Category Archives: Molecular Medicine

Long-term and deep reprogramming of immune cells

The immune systems response to infection with SARS-CoV-2 has a significant impact on the course of COVID-19 and an overactive immune response is responsible for many serious complications. A new study demonstrates the far-reaching changes that the virus causes in the innate immune system.

The research team about the first author d. Sebastian Theobald of the University Hospital Cologne examined the effect of the spike protein, a typical feature of the coronavirus, on the innate immune system. It turns out that SARS-CoV-2 infection causes profound and long-term reprogramming of macrophages, the researchers wrote. The results of the corresponding study were published in the specialized journal .EMBO Molecular Medicine.

According to the researchers, the reason why some people with an excessive immune response to SARS-CoV-2 are still not well understood. Clearly, SARS-CoV-2 infection can lead to a massive release of inflammatory signaling substances, called cytokines, that cause severe organ damage in some infected people and lure active defense cells in tissues into a chain reaction. . How the virus releases cytokines has not been clearly established.

For the first time, researchers were able to demonstrate the effect of the spike protein on the innate immune system and found that human defense cells (macrophages, also called scavenger cells) are highly stimulated by the viral spike protein to produce the inflammatory signaling substance. interleukin 1.

However, this was only the case if the macrophages of people with COVID-19 were examined in the trials. The researchers reported that macrophages from people who had not yet been in contact with SARS-CoV-2 did not react by releasing interleukin-1.

Dr. confirms. Jan Riebniker, Head of the Infectious Disease Research Laboratory at the University Hospital Cologne. The expert also sees many starting points here to understand why some people react with an overreaction of the immune system.

Interestingly, macrophages can still be very strongly activated by the sparse protein several weeks to months after SARS-CoV-2 infection. Because macrophages have a very short lifespan of only a few days, this indicates changes in the DNA of the macrophage progenitor cells, explains Dr. Sebastian Theobald. The researchers were also able to demonstrate so-called epigenetic changes through complex sequencing experiments.

The research team continues that profound changes from macrophages to the genetic makeup of cells can now also be used to better understand the long-term consequences of COVID-19. Last but not least, the results of the study are also important in relation to vaccines, as the spike protein plays a major role in these vaccines.

For the success of different vaccine formulations, it is certainly beneficial that the spike protein leads to a strong activation of the innate immune system, says Riebnecker.

In addition, the inflammatory signaling pathway investigated here, which ultimately leads to the release of interleukin-1, is also a potential therapeutic starting point for immune-modulating therapies in severe COVID-19 cycles, and the study provides a scientific basis for this. (fp)

This text complies with the requirements of the specialized medical literature, clinical guidelines and current studies and has been examined by medical professionals.

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important note:This article is for general guidance only and is not intended to be used for self-diagnosis or self-treatment. It cannot replace a visit to the doctor.

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The innate immune system has been deeply reprogrammed - the practice of healing - BioPrepWatch

CAMBRIDGE, Mass.--(BUSINESS WIRE)--Foundation Medicine, Inc. and its collaborators announced today the presentation of new data analyzing the genomic landscape, comprehensive genomic profiling (CGP) utilization and treatment patterns among more than 11,000 men with advanced prostate cancer, including 12% with a predicted African genomic ancestry. In what is believed to be the largest known cohort of its kind, researchers found that despite similar rates of actionable gene alterations between men of European and African ancestry, men of African ancestry were less likely to receive CGP early in their treatment course and less likely to be enrolled in clinical trials. These findings highlight the importance of additional factors, beyond inherent differences in disease biology, in potentially driving disparities in outcomes. They also underscore the need to expand access to precision medicine and clinical trial enrollment. Data will be presented during an oral presentation on June 8 at the 2021 American Society of Clinical Oncology Virtual Scientific Program (ASCO21).

Prostate cancer incidence and clinical outcomes vary widely across race and ethnicity, and the underlying drivers of these outcomes are multifactorial, including systemic barriers that lead to differences in access to genomic and precision medicine. Men of African ancestry are particularly underrepresented in prostate cancer research. With this study, Foundation Medicine and collaborators at Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine, the University of Michigan and Harvard Medical School explored the interplay between ancestry and patient care.

Men of African ancestry experience the greatest burden of disease in prostate cancer, and this research indicates that differences in cancer care are not solely based on biological factors, but rather points to socioeconomic factors such as access to comprehensive genomic profiling and clinical trial enrollment, said study investigator Brandon Mahal, M.D., Assistant Professor, Radiation Oncology and Assistant Director of Community Outreach and Engagement, Sylvester Comprehensive Cancer Center. To ensure equitable opportunities for precision medicine, we need to expand access to and awareness of advances that impact patient care and outcomes, including timely use of genomic testing to help make informed treatment decisions.

The study analyzed 11,741 men with advanced prostate cancer who received CGP as part of routine clinical care, along with a subset of 897 patients with real-world clinical data from Foundation Medicine and Flatiron Healths joint clinico-genomic database (CGDB). Results showed that the rates of genomic alterations were largely similar across ancestry, including alterations in BRCA1/2, androgen receptor, DNA damage response pathway genes and actionable genes with therapy implications. Within the CGDB cohort, the proportion of patients receiving immunotherapy and PARP inhibitors was also similar across ancestry. However, men of African ancestry were less likely to receive a clinical study drug than men of European ancestry (11% vs. 30%). Further, men of African ancestry received a median of two lines of therapy prior to CGP, compared to one line of therapy for men of European ancestry, highlighting the extended time from diagnosis to implementation of precision medicine. These factors may potentially impact the genomic landscape, outcomes, and ultimately disparities.

