Clinical laboratories continue to report positive COVID-19 tests for individuals that have been vaccinated and even previously infected with the same variant of the coronavirus
Researchers across the globe continue to study the SARS-CoV-2 coronavirus and its many variants. Their goals are to curb the spread of the disease and develop new therapies and treatments for optimal patient outcomes. Now, a study conducted by scientists at the University of Missouri (UM) provides deeper insight into the processes the virus uses to mutate and overpower the human immune system. These findings could lead to improved antivirals and clinical laboratory tests for COVID-19.
The UM team identified specific mutations occurring within the virus’ spike protein that help Omicron subvariants evade existing antibodies and create an infection. These mutations may explain why some people who have had previous COVID-19 infections and/or who are fully vaccinated continue to test positive for SARS-CoV-2, and why the virus continues to evolve.
“Omicron now has more than 130 sublineages and they have been here for quite a while. We are now just finally able to detect them and differentiate among them with this research,” said Kamlendra Singh, PhD, associate research professor in the Department of Veterinary Pathobiology at UM’s College of Veterinary Medicine, in a UM press release.
“Previous variants, including Alpha, Beta, Gamma, and Delta, contributed to many of the mutations occurring now with these Omicron variants. So, our research shows how the virus has evolved over time with new mutations,” he added.
“Throughout the pandemic, the [SARS-CoV-2] virus has continued to get smarter and smarter. Even with vaccines, it continues to find new ways to mutate and evade existing antibodies,” said Kamlendra Singh, PhD (above), Associate Research Professor, College of Veterinary Medicine at University of Missouri, in a UM press release. This research team’s findings may help clinical laboratories further develop their SARS-CoV-2 antibody tests. (Photo copyright: University of Missouri.)
Antibodies for One Variant, but Not for Another
The scientists began their investigation by researching online databases that track COVID-19 cases and analyzing the protein sequences from more than 10 million Omicron-related samples that were collected from around the world since November of last year.
They examined the available sequences, structures of spike/receptor and spike/antibody complexes of the samples, and then conducted molecular dynamics simulations. The team utilized 3D modeling to locate where mutations occur and created structures of the spike protein to determine how the mutations are affected by antibodies and vaccinations.
The researchers found that the Omicron variant continues to mutate and has become extremely efficient at adaptation. Reinfections are happening because many individuals do not possess the antibodies for the new subvariants that continue to develop.
“Vaccinated individuals, or those who have previously tested positive, may have the antibodies for one variant but not necessarily for any of the other variants,” Singh explained. “The various mutations may seem like only subtle differences, but they are very important.”
The UM scientists’ research shows it is possible to differentiate Omicron subvariants from each other and pinpoint how certain mutations might become problematic for patients. According to Singh, many people can be infected with multiple variants at the same time. He is hopeful that their work will make it possible for vaccines and other treatments to specifically target different strains of the virus.
Singh also believes that the coronavirus is most likely never going to disappear from society and that new variants and their sublineages will continue to appear and evolve.
“The ultimate solution going forward will likely be the development of small molecule, antiviral drugs that target parts of the virus that do not mutate,” Singh said. “While there is no vaccine for HIV, there are very effective antiviral drugs that help those infected live a healthy life, so hopefully the same can be true with COVID-19.”
Omicron Subvariants May Be Here to Stay
“I am proud of my team’s efforts, as we have identified specific mutations for various variants throughout the pandemic, and it feels good to be contributing to research that is assisting with the situation,” Singh said. “We will continue to help out, as there will surely be new variants in the future.”
Singh is also part of a team that developed a supplement called CoroQuil-Zn, which was designed to reduce a patient’s viral load after being infected with SARS-CoV-2. The drug is currently being used in parts of India and is awaiting approval from the US Food and Drug Administration (FDA).
