolic lineages can tell a different story, the researchers found. For instance, while there is a clear delineation between genetic variants among African-Americans and Americans of European descent, researchers found that metabolically these two groups are more closely related. Conversely, while people of Japanese and Chinese descent, for instance, are closely related genetically, the researchers found larger differences in their metabolic profiles.

"This attests to the role of environment in forming our metabolism," Scharfe said. "Where people share the same culture and food, metabolic profiles are more similar. Where people are separated by circumstances, such as language or lifestyles, then differences in metabolism are greater than genetic variations."

Scharfe cautions that more work needs to be done before findings can be applied clinically. Researchers only analyzed 41 out of many hundreds of metabolites and relied on parents own reports of their ethnic heritage, which might not always correspond to reality.

"This is just a first snap shot, but understanding our metabolic ancestry has a promising future," Scharfe said.

Gang Peng, an associate research scientist of biostatistics and bioinformatics in Yale's departments of Biostatistics and Genetics, is the first author of the study.

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Story Source:

Materials provided by Yale University. Original written by Bill Hathaway. Note: Content may be edited for style and length.

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Journal Reference:

1. Gang Peng, Andrew J. Pakstis, Neeru Gandotra, Tina M. Cowan, Hongyu Zhao, Kenneth K. Kidd, Curt Scharfe. Metabolic diversity in human populations and correlation with genetic and ancestral geographic distances. Molecular Genetics and Metabolism, 2022; 137 (3): 292 DOI: 10.1016/j.ymgme.2022.10.002

https://www.sciencedaily.com/releases/2022/10/221017161110.htm

Commonwealth Fund: Insurance coverage often not enough to stave off high healthcare costs

 Even amid high levels of insurance coverage, more and more Americans are finding it difficult to afford healthcare, a new survey found. 

The survey, released Thursday by the Commonwealth Fund, showed insurance coverage doesn’t always provide enough financial protection against rising costs. It also found that certain groups such as Hispanics and lower-income individuals were chronically uninsured. 

“The Affordable Care Act made great strides for better access to health insurance,” said David Blumenthal, M.D., president of the Commonwealth Fund, in a reporter briefing Wednesday. “However, more work is needed to fill the remaining coverage gaps.”

The survey, fielded from March 28 through July 4, found 43% of working-age adults surveyed were inadequately insured. This figure includes 9% who were uninsured, another 11% which had a gap in coverage over the past year and 23% that were underinsured where their benefits didn’t give them access to affordable care. 

“More than one-quarter (29%) of continuously insured people with employer coverage and 44% of those with coverage purchased in the individual market or marketplaces are underinsured because of high out-of-pocket costs and deductibles, relative to their income,” according to a release on the survey. 

Those surveyed who had poor insurance were unable to handle unexpected healthcare costs. 

“Half (49%) of people surveyed said they would be unable to pay for an unexpected $1,000 medical bill within 30 days, including 68% of adults with low income, 69% of Black adults and 63% of Latinx/Hispanic adults,” the release added. 

Researchers identified underinsurance as individuals that had out-of-pocket costs over the past year, excluding premiums, that equal 10% or more of their household income. 

“Because out-of-pocket costs occur only if a person uses their insurance to obtain healthcare, we also consider the deductible when determining whether someone is underinsured,” according to the survey brief. 

The Commonwealth Fund’s survey is based on a sample of 8,022 adults 19 and older. 

The results come amid major gains in insurance coverage in the past several years thanks in part to record sign-ups on the Affordable Care Act’s (ACA's) exchanges due to enhanced tax credits and gains in Medicaid due to the pandemic. 

However, experts caution that coverage alone isn’t enough to ensure people are protected from high healthcare costs. 

In addition, coverage gains over the past several years could be threatened if the enhanced credits (which expire in 2025) are not made permanent and when pandemic emergencies eventually wind down, said Sara Collins, lead author of the survey.

She added Congress could also help enhanced ACA exchange costs further by setting the benchmark plan from silver to gold tier. The benchmark plan is the one used to calculate income-based tax credits that lower the cost of insurance. By increasing the benchmark plan to the higher gold tier, the credits would expand to cover more of the costs. 

“It’s a significant improvement in terms of cost protection,” Collins said.

https://www.fiercehealthcare.com/payers/commonwealth-fund-insurance-coverage-often-not-enough-stave-high-healthcare-costs

Highly evasive BQ.1.1 appears on CDC's COVID-19 variants charts for first time

 The highly infectious and evasive BQ.1.1 variant not only has a foothold in the U.S., it may have established that foothold weeks ago. The data on the variant have prompted the Centers for Disease Control and Prevention (CDC) to redo previous weeks’ variants tracking charts.