At Foundation Medicine, we strive to better understand barriers at different stages of a patients journey and identify opportunities to mitigate disparities in cancer care. Our study highlights the need for the cancer community to understand and systematically define barriers to care across different populations, especially those traditionally underrepresented in clinical research," said study co-lead Smruthy Sivakumar, PhD, scientist at Foundation Medicine. "The results contribute to our knowledge of comprehensive genomic profiling and real-world data to better understand the barriers patients face in accessing quality cancer care a critical step toward addressing persistent disparities," added Jessica Lee, study co-lead and scientist at Foundation Medicine.

A full list of research being presented by Foundation Medicine and its collaborators at ASCO21 can be found at http://www.foundationmedicine.com/event/asco2021.

About Foundation MedicineFoundation Medicine is a molecular information company dedicated to a transformation in cancer care in which treatment is informed by a deep understanding of the genomic changes that contribute to each patient's unique cancer. The company offers a full suite of comprehensive genomic profiling assays to identify the molecular alterations in a patients cancer and match them with relevant targeted therapies, immunotherapies and clinical trials. Foundation Medicines molecular information platform aims to improve day-to-day care for patients by serving the needs of clinicians, academic researchers and drug developers to help advance the science of molecular medicine in cancer. For more information, please visit http://www.FoundationMedicine.com or follow Foundation Medicine on Twitter (@FoundationATCG).

Foundation Medicine is a registered trademark of Foundation Medicine, Inc.

Source: Foundation Medicine

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New Study Results Presented by Foundation Medicine and Collaborators at ASCO21 on Ancestry-Based Disparities in Prostate Cancer Care Underscore...

The goal of deploying two new antiviral drugs to prevent and treat COVID-19 by year end, as set by the UK Government, might not be as far-fetched as it sounds, according to plans and trials already underway said experts in the fields of virology and pharmaceuticals at a media briefing last week.

To meet the Governments challenge, antiviral drugs active against SARS-CoV-2 would most likely be administered orally, intranasally or inhaled; already be at the phase 1 or 2 stage of development or beyond; be for short-term use only; and exhibit targeted anti-viral activity without adversely affecting other parts of the body, said Ruth McKernan, PhD, chair of the BioIndustry Association. "Any drug that has more complicated administration, or has longer use, will have too high hurdles to jump," she highlighted.

A handful of candidate drugs meet these criteria and include favipiravir, niclosamide, iota-carrageenan, and molnupiravir, among others.

Despite a successful vaccination programme in the UK, there remains a pressing need for antiviral drugs to plug the gap between those protected via vaccination and those in whom vaccinations are ineffective, vaccination is contraindicated, or who choose to opt out of vaccination. New variant escape from vaccine protection also presents a threat and is likely to persist for some time to come.

Most pharmaceuticals take around 15 years from concept to market, but this development time is approximately halved in antiviral drugs, said McKernan. "The making of antivirals, along with anti-bacterial drugs has a higher probability of success than most other pharmaceuticals."

She also noted that the availability of human challenge studies where volunteers are purposefully infected with SARS-CoV-2 for study purposes were "hugely enabling" and were key given that case numbers limited the availability of trial volunteers, although there remains the possibility of conducting trials in countries with higher incidence of COVID-19.

Speaking alongside McKernan was Dr Ian Hall, professor of molecular medicine, University of Nottingham. He explained that successful candidate drugs would need to take effect early in disease where the drugs would be more effective. "Essentially, administration would be community based, so as soon as a positive test confirms infection, or as a prophylaxis in people notified as having been in contact with a positive individual. Other likely users will be those who become infected via nosocomial spread in hospitals who often have worse outcomes due to other conditions, and subgroups such as patients with haematological malignancies who typically have worse outcomes."

McKernan added that here in the UK, with government support and enablement, vaccine development had provided a good example of how to expedite manufacturing and supply issues. "This is likewise important for antiviral drugs too. In addition, the MHRA [Medicinesand Healthcare products Regulatory Agency] has also shown how it can evaluate products efficiently. However, she drew attention to maintaining a good testing and contact tracing system. "Antivirals work best early on in disease. If you cant detect, you cant treat, so you need a very good testing system."

In April, the Government announced that it was establishing a new Antivirals Taskforce to identify and deploy innovative, home-based, COVID-19 treatments as early as this autumn. Treatments would be taken after testing positive or being exposed to COVID-19 and would be aimed at reducing transmission and speeding up recovery.

Last Thursday, Eddie Gray, previously president of the European Pharmaceutical Business at GlaxoSmithKline, and CEO of Dynavax Technologies, accepted the role as chair of the new COVID-19 Antivirals Taskforce. "I do think the antiviral programme and the story around antivirals is an important one and has a real contribution to make to the overall response to COVID, and I am looking forward to moving that programme forward," he told journalists in a briefing hosted by the Science Media Centre.

Antiviral agents exert activity at the virus level, potentially interfering at one or more mechanistic stages of viral infection, for example, how the virus enters the cell, amplifies, makes new proteins, repackages itself into new viral particles, or bursts out to infect other areas of the body.

McKernan explained that there are four key ways that an anti-SARS-CoV-2 drug might work, in principle. Firstly, a drug can stop the virus entering the cell by interfering with the two main receptors that permit viral entry the angiotensin-converting enzyme (ACE) 2 receptor and/or the serine protease TMPRSS2 used for S protein priming. Secondly, because the virus needs to make new proteins, drugs can target the protein synthesis pathway of the virus specifically. Thirdly, a drug can target enzymes involved in the assembly of new viral particles called protease inhibitors; and fourthly drugs can interfere with RNA synthesis.

Good laboratory-based assays are also needed to test whether the molecules work, McKernan pointed out. "Its also necessary to have molecules that are as selective as possible so they dont interfere with other processes of the human body, making them safe to use."