Clinical laboratories that perform antibody testing for SARS-CoV-2 infections should be aware that the coronavirus will likely be moving among humans for many years to come. This recent research may aid in the development of new antivirals, treatments, and vaccines that target specific subvariants for the best patient outcomes.
Findings could lead to new clinical laboratory involvement in diagnostics targeted at overweight patients
Does the SARS-CoV-2 coronavirus make us fat so it can better take over our bodies? It sounds like the plot for a science fiction horror movie! But a team of scientists in the Pacific Northwest say that is exactly what the virus does, and their findings could lead to clinical laboratories playing a role in evaluating how the virus highjacks fat cells to aid in its invasion of humans.
They found that certain types of lipids support replication of the COVID-19 virus. Their study illustrates how lipids may play a more important role in the human body than scientists previously understood.
“This is exciting work, but it’s the start of a very long journey,” said Fikadu Tafesse, PhD (left), Assistant Professor of Molecular Microbiology and Immunology, OHSU School of Medicine and corresponding author of the study in an OHSU press release. “We have an interesting observation, but we have a lot more to learn about the mechanisms of this disease.” Clinical laboratories may eventually be part of a new diagnostic process for overweight COVID-19 patients. (Photo copyright: Oregon Health and Science University.)
Does Obesity Promote COVID-19 Infection?
The OHSU and PNNL scientists performed their research by examining the effect of SARS-CoV-2 on more than 400 lipids in two different cell lines. They observed that individuals with a high body mass index (BMI) appear to be more sensitive to the COVID-19 virus.
The researchers discovered there is a tremendous shift in lipid levels in those cell lines when the virus was present, with some fats increasing by a massive 64 times! Nearly 80% of the fats in one cell line were changed by the virus and more than half of the fats were altered in the other cell line.
The lipids that were most affected by the COVID-19 virus were triglycerides which are critical to human health. Triglycerides are basically tiny bundles of fat that allow the body to store energy and maintain healthy cell membranes. When a body needs energy, these fat parcels are broken up into useful, raw materials to provide the required energy.
“Lipids are an important part of every cell. They literally hold us together by keeping our cells intact, and they’re a major source of energy storage for our bodies,” said Jennifer Kyle, PhD, in the OHSU press release. Kyle is a research scientist at PNNL who specializes in all stages of lipidomic research. “They are an attractive target for a virus,” she noted.
Stopping SARS-CoV-2 Replication
The scientists discovered that SARS-CoV-2 alters our fat-processing system by boosting the number of triglycerides in our cells and changing the body’s ability to utilize stored fat as fuel. The team also analyzed the effects of lipid levels in 24 of the virus’ 29 proteins. They identified several proteins that had a strong influence on triglyceride levels.
The team then searched databases and identified several compounds that interfered with the body’s fat-processing system by cutting off the flow of fatty fuel. They found that several of these compounds were successful at stopping the SARS-CoV-2 virus from replicating.
A synthetic organic compound known as GSK2194069, which selectively and potently inhibits fatty acid synthase (FAS), and a weight-loss medication called Orlistat, were both able to stop viral replication in the lab.
Although the scientists believe their work is an important step in understanding the SARS-CoV-2 coronavirus, they also note that their results occurred in cell culture (in vitro) and not in people (in vivo). Therefore, more research is needed to determine if the compounds will work in the same manner in human trials.
“As the virus replicates, it needs a continuous supply of energy. More triglycerides could provide that energy in the form of fatty acids. But we don’t know exactly how the virus uses these lipids to its advantage,” Tafesse said in the press release.
“Our findings fill an important gap in our understanding of host dependency factors of coronavirus infection. … In light of the evolving nature of SARS-CoV-2, it is critical that we understand the basic biology of its life cycle in order to illuminate additional avenues for protection and therapy against this global pandemic pathogen, which spreads quickly and mutates with ease,” the OHSU/PNNL scientists wrote in Nature Communications.