“It’s been hiding in plain sight,” Kevin Kavanagh, M.D., founder of the patient advocacy group Health Watch USA, told Fierce Healthcare.

The charts below tell the story. The left shows the first version of CDC tracking data for the week ending Oct. 8, where BQ.1.1 (and its cousin, BQ.1) don’t even appear. The CDC had grouped those data under the BA.5 label, which has been the most dominant subvariant of omicron since early July.

After examining additional data, the CDC this week reconfigured the chart to show BQ 1.1. accounting for 2.4% of new cases of COVID-19 for the week ending Oct. 8 and BQ.1 accounting for 3.3%.

(Centers for Disease Control and Prevention)

Now look at the chart for the week ending Oct. 15. Both variants now account for 5.7% of new COVID-19 cases in the U.S.

(Centers for Disease Control and Prevention)

Kavanagh said BQ.1.1 “appears to be doubling every week. Data from CDC appears delayed in being posted on this variant. Once it became apparent in the last few weeks that the variant is having a significant impact, the data were separated.”

As far as his patient advocacy concerns, Kavanagh added that “this underscores the importance of obtaining the bivalent BA.5 booster. For most individuals, the benefits of the booster far outweigh risks.” The take-up of the latest bivalent vaccine has been lackluster, with fewer than 5% of eligible Americans getting inoculated, according to the CDC.

Despite concern about what has become known as the splintering of omicron into subvariants and sub-subvariants (Kavanagh called BQ 1.1 the great-grandchild of BA.5), almost all experts agree that the U.S. will not see the levels of hospitalizations and deaths that occurred in the fall and winter of 2020‑21 and 2021‑22 in the 2022‑23 season.

The public, for the most part, considers the pandemic over, as daily deaths and hospitalization rates plummet, according to the CDC. The Johns Hopkins Coronavirus Resource Center records that the seven-day moving average for deaths as of today is 344; for new cases, 35,747.

President Joe Biden last month declared the pandemic over but added that we need to continue to keep an eye on the always unpredictable SARS-CoV-2. The president last Thursday extended the public health emergency for COVID-19 through Jan. 11. That means, among other things, that COVID-19 tests and vaccines will still be free, pushing back the long-term goal of shifting costs for those to health insurance plans.

For now, BQ.1.1 concerns health officials the most, but others wait in the wing. Yunlong Richard Cao, an immunologist at Peking University in Beijing, tweeted that “XBB is currently the most antibody-evasive strain tested, and BR.2, BM.1.1.1, CA.1 are more immune evasive than BA.2.75.2 and BQ.1.1.”

Cornelius Roemer, a physicist major at Cambridge University who closely tracks variants, predicted on Twitter that there will be another COVID-19 “variant wave in Europe and North America before the end of November.” Speaking about Great Britain, Roemer adds that BQ.1.1’s “relative share has kept more than doubling every week. It has taken just 19 days to grow 8-fold from 5 sequences to 200 sequences.”

Eric Topol, M.D., founder of the Scripps Translational Institute, tweeted last week that “XBB and BQ.1.1 are 2 of the most important variants [to] watch right now.” Topol also notes that Germany, France and Belgium are experiencing waves of BQ.1.1

Vaccines and treatments keep us safe, for the most part. Hope abounds that COVID-19 will become like the flu: potentially dangerous, especially for vulnerable groups like the very young or old, but something society can live with.

Tom Peacock, a virologist at Imperial College London, told Stat that the splintering of omicron does make SARS-CoV-2 in some ways more like influenza, but a speeded up version. “It’s a little bit like what we would expect to see over a couple years of flu, but crammed into about three months with SARS-CoV-2,” Peacock tells Stat. Peacock said that it’s telling that we’re facing subvariants of omicron rather than totally new variants, an indication that though different subvariants might spring up in different parts of the globe, they share a common enemy: the immunity people have gotten through vaccines and/or prior infection.

Some of the therapies developed for earlier iterations of SARS-CoV-2 don’t work against the newer subvariants. For instance, the Food and Drug Administration warned last week that Evusheld for immunocompromised individuals can’t protect them from the subvariants.

Kavanagh suggested that it might be time to reconfigure variant grouping methods. “With different lineages developing similar mutations and the myriad of concerning mutations which are having an impact on viral infectivity and severity, one may need to consider a different method of classification, such as using levels of variant mutations,” he said. “A Level 4 Variant would have 4 mutations of concern and a Level 6, six mutations. This may produce a more rapid flagging of variants of concern rather than waiting for data regarding the impact of specific lineages.”

https://www.fiercehealthcare.com/providers/highly-evasive-bq11-appears-cdcs-covid-19-variants-charts-first-time