Safety is essential and preclinical safety studies cannot be rushed, she stressed. "The duration of drug treatment is instrumental in the assessment of safety. If the duration is 5 days to 2-weeks then the safety hurdles are lower than a drug designed for longer duration of use."

Prof Hall is chair of the UK COVID-19 Therapeutics Advisory Panel (UK-CTAP) antiviral sub-panel. UK-CTAP was set up to advance agents most likely to be effective against COVID-19.

He explained that UK-CTAP had overseen 300 approaches with candidate drugs to tackle COVID-19. "Its impossible to study all of these and take them forward so weve strategically prioritised those drugs which have the greatest chance of success. Weve made 15 recommendations to the CMO [Chief Medical Officer] for trials in COVID-19."

The three leading recommendations are: favapiravir, an antiviral drug used for influenza and similar viruses; niclosamide (an oral antihelminthic drug used to treat tapeworm infections and which has shown activity against SARS-CoV-2 in vitro); and iota-carrageenan (a seaweed derivative and nasal spray shown to reduce symptoms of cold and flu, which has demonstrated in vitro activity against SARS-CoV-2).

UK-CTAP has considered 150 agents that currently have insufficient evidence to advance to existing clinical platforms, explained Prof Hall.

He also identified a significant challenge going forward. "To take these drugs forward through clinical trials we need to test them on patients with COVID-19. But since the vaccine strategy has been so successful to date the number of cases available is low and without sufficient cases then it is difficult to prove efficacy and pick up rare side effects."If we see escape variants it would be easier to do trials but the need for these drugs would be greater," he added.

Also in the race is molnupiravir (MK4482), a novel antiviral agent being jointly developed by pharmaceutical companies MSD and Ridgeback Biotherapeutics in the phase 3 MOVe-OUT Study.

"Molnupiravir inhibits a critical step in the replication of SARS-CoV-2, other coronaviruses and multiple RNA viruses. Early phase 2 studies show activity against SARS-CoV-2 and we believe it has potential to be a broad spectrum antiviral drug effective against a range of diverse coronaviruses as well as influenza and RSV [respiratory syncytial virus]," said Dr Daria Hazuda,vice president research, chief scientific officer, MSD.

Preclinical models suggest it can block transmission of SARS-CoV-2. Hazuda explained that based on results of a phase 2 study, the phase 3 trial will now focus on outpatient use because the highest efficacy impact on disease was seen in early community-based infection. Results are expected later in 2021.

The Prophylactic Therapy in Care Homes (NIHR-PROTECT-CH) trial platform is assessing two potential antiviral compounds in one of the most vulnerable population groups. PROTECT-CH will recruit 9300 residents across 300 UK care homes.

"Lets remember that 30-50% of COVID-19 deaths have occurred in care homes, but care homes are a highly neglected area of research," remarked Dr Philip Bath, professor of stroke medicine, University of Nottingham and lead researcher for PROTECT-CH.

Prof Bath explained that most virus enters the home with staff, relatives, or friends. Despite an effective vaccination campaign, a back-up and additional plan involving antiviral drugs is needed to prevent and treat cases in care homes. "Our vaccines are around 90% effective against the Wuhan variant but may be less so for the Kent and Indian variant, while reduction of transmission is only around 50%," he said, stressing that "vaccines dont work for everyone, and around 8% of residents and 15% of care home staff are not vaccinated".

Two antiviral drugs versus a control group will be assessed in the PROTECT-CH trial with the aim of preventing hospitalisation and mortality. The names of the trial drugs remain confidential currently, but they both have antiviral and anti-inflammatory activity, one is given by inhaler and the other intranasally.

PROTECT-CH takes a post-exposure prophylaxis approach. "We wait for a confirmed infection in the care home before randomisation (cluster randomisation of the whole care home) and treatment," explained Prof Bath, adding that as a platform, new interventions can be added over time.

The primary outcome is comprised of four-levels: no SARS-CoV-2 infection; SARS-CoV-2 infection but resident remains in care home; hospitalisation, and death.

Saye Khoo, professor of pharmacology and therapeutics, University of Liverpool, also runs a platform in the early phase trial area. He is chief investigator for the AGILE Coronavirus Drug Testing Initiative.

AGILE is in the early phase space up to phase 2 of drug development. "[The programme] takes a lot of potential candidates and advances the most plausible at speed and with rigour," he said. "Its an umbrella off which hang various trials of candidate drugs being tested at the same time. It is largely tuned to look at antiviral drugs mainly the game-changers to advance quickly and reject others."

He added that, "Vaccines do the bulk of heavy-lifting, but antivirals are important in managing the disease."

Prof Khoo drew attention to the threat of antiviral resistance without careful use. "Dont bet against the virus becoming resistant. Mutating is their core business and its how they survived for millions of years. We want to get ahead of this virus."

Prof Hall suggested that combination therapies might help prevent the development of resistance. "We have seen viruses develop resistance to other antiviral drugs. For example, by altering their genetic code, an antiviral becomes resistant to protease inhibitors as seen with hepatitis C or HIV, and here we use a combination of two or three drugs to help overcome that. It is currently, a theoretical risk in the long-term in the same way as we see variants escape from the vaccine."

Hazuda agreed but added that resistance was less likely when using an antiviral for an acute infection compared to use in a patient with chronic disease. "But we cant bet against a virus. When we start a drug development programme, it is in our interest to understand the potential for resistance."

Based on a briefing at the Science Media Centre, London, given on Thursday 27 May, 2021.

Smith and Jones report no relevant financial relationships. OR

Smith reports receiving grant funding from Merck. Jones reports no relevant financial relationships. The study was funded by Merck.