More research is needed to validate the findings of this study and to better understand the dynamic between lipids and SARS-CoV-2 infection. However, it is reasonable to assume that, in the future, some COVID-19 patients may require a clinical laboratory work-up to determine how the coronavirus may be hijacking their fat cells to exacerbate the illness.
Study may lead to clinical laboratory involvement in repurposing hormonal treatments to prevent cancer treatment resistance
Diagnosing prostate cancer and identifying which patients have aggressive forms of the cancer has been a challenge. But new insights into how aggressive cancers become resistant to drug therapies—and the discovery of a way to repurpose hormonal treatment to block or slow aggressive prostate cancer—may lead to clinical laboratories monitoring the progress of patients’ being treated with this new type of therapy.
Instead of treating tumors directly, the new approach developed by an international team of scientists would target proteins that typically regulate a cell’s circadian rhythm, but which have been found to be helping cancerous cells become resistant to treatment therapies.
“Our discovery has shown us that we will need to start thinking outside the box when it comes to new drugs to treat prostate cancer and test medicines that affect the circadian clock proteins in order to increase sensitivity to hormonal therapy in prostate cancer,” said Wilbert Zwart, PhD (above), Lead Researcher and Senior Group Leader Oncogenomics Division at NKI, in a news release. This discovery could give clinical laboratories and anatomic pathology groups an effective way to monitor new forms of cancer hormonal treatments. (Photo copyright: Netherlands Cancer Institute.)
Breakthrough Could Mean New Treatment for Aggressive Cancer
The aim of prostate cancer hormone therapy (AKA, androgen suppression therapy) is to halt signals by male hormones (usually testosterone) that stimulate tumor growth. This approach works until cancer becomes resistant to the drug therapy.
So, the challenge in metastatic prostate cancer treatment is finding a drug that prevents resistance to hormonal therapy.
In addressing the challenge, the researchers made a surprising discovery about what exactly dilutes anti-hormonal therapy’s effectiveness. Proteins that regulate the body’s sleep-wake cycle, or circadian rhythm, were found to also “dampen the effects of the anti-hormonal therapy,” according to the study.
“Prostate cancer cells no longer have a circadian rhythm. But these ‘circadian clock’ proteins acquire an entirely new function in the tumor cells upon hormonal therapy: they keep these cancer cells alive, despite treatment. This has never been seen before,” said Wilbert Zwart, PhD, Lead Researcher and Senior Group Leader Oncogenomics Division, NKI, in the news release.
The research suggests treatment for metastatic prostate cancer requires drugs “which influence the day-and-night rhythm of a cell,” and not necessarily medications that fight cancer, Technology Networks noted.
“Fortunately, there are already several therapies that affect circadian proteins, and those can be combined with anti-hormonal therapies. This lead, which allows for a form of drug repurposing, could save a decade of research,” Zwart added.
Questioning Hormonal Therapy Resistance
In their paper, the Dutch researchers acknowledged that androgen receptor (AR)-targeting agents are effective in prostate disease stages. What they wanted to learn was how tumor cells bypass AR suppression.
For the study, the scientists enrolled 56 patients with high-risk prostate cancer in a neoadjuvant clinical trial. Unlike adjuvant therapy, which works to lower the risk that cancer will return following treatment, the purpose of neoadjuvant therapy is to reduce the size of a tumor prior to surgery or radiation therapy, according to the National Institute of Health (NIH) National Cancer Institute (NCI).
The researchers performed DNA analysis of tissue samples from patients who had three months of anti-hormonal therapy before surgery. They observed that “genes keeping tumor cells alive were controlled by a protein that normally regulates the circadian (body) clock,” said Simon Linder, PhD student and researcher at NKI, in the news release.
“We performed integrative multi-omics analyses on tissues isolated before and after three months of AR-targeting enzalutamide monotherapy from patients with high-risk prostate cancer enrolled in a neoadjuvant clinical trial. Transcriptomic analyses demonstrated that AR inhibition drove tumors toward a neuroendocrine-like disease state,” the researchers wrote in Cancer Discovery.