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Headway in the Challenge to Develop Two Antivirals Against COVID-19 This Year - Medscape

Samples from a study suggesting the coronavirus was circulating outside China by October 2019 have been re-tested at the World Health Organization's (WTO) request, two scientists who led the Italian research said. There is growing international pressure to learn more about the origins of the pandemic that has killed more than 3 million people worldwide and U.S. President Joe Biden last week ordered his aides to find answers.

The WHO said on Friday experts were preparing a proposal on the next studies to be carried out into the origins of the virus, but that there was no set timeline. The UN body reacted to Biden's announcement that intelligence agencies were pursuing rival theories, including the possibility of a laboratory accident in China, by saying the search was being "poisoned by politics".

COVID-19 was first identified in the central Chinese city of Wuhan in December 2019, while Italy's first patient was detected on Feb. 21 last year in a small town near Milan. However, a study published last year suggested antibodies to either the virus or a variant were detected in Italy in 2019.

That prompted Chinese state media to suggest the virus might not have originated in China, although the Italian researchers stressed the findings raised questions about when the virus first emerged rather than where. "The WHO asked us if we could share the biological material and if we could re-run the tests in an independent laboratory. We accepted," Giovanni Apolone, scientific director of one of the lead institutions, the Milan Cancer Institute (INT), said.

The WHO's request has not previously been reported. "WHO is in contact with the researchers that had published the original paper. A collaboration with partner laboratories has been set up for further testing," a WHO spokesman said.

The spokesman said the WHO was aware that the researchers are planning to publish a follow-up report "in the near future". He said the UN agency has contacted all researchers who have published or provided information on samples collected in 2019 that were reported to have tested positive for SARS-CoV-2, but does not yet have the final interpretation of the results.

The Italian researchers' findings, published by the INT's scientific magazine Tumori Journal, showed neutralising antibodies to SARS-CoV-2 in blood taken from healthy volunteers in Italy in October 2019 during a lung cancer screening trial. Most of the volunteers were from Lombardy, the northern region around Milan, which was the first and hardest hit by the virus in Italy.

"None of the studies published so far have ever questioned the geographical origin," Apolone told Reuters. "The growing doubt is that the virus, probably less powerful compared to later months, was circulating in China long before the reported cases," Apolone added.

DUTCH TEST The WHO chose the laboratory of the Erasmus University in Rotterdam for the re-test, Emanuele Montomoli, co-author of the original study and professor of Public Health at the Molecular Medicine Department in the University of Siena, said.

The Erasmus University did not reply to requests for comment. Italian researchers sent the team in Rotterdam 30 biological samples from October-December 2019 that they had found positive, 30 samples from the same period they had tested negative and 30 samples from as far back as 2018, negative.

"We sent them blind, that means our colleagues did not know which samples were positive and which negative," Apolone said. "They rechecked our samples with commercial tests, which are much less sensitive than the ones we devised and validated," Montomoli said.

Despite the differences in the two detection methods, both Italian scientists said they were satisfied with the results, delivered to them in late February, adding that they could not comment further until the team of Italian and Dutch scientists have published their findings. "We did not say in our study that we could establish without a doubt that the coronavirus, later sequenced in Wuhan, was already circulating in Italy in October," Montomoli said.

"We only found the response to the virus, namely the antibodies. So we can say that this coronavirus or a very similar one, perhaps a less transmissible variant, was circulating here in October," he added.

(This story has not been edited by Devdiscourse staff and is auto-generated from a syndicated feed.)

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WHO asks for re-checks of research on when coronavirus first surfaced in Italy - Devdiscourse

IRVINE, Calif. & AMSTERDAM--(BUSINESS WIRE)--Agendia, Inc., a world leader in precision oncology for breast cancer, announced today that an oral presentation at the 2021 American Society of Clinical Oncology (ASCO) Annual Meeting revealed new data from the national FLEX registry that identify differences in tumor biology between ethnic groups that can lead to meaningful treatment decisions, reinforcing the need for appropriate representation of diverse patient populations in breast cancer studies.

A major theme of this years ASCO meeting centers around disparities in care and outcomes, which Agendias FLEX study aims to combat by prospectively enrolling 30,000 patients from various ethnicities, ages and demographic groups representative of the total breast cancer population. The data presentation from this study, Disparities within Luminal breast cancer: clinical and molecular features of African American and non-Hispanic White patients, delivered by first author of the study Kent Hoskins, MD, Co-Leader of the Breast Cancer Research Group and Director of Cancer Genetics at the University of Illinois Cancer Center, details significant biological differences in luminal breast tumors from African American and non-Hispanic White women, suggesting that shared adverse socioeconomic exposures and/or genetic ancestry may be driving disproportionately aggressive tumor biology in African American women. This finding further underscores the need for inclusion of diverse patient groups in clinical trials to ensure equity in drug development.

The data presented at ASCO 2021 show significant transcriptomic differences between Luminal tumors from African American and non-Hispanic White patients, seen even more starkly as our study controlled for age, obesity, and genomic classification, said Dr. Hoskins. The data show ER+ breast cancers in African American women more often had upregulation of the mTOR pathway and cell cycle genes, which require different treatment approaches than other ER+ breast cancers. These data tell us that we desperately need proper representation of diverse populations in clinical trials, and future studies focused on the efficacy of these agents specifically in African American women with breast cancer, so that all patients can benefit from precision medicine, tailored to them, and accounting for their ancestry and genomic profiles.

Additional data from Agendia regarding breast cancer in African American women was shared in an abstract titled Genomic risk classification by the 70-gene signature and 21-gene assay in African American, early-stage breast cancer patients. This study was triggered by recent research showing less accurate prognostic performance of OncotypeDX in African American women with early stage breast cancer. The abstract compared MammaPrint and OncotypeDX results in a cohort of African American women with ER+ breast cancer, and observed an overall discordance of 51% between the two tests in African American patients; notably, of tumors with a TAILORx intermediate risk score (11-25), 61% were classified as MammaPrint High Risk. Combined with previously published data in African American patients, 57% of OncotypeDX low risk score tumors are re-classified as MammaPrint High Risk, suggesting that OncotypeDX results could be less accurate in African American patients.

In addition, recent data indicate that African American patients who receive a low or intermediate OncotypeDX risk score have higher recurrence rates and lower survival than Caucasian patients with early stage breast cancer with the same risk score, a difference that can have meaningful clinical implications and requires further investigation.1

It is essential that genomic tests either work consistently across diverse groups of patients, or have the ability to be calibrated to do so, said Patricia Robinson, MD, Associate Professor of Hematology and Oncology at Loyola University Medical Center, and Assistant Dean of Diversity, Equity and Inclusion at the Strich School of Medicine, We cannot be using genomic tests that work for some people and not others, or accepting that the tests, which offer such crucial information, work better for some than for others. While the clinical evaluation of the discrepancy between OncotypeDX and MammaPrint may be ongoing, this data still captures the diversity of pathways driving tumor metastasis, and reinforces the importance of proper representation in trials and in test development and optimization.

Agendias large-scale, prospective FLEX registry continues to highlight data from real-world practices in one of the most flexible and inclusive studies in breast cancer research to date, playing an important part in the companys mission to help guide the diagnosis and personalized treatment of breast cancer for all patients throughout their treatment journey.

About Agendia

Agendia is a precision oncology company headquartered in Irvine, California, committed to bringing patients with early stage breast cancer and their physicians the information they need to make the best decisions for the full treatment journey. The company currently offers two commercially-available genomic profiling tests, supported by the highest levels of clinical and real world evidence, that provide comprehensive genomic information that can be used to identify the most effective breast cancer treatment possible for each patient.

MammaPrint, the 70-gene breast cancer recurrence assay, is the only FDA-cleared risk of recurrence test backed by peer-reviewed, prospective outcome data and inclusion in both national and international treatment guidelines. BluePrint, the 80-gene molecular subtyping assay, is the only commercially-available test that evaluates the underlying biology of a tumor to determine what is driving its growth. Together, MammaPrint and BluePrint provide a comprehensive genomic profile to help physicians make more informed decisions in the pre- and post-operative treatment settings.

Agendia develops evidence-based novel genomic tests and forges partnerships with groundbreaking companies to develop next-generation digital treatment tools. The ongoing research builds an arsenal of data that improve patient outcomes and support the evolving clinical needs of patients with breast cancer and their physicians every step of the way, from initial diagnosis to cancer-free.

Agendias assays can be ordered on core biopsies or surgical specimens to inform pre- and post-operative treatment decisions. For more information on Agendias assays and ongoing trials, please visit http://www.agendia.com.

1 Hoskins, Kent F., et al. Association of Race/Ethnicity and the 21-Gene Recurrence Score With Breast CancerSpecific Mortality Among US Women. JAMA Oncology, vol. 7, no. 3, 2021, p. 370., doi:10.1001/jamaoncol.2020.7320.

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ASCO 2021 Podium Presentation on Agendia FLEX Study Shows Clinical & Molecular Differences in Tumors of African American and Caucasian Patients...

Medical researchers say within a few years major breakthroughs in blood testing technology that use immune system response and genetic analysis to identify disease quickly and cost-effectively will be on the market.

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One morning last May, Tayah Fernandes's mother Shannon realized her four-year-old daughter was seriously unwell, and rushed her to the nearest ER in the English city of Manchester. The coronavirus had crashed onto Britain's shores weeks earlier, and emergency doctors were initially uncertain how best to treat Tayah's constellation of symptoms, which included stomach pains and a bright red rash.

They gave her antibiotics for a suspected bacterial infection, but her condition only worsened, her fever spiking. For her parents, for any parents, this was the ultimate medical nightmare; doctors in the dark for days over the cause of their daughter's illness.

Eventually, after further blood tests, physicians decided Tayah was suffering from an unusual inflammatory syndrome that pediatric infectious disease specialists had only just started to see, but suspected had links to Sars-COV-2.

Young patients across the U.K. and U.S. were arriving in intensive care units with symptoms similar to another disease doctors already recognized, called Kawasaki. But they had no guarantee that the same course of treatment injecting a solution of donors' antibodies into the bloodstream would prove successful.

In Tayah's case the antibodies solution, known as immunoglobulin, worked, to her parents' relief. But at around that same time last May a team of researchers at Imperial College, London confirmed through complex analyses of blood samples, taken from patients like Tayah, that this was indeed a new disease, distinct from Kawasaki.

A related breakthrough in that same laboratory, focused specifically on the way individual genes behave, could have seismic implications for a multi-billion dollar diagnostics sector that has received unprecedented attention from patients, regulators and the business world over the course of this pandemic.

A new method for identifying a specific illness from blood samples relies on the correlation between the activity in small set of genes, which represents the immune response, and specific pathogens that cause a specific disease just as the poliovirus causes polio, the coronavirus (SARS-COV-2, a pathogen) causes Covid-19. Scientists believe that by studying a small number of genes, they can quickly discern which pathogen is in a patient's system, what disease they have, and so how best to treat them.

Companies from small research university spin-offs to industry giants like Abbott Laboratories and Danaher's Cepheid are looking to build on two decades of research into the way our own immune systems naturally respond to foreign substances in our bodies, including pathogens like bacteria or viruses. A current technology like Cepheid's GeneXpert technology is able to distinguish between the different RNA of various viruses, such as SARS-COV-2, or a particular influenza strain, but experts say it's become increasingly clear that our body's immune systems can be faster, more accurate detection systems.