“Understanding how prostate cancers adapt to AR-targeted interventions is critical for identifying novel drug targets to improve the clinical management of treatment-resistant disease. Our study revealed an enzalutamide-induced epigenomic plasticity toward pro-survival signaling and uncovered the circadian regulator ARNTL [Aryl hydrocarbon receptor nuclear translocator-like protein 1] as an acquired vulnerability after AR inhibition, presenting a novel lead for therapeutic development,” the scientists concluded.
More Research Planned
The scientists expressed intent to follow-up with Oncode to develop a drug therapy that would increase anti-hormonal therapy’s effectiveness in prostate cancer patients.
Given the molecular processes involved in the researchers’ discovery, there may be a supportive role for clinical laboratories and anatomic pathology groups in the future. But that can only happen after more studies and a US Food and Drug Administration (FDA) review of any potential new therapy to combat hormonal treatment resistance in prostate cancer patients.
Understanding why some mutations impair normal bodily functions and contribute to cancer may lead to new clinical laboratory diagnostics
New insight into the human genome may help explain the ageing process and provide clues to improving human longevity that can be useful to clinical laboratories and researchers developing cancer diagnostics. A recent study conducted at the Wellcome Sanger Institute in Cambridge, United Kingdom, suggests that the speed of DNA errors in genetic mutations may play a critical role in the lifespan and survival of a species.
To perform their research, the scientists analyzed genomes from the intestines of 16 mammalian species looking for genetic changes. Known as somatic mutations, these mutations are a natural process that occur in all cells during the life of an organism and are typically harmless. However, some somatic mutations can impair the normal function of a cell and even play a role in causing cancer.
“Aging is a complex process, the result of multiple forms of molecular damage in our cells and tissues. Somatic mutations have been speculated to contribute to ageing since the 1950s, but studying them had remained difficult,” said Inigo Martincorena, PhD (above), Group Leader, Sanger Institute and one of the authors of the study. Greater understanding of the role DNA mutations play in cancer could lead to new clinical laboratory tools and diagnostics. (Photo copyright: Wellcome Sanger Institute.)
Lifespans versus Body Mass
The mammalian subjects examined in the study incorporated a wide range of lifespans and body masses and included humans, giraffes, tigers, mice, and the highly cancer-resistant naked mole-rat. The average number of somatic mutations at the end of a lifespan was around 3,200 for all the species studied, despite vast differences in age and body mass. It appears that species with longer lifespans can slow down their rate of genetic mutations.
The average lifespan of the humans used for the study was 83.6 years and they had a somatic mutation rate of 47 per year. Mice examined for the research endured 796 of the mutations annually and only lived for 3.7 years.
Species with similar amounts of the mutations had comparable lifespans. For example, the small, naked mole-rats analyzed experienced 93 mutations per year and lived to be 25 years of age. On the other hand, much larger giraffes encountered 99 mutations each year and had a lifespan of 24 years.
“With the recent advances in DNA sequencing technologies, we can finally investigate the roles that somatic mutations play in ageing and in multiple diseases,” said Inigo Martincorena, PhD, Group Leader, Sanger Institute, one of the authors of the study in a press release. He added, “That this diverse range of mammals end their lives with a similar number of mutations in their cells is an exciting and intriguing discovery.”
The scientists analyzed the patterns of the mutations and found that the somatic mutations accumulated linearly over time. They also discovered that the mutations were caused by similar mechanisms and the number acquired were relatively similar across all the species, despite a difference in diet and life histories. For example, a giraffe is typically 40,000 times larger than a mouse, but both species accumulate a similar number of somatic mutations during their lifetimes.
“The fact that differences in somatic mutation rate seem to be explained by differences in lifespan, rather than body size, suggests that although adjusting the mutation rate sounds like an elegant way of controlling the incidence of cancer across species, evolution has not actually chosen this path,” said Adrian Baez-Ortega, PhD, postdoctoral researcher at the Sanger Institute and one of the paper’s authors, in the press release.
“It is quite possible that every time a species evolves a larger size than its ancestors—as in giraffes, elephants, and whales—evolution might come up with a different solution to this problem. We will need to study these species in greater detail to find out,” he speculated.
Why Some Species Live Longer than Others
The researchers also found that the rate of somatic mutations decreased as the lifespan of each species increased which suggests the mutations have a likely role in ageing. It appears that humans and animals perish after accumulating a similar number of these genetic mutations which implies that the speed of the mutations is vital in ascertaining lifespan and could explain why some species live substantially longer than others.
“To find a similar pattern of genetic changes in animals as different from one another as a mouse and a tiger was surprising. But the most exciting aspect of the study has to be finding that lifespan is inversely proportional to the somatic mutation rate,” said Alex Cagan, PhD, Postdoctoral Fellow at the Sanger Institute and one of the authors of the study in the press release.
“This suggests that somatic mutations may play a role in ageing, although alternative explanations may be possible. Over the next few years, it will be fascinating to extend these studies into even more diverse species, such as insects or plants,” he noted.
Benefit of Understanding Ageing and Death
The scientists believe this study may provide insight to understanding the ageing process and the inevitability and timing of death. They surmise that ageing is likely to be caused by the aggregation of multiple types of damage to the cells and tissues suffered throughout a lifetime, including somatic mutations.
Some companies that offer genetic tests claim their products can predict longevity, despite the lack of widely accepted evidence that such tests are accurate within an acceptable range. Further research is needed to confirm that the findings of the Wellcome Sanger Institute study are relevant to understand the ageing process.
If the results are validated, though, it is probable that new direct-to-consumer (DTC) genetic tests will be developed, which could be a new revenue source for clinical laboratories.
Genetic testing for the health and wellbeing of beloved pets is not unlike clinical laboratory testing to develop personalized treatments for humans
Clinical laboratory professionals know that the same patients who complain about a $10 copay for their own laboratory testing will happily pay veterinarians tons of cash to test and treat their beloved pets. And as genetic testing for humans becomes commonplace, more people are seemingly willing to pay for genetic analyses of their pets as well.
In June, animal health company Zoetis, Inc. announced it had completed the acquisition of pet care genetics company Basepaws. The financial terms of the deal were not disclosed.
California-based Basepaws is a privately-held company that provides pet owners with analytics, genetic tests, and early health risk assessments for their pets through oral microbiome analysis. Founded in 2017, Basepaws was responsible for the creation of the first at-home genetic testing platform for cats.
Basepaws sells easy-to-use genetic testing kits for cats that allow pet owners and veterinarians to better understand an individual pet’s predisposition to certain illnesses and increase the likelihood of early detection and treatment of those diseases.
It’s not unlike the drive toward personalized medicine and genetic testing that is at the core of human precision medicine.
Different Breeds, Different Needs
Basepaws has a slogan: “Different breeds, different needs.” This means, according to their website, each individual cat has a unique composition of genetic traits that can relate to its needs for optimal health and wellbeing. Obviously, this would apply to all pets.
“As a pioneer in pet care genetics, the California-based Basepaws offers easy-to-use genetic screening tools for the early detection of disease risk in pets, as well as individualized breed and health reports that can identify traits, biomarkers, and potential hereditary conditions for pets. Basepaws helps pet owners and veterinarians understand an individual pet’s risk for disease and can lead to more meaningful engagements and increased likelihood of early detection and treatment of disease,” states a Zoetis press release announcing the acquisition.
“The addition of Basepaws will enhance our portfolio in the precision animal health space and inform our future pipeline of pet care innovations,” said Kristin Peck, CEO of Zoetis, in the press release. “Working together, we can continue to provide veterinarians and pet owners with more comprehensive ways to proactively manage the health, wellness, and quality of care for their animals.”