Historically, doctors have had to rely on a patient's case history and symptoms to narrow down the cause of an illness and develop a treatment plan. More recently, laboratory inspections at the molecular level such as the Cepheid technology have allowed clinicians to identify specific pathogens in nasal mucus, throat swabs or blood samples that might have caused an illness. But hunting for bacteria or a virus in this way can be time-consuming, costly and sometimes simply ineffective. The specific RNA signature of a virus can be hard to detect.

Abbott and Cepheid did not respond to requests for comment.

The team at Imperial College, London, working separately but at the same time as several counterparts around the world, are now convinced that future diagnoses can soon be conducted using table-top tests that will take just a matter of minutes.

These tests would not explicitly screen for a specific pathogen, but instead, allow scientists and medical professionals to simply watch how specific genes in the body are behaving as an indication of how an immune system is already responding to a pathogen that may not be easily otherwise detectable.

Imperial College professor Mike Levin currently leads an ongoing European Union-funded study focused on this potential, called "Diamonds." In recent years he and other scientists have shown how the observed activity in a small number of our genes can work as a kind of shorthand for our body's immune response to a pathogen. If a handful of specific genes out of thousands in a blood sample are seen to be activated or the opposite, inhibited it can indicate that a person is preparing to fight off a specific pathogen.

We think this is a completely revolutionary way of doing medical diagnosis.

Imperial College professor Mike Levin

Levin and colleagues already have a proof of concept for this diagnostic approach after studies involving thousands of patients with fever caused by tuberculosis, and hundreds of Kawasaki patients. And his Imperial College team's work with the "Diamonds" study are starting to bear fruit and could helpidentify the distinct immunological markers of illnesses like the coronavirus-linked multi-system inflammatory syndrome in children like Tayah Fernandes, now commonly known as MIS-C.

When Covid-19 turned up in multiple locations, with MIS-C in its wake, it presented Levin and his researchers with an unprecedented opportunity to test this technique on an entirely new disease.

In the future, these tests by relying on huge amounts of data and machine learning should be able to produce multi-class rather than just binary results. This means they could confirm not only if a pathogen is bacterial or viral, or whether someone has a specific disease or not, but could distinguish which one of a multitude of illnesses is afflicting their patient.

In short, Levin expects that by examining the behavior of a relatively small number of genes, clinicians will be able to assign patients to all the major disease classes within an hour.

"We think this is a completely revolutionary way of doing medical diagnosis," Levin said. He expects the research will provide the basis for new technology, but has no financial interest in any business related to it.

Rather than what he calls the "stepwise process" of first eliminating bacterial infections, treating for the most common conditions, and then doing more investigation, "this idea is the very first blood test can tell you, has the patient got an infection or not an infection, and what group of infection that is, right down to the individual pathogens."

Purvesh Khatri, an associate professor at the Stanford Institute for Immunity, Transplantation and Infection and Department of Medicine, says our immune systems have been evolving for millennia to combat pathogens, and so it may prove more effective, and efficient, to examine the response of our bodies.

"We didn't have a technology, until now, that could measure a set of genes in a rapid point of care way," he said. "But in the last couple of years, there have been enough technologies available that now allow us to measure a few genes in a rapid multiplex point of care assay way."

While neither the FDA nor any European regulators have approved these kinds of gene-based pathogen detection systems, Khatri, who is helping launch a related commercial venture, says they're coming soon. "In the next year or two, there will be several that will be available on the market."

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Theranos is history, but big blood testing breakthroughs are coming post-Covid - CNBC

A team of researchers received a $1 million grant late last month to study how memory cells recall past events when responding to attacks on the immune system and injuries on the skin.

The projects lead researchers said the team is looking into how memory T cells can memorize certain events, like an attack from a virus, and recall that memory once those events appear a second time. Rong Li, the chair of the Department of Biochemistry and Molecular Medicine in the School of Medicine and Health Sciences and the lead researcher on the project, said the team hopes to learn the molecular process these memory cells use to recall past events and to eventually mimic this process in treatments like cancer therapies and inflammation care.

That phenomena has been around for quite some time, Li said. But really, at the molecular level, at the cellular level, you ask really the fundamental question, In that case, how did cells remember that? That is really what this grant is about.

Li said the three-year grant from the W.M. Keck Foundation is exclusively for pre-clinical work, meaning the funds will cover the investigation of animal models and molecular tools. But he said if his research team is successful at working with the animal models, their findings could be applied to humans.

It would be very interesting to, for example, take human memory T cells from cancer patients, culture them in a laboratory setting and then introduce this human version of that key molecule back into those memory T cells and then put them back in the same cancer patient and see whether that can boost the hosts immune system to fight tumors, Li said. We are very excited about the long-term potential.

Li said the key to this research is the different expertise of each member of the research team.

He said he comes from the molecular biology perspective, while Brett Shook, an assistant professor of biochemistry and molecular medicine, is looking at this research through a physiology lens, including the healing of skin cell wounds and inflammation. He said other contributing researchers are helping with the immunological side of the research.

Shook said the team is applying an irritant to mices skin and then will precisely manipulate one gene at a time to determine the effect it has on memory. He said they can use tools in their lab to express a gene at a higher level than its typically expressed to try to emphasize a memory in certain cells, or they can eliminate the gene of interest entirely, completely disrupting the cells ability to remember any previous events.

Shook said the researchers are using these mice models to observe skin inflammation to determine how the memory cells respond.

He said they first apply an irritant to mices skin, which will cause inflammation in the tissue and eventually a rash. The researchers then manipulate the specific gene in the mice, which they believe controls the skin cells memory of the inflammation, and then reapply the irritant to determine whether the memory cells can recall the event and eliminate the rash more quickly.