“Basepaws and Zoetis both consist of pet lovers with a passion for science, and our mission is to create better and longer lives for our pets through knowledge and data,” Anna Skaya (above), CEO of Basepaws, told ROI-N.J. “We look forward to expanding our business and the impact of our genetic products with the global scale and [research and development] experience of Zoetis, the world leader in animal health. We believe that, together, we can bring the benefits of a more proactive healthcare approach to pet parents around the world.” Genetic testing for optimum pet health is not unlike the drive for personalized clinical laboratory genetic testing for humans. (Photo copyright: Los Angeles Times.)
Test Results for Hundreds of Genetic Disorders and Health Markers
Basepaws currently sells three DNA test kits for felines on their webpage. The current price for an oral health test kit that identifies active signs of dental diseases is $69. Their breed and cat health DNA test kit, which provides results for over 115 known feline genetic markers, is $129. Their most comprehensive testing kit is a whole genome sequencing (WGS) kit which is currently on sale for $399.
After receiving a test kit by mail, the purchaser registers the kit online, takes a single buccal swab from their kitty’s inner cheek, and then mails the sample to Basepaws. Lab personnel then extract the cat’s DNA from the sample and perform quality checks to ensure the sample is acceptable for genetic testing. It takes four to six weeks for consumers to receive test results.
According to the company’s website, Basepaws’ WGS test provides results related to 43 genetic disorders that are represented by 65 health markers. The listing of genetic disorders contained in the Health Marker section of the Basepaws report includes data on:
Metabolic disorders,
Musculoskeletal and connective tissue disorders,
Renal disorders,
Cardiovascular disorders,
Blood disorders,
Eye disorders,
Endocrine disorders,
Skin disorders, and
Autoimmune disorders.
“The Basepaws team has done an amazing job demonstrating how genetic testing and data can improve how we care for the pets in our lives,” Abhay Nayak, Executive Vice President at Zoetis, told ROI-NJ. “With the addition of Basepaws, Zoetis will continue to strengthen our portfolio of products for precision animal health, across genetics, diagnostics, and data analytics for pets and livestock. We are also excited by how Basepaws’ feline genomic and microbiome database will help enhance our [research and development] capabilities and inform the future of our pet care pipeline.”
Zoetis, based in Parsippany, N.J., manufactures vaccines, medicines, clinical laboratory diagnostics, and other technologies for the benefit of companion pets and livestock. The Fortune 500 company generated $7.8 billion in revenue in 2021, according to its website.
The article also stated that the global animal genetic testing market was valued at $990 million in 2020 and is only expected to rise.
Thus, spending money keeping our pets healthy is not only a typical element of Americans’ lives, but also a mega-billion-dollar industry. With at-home genetic testing for humans increasing in popularity, it’s likely testing for animals will follow that trend as well.
In the future, some clinical laboratory organizations may want to consider assessing the animal DNA testing market for its potential to be a useful source of new revenue, especially because potential customers will pay cash when they order genetic tests for their dogs and cats.
In fact, the UB study suggests traditional anatomical methods for determining the evolutionary relationships between species may not be as accurate as once thought, an article in SciTechDaily reported.
Nevertheless, the UB’s research into convergent evolution is unlocking new insights into how genes evolve over time and this new knowledge may help researchers develop genetic tests that more accurately identify different diseases and health conditions.
Additionally, studies that bring a better understanding of how beneficial genetic mutations work their way into a species’ genome might also aid researchers in developing personalized clinical laboratory testing and therapies based on manipulating a patient’s genetic sequences in ways that would be beneficial.
Gene Sequencing More Accurate at Determining Evolutionary Relationships
The UB study suggests that existing evolutionary (phylogenetic) trees may need to be reconsidered. To put a finer point on the findings, a UB news release on the study states, “determining evolutionary trees of organisms by comparing anatomy rather than gene sequences is misleading.”
The UB scientists used genetic sequencing to quickly—and more cost effectively—determine evolutionary relationships as compared to traditional morphology (anatomy and structure), according to the news release.
They found genetic data that revealed surprising relationships about where the sequenced species originated, and which differed with prior conclusions that were drawn based on the species’ appearance. The findings suggest there may be need to “overturn centuries of scientific work in classifying relation of species by physical traits,” the UB scientists said.
“For over a hundred years, we’ve been classifying organisms according to how they look and are put together anatomically, but molecular data often tells us a rather different story,” said Matthew Wills, PhD (above), Professor of Evolutionary Paleobiology, Milner Center for Education at the University of Bath, in the news release. “Our study proves statistically that if you build an evolutionary tree of animals based on their molecular data, it often fits much better with their geographical distribution.” This new use of genetic sequencing could lead to improved precision medicine treatments and clinical laboratory testing. (Photo copyright: University of Bath.)
Molecular Data Leads to New Insights into Convergent Evolution
The UB study’s use of genetic sequencing led the researchers to a greater understanding of convergent evolution, defined by “a characteristic evolving separately in two genetically unrelated groups of organisms,” according to UB.
For example, wings are a widely developed characteristic. But they are not necessarily a sign of relatedness when it comes to birds, bats, and insects.
“Now with molecular data, we can see that convergent evolution happens all the time—things we thought were closely related often turn out to be far apart on the tree of life,” Wills said, adding, “Individuals within a family don’t always look similar; it’s the same with evolutionary trees, too.”
Family Trees: Morphology Versus Molecular
In their paper, the UB researchers acknowledged the importance of phylogenies (evolutionary history of species) in areas of biology, including medicine. They aimed to study a better way to produce accurate phylogenetic trees.
“Phylogenetic relationships are inferred principally from two classes of data: morphological and molecular,” they wrote, adding, “The superiority of molecular trees has rarely been assessed empirically.”
So, they set out to compare the two approaches to building evolutionary trees:
Traditional morphology analysis, and
Phylogenetic trees developed using molecular data.
Using 48 pairs of morphological and molecular trees, they mapped data geographically.
“We show that, on average, molecular trees provide a better fit to biogeographic data than their morphological counterparts, and that biogeographic congruence increases over research time,” the researchers wrote.
Biogeography a Better Gauge of Relatedness than Anatomy
The study also found animals on molecular trees lived geographically closer as compared to groups on morphological trees.
For example, molecular studies put aardvarks, elephants, golden moles, swimming manatees, and elephant shews in an Afrotheria group, named for Africa, which is where they came from. Therefore, the biogeography matches, however the appearances of these mammals clearly do not, the UB scientists point out.
“What’s most exciting is that we find strong statistical proof of molecular trees fitting better not just in groups like Afrotheria, but across the tree of life in birds, reptiles, insects, and plants,” said Jack Oyston PhD, UB Department of Biology and Biochemistry Research Associate and first author of the study, in the news release.
The researchers believe their findings support the accuracy of genetic-themed trees.
“It being such a widespread pattern makes it much more potentially useful as a general test of different evolutionary trees. But it also shows just how pervasive convergent evolution has been when it comes to misleading us,” Oyston added.
Advantages of Molecular Data
In their Nature Communications Biology paper, the UB scientists wrote that molecular data offer up these advantages over morphology:
Widely available in vast quantity.
Opportunity exists to “search, repurpose, and reanalyze sequenced data alongside novel sequences.”
Less subjectivity in researchers’ analysis.
Well-developed data at the ready and “still in their infancy.”
The University of Bath’s study of convergent evolution, phylogenetic trees, and comparison of molecular data versus morphology, has implications for medical laboratories. Should their research lead to new insights into how genes evolve over time, diagnostics professionals may have new information to identity diseases and work with others to precisely treat patients.