Anytime you have a rash, that area now has some memory of inflammation, Brett said. We are able to injure the same area, and what has been documented is that regions of skin that have previously experienced inflammation will heal faster.

Experts in medicine and infectious diseases said this research is a relatively unexplored area and the findings could pave the way for enhanced cancer treatments.

Joaquin Madrenas, a professor of medicine at UCLA, said the implications of this research are very important, especially in terms of immunological memory. He said vaccines give the immune system exposure to foreign antigens so that upon exposure, the immune system can mount a memory response.

If we know what is the mechanism to induce memory, you can make better vaccines that will ensure the development of long lasting memory, Madrenas said.

Madrenas said studying cellular memory may also help cancer patients, especially those with types of cancer associated with a lack in immune response.

If you know the mechanisms of memory, you can induce memory in the immune system of a patient that can then get rid of the cancer and keep the cancer from growing, Madrenas said.

He said laboratory mice are inbred animals that are kept under clean conditions and should have no history of exposure to infections, making the task of translating the research findings to humans complicated.

We live in a completely exposed and uncontrolled environment, Madrenas said. Each one of us has a completely different antigen history. Your exposure to different viruses and bacteria and other infectious diseases is very different from mine, so the ability to manipulate your memory pool may be very different from mice.

Girish Kirimanjeswara, a professor of immunology and infectious diseases at Pennsylvania State University, said studying memory cells allow researchers to understand how the body encounters and responds to infectious diseases. He said this area of research is relatively less explored and this project could pave the way for a deeper understanding of how immune cells can recall a past exposure to a virus or cancer.

While we know how memory T cells may recognize a second encounter of a foreign substance, we are still learning about how these cells may be regulated, how long can they last, how do they function at various times etc, he said in an email. This research will explore many of those areas and also study the inherent cellular memory.

This article appeared in the March 8, 2021 issue of the Hatchet.

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Medical school researchers receive grant to study cell memory - GW Hatchet

--(BUSINESS WIRE)--Leaps.org:

WHAT:

COVID Vaccines and the Return to Life: Part 1 First of four virtual symposiums reviewing the most pressing, timely questions around the COVID-19 vaccines. Featuring leading scientific and medical experts, marking the one-year anniversary of the global declaration of the COVID-19 pandemic.

Topics include: the effect of the new circulating variants on the vaccines, what we know so far about transmission dynamics post- vaccination, the myths of good and bad vaccines as more alternatives come on board, and more. Public Q&A will follow the expert discussion.

WHEN:

Thursday, March 11, 2021

12:30 1:45 pm EST / 9:30 10:45 am PST

WHO:

Co-Host: Kira Peikoff, Editor-in-Chief, Leaps.org

Monica Gandhi, M.D., MPH, Professor of Medicine and Associate Division Chief (Clinical Operations/ Education) of the Division of HIV, Infectious Diseases, and Global Medicine at UCSF/San Francisco General Hospital.

Paul Offit, M.D., Director of the Vaccine Education Center, attending physician in infectious diseases at the Childrens Hospital of Philadelphia, and advisor to CDC and FDA vaccine committees.

Onyema Ogbuagu, MBBCh, Associate Professor at Yale School of Medicine and Yale Medicine infectious disease specialist treating COVID-19 patients and leading Yales COVID-19 vaccine trials.

Eric Topol, M.D., cardiologist, scientist, professor of molecular medicine, and the director and founder of Scripps Research Translational Institute.

CO-HOSTS:

Aspen Institute Science & Society Program

SabinAspen Vaccine Science & Policy Group

With generous support from the Gordon and Betty Moore Foundation and the Howard Hughes Medical Institute.

REGISTER:

https://leaps.org/covid-vaccines-and-the-return-to-life-part-1/

Leaps.org is a not-for-profit program within the Good Worldwide ecosystem, which also includes Upworthy a media platform that reaches over 150 million people monthly whose mission is to share the best of humanity and inspire others to do the same.

Leaps.org publishes award-winning journalism, popularizes scientific progress on social media, and hosts forums about innovation, ethics, and the future of humanity. Leaps.orgs projects and activities are supported by a consortium of like-minded partners including the Aspen Institute Science & Society Program, and supporters Leaps by Bayer, the Gordon and Betty Moore Foundation and the Howard Hughes Medical Institute.

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Leaps.org & Aspen Institute Feature COVID Vaccines & the Return to Life, March 11 Webinar with Major Health & Science Experts - Business...

A new study has revealed that immunoglobulin-M antibodies recognise microvesicles, which are critical for the progression of thrombosis.

A new study has revealed the important role of immunoglobulin-M (IgM) antibodies in preventing thrombosis. The researchers, from the CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences and the Medical University of Vienna, both Austria, say that these antibodies recognise microvesicles, which are membrane blebs shed by cells and recognised for their critical role in thrombosis, so therefore prevent pro-thrombotic effects.

According to the authors, earlier studies have demonstrated that people with a low number of IgM antibodies have an increased risk for thrombosis. The team also previously demonstrated that a high percentage of natural IgM antibodies bind oxidation-specific epitopes, molecular structures that are present on dying cells and serve as signals for the immune system.

In the new study, the researchers identified the mechanisms explaining the anti-thrombotic effects of natural IgM antibodies. They demonstrated that the antibodies that bind oxidation-specific epitopes can prevent coagulation and thrombosis induced by microvesicles. This provides a mechanistic explanation for the previously published observation that low levels of these antibodies are associated with an increased risk of thrombosis.

We assume that natural IgM antibodies recognise microvesicles that are particularly pro-inflammatory and pro-coagulant, say the scientists in their paper.

In experiments on a mouse model and directly on human blood samples, the scientists were able to show that the addition of IgM antibodies inhibited blood clotting caused by specific microvesicles and protected mice from lung thrombosis. Conversely, it was also shown that depletion of the IgM antibodies increased blood clotting.

The study for the first time provides an explanation why people with a low number of natural IgM antibodies have an increased risk of thrombosis, write the authors.

The results offer high potential for novel treatments to reduce the risk of thrombosis. Influencing IgM antibody levels in high-risk patients could be a viable addition to the previously established blood thinning treatment, as this is also known to be associated with side effects such as an increased tendency to bleed in the case of injuries, said principal investigator Professor Christoph Binder.Microvesicles are already recognised as an important component of blood coagulation. However, our study created a novel possibility of targeting them therapeutically for the first time.

The study was published in Blood.

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Study shows role IgM antibodies play in preventing thrombosis - Drug Target Review

From the start of the COVID-19 pandemic, diagnostic testing has been highlighted as a key part of global measures to contain the spread of SARS-CoV-2. In a media briefing on March 16, 2020, Dr Tedros Adhanom Ghebreyesus, WHO Director-General, remarked that testing, isolation and contact tracing were the backbone of the response and urged all countries to test, test, test.RT-qPCR testing, which detects SARS-CoV-2 genetic material present in a patient sample, quickly became the predominant method used to identify infected individuals. However, several claims and allegations about the capabilities and value of PCR have been circulated throughout the course of the pandemic, leading to questions about its use.

To address these misconceptions and communicate the true strengths and limitations of the technology, a group of PCR experts recently published a commentary in the International Journal of Molecular Sciences. Technology Networks had the pleasure of speaking to Professor Stephen Bustin, professor of molecular medicine at Anglia Ruskin University, and lead author of the commentary, to learn more about some of the facts and fallacies highlighted.

The views and opinions expressed below are those of Stephen Bustin and do not necessarily reflect the official policy or position of Anglia Ruskin University.

Anna MacDonald (AM): RT-qPCR was quickly adopted at the start of the pandemic as the predominant method of detecting SARS-CoV-2. Can you describe some of the key strengths of the technology that made it a suitable choice?Stephen Bustin (SB): Indeed, the first three PCR tests for SARS-CoV-2 were designed within a day of its genome sequence having been published by Chinese scientists. Such lightning speed is unthinkable with any antigen-based test, hence PCR being the predominant method. Furthermore, a properly designed, optimized and validated RT-qPCR test is the most sensitive, specific, reliable and robust method for detecting a pathogen. Current protocols are not as fast as antigen tests, but they will be so in the future (see below).

Crucially, RT-qPCR tests are also easily modified to accommodate the appearance of mutations and variants and so are characterized by exceptional flexibility, an important advantage when dealing with an RNA virus that, against initial expectation, continually and rapidly changes. Once genetic changes that characterize variants have been identified by sequencing, it is straightforward to design tests and, crucially, use them immediately. Again, this is unlike antigen tests, that require the development and production of new antibodies, a process that takes months and is very expensive. PCR tests can distinguish the original virus from the variant even if they differ by only a single nucleotide change (e.g., variant B.1.1.7 N501Y which has a nucleotide change of A to T within the sequence coding for the spike protein).

Although mainstream PCR instruments take between 30 minutes and 1.5 hours to complete a test, a combination of fast protocols and instruments can reduce that time to less than 15 minutes. Even that does not fully exploit the potential of this technology, with extreme PCR shown to complete a test in less than 20 seconds. I have no doubt that in a year or twos time such instruments will be available commercially. Furthermore, there will be inexpensive hand-held personal and point-of-care devices that will give rapid results when and where needed.

AM: Several claims have been made suggesting that PCR-based testing is not fit for purpose. What has led to these allegations and what effect is this misinformation having?SB: These sentiments arise from the deliberate spreading of false information, coupled with misleading quotes and incomplete reporting. They are made by people who have little knowledge and no understanding of the technology, but are articulate and rely on the general publics ignorance and lack of interest in scientific detail. The media also are at fault, because they have generally failed to distinguish between authoritative scientific conclusions based on data and facts versus false and unreliable opinions based on mendacity and sophistry.

The most common falsehood is that the inventor of PCR, Kary Mullis, claimed that PCR should not be used for diagnostics. He did make an unfortunate comment about the reliability of diagnostic testing, but this related specifically to the detection of HIV in AIDS patients, was aimed at conventional gel-based PCR and was made in 1993, before real-time (qPCR) was in use as a diagnostic tool. I knew Kary Mullis personally and I know for certain that this was not his opinion as we discussed, and he was interested, in the use of RT-qPCR as a prognostic tool for colorectal cancer patients.

Without a shadow of a doubt, qPCR is highly suitable for diagnostic testing for pathogens for at least three reasons: (1) it has two levels of specificity that minimize the risk of false positive results, (2) its sensitivity minimizes the risk of false negative results and (3) as a closed-tube procedure amplified DNA is never released into the environment, minimising the chances of contamination. In a way we are seeing the same dishonest campaign resurrected that caused so much unnecessary heart-ache in the late 1990s concerning the MMR vaccine and autism.

These operations are driven by callous individuals and groups with an agenda, and unfortunately are not open to persuasion of any kind. PCR testing is just another topic that has become entangled in todays doctrine that feelings and opinions matter as much or, indeed, more than facts, a phenomenon that has become familiar in politics, education as well as in a health-related environment. Whilst it is easy to come up with a simple slogan that denigrates something and reduces a complex issue to a single catch phrase, it takes much longer to explain that matter adequately and sensitively. Ultimately, there is an obnoxious fringe element in our society that is not interested in listening or learning and, sadly, there is neither vaccine nor cure for stupidity. A serious consequence of this trend is that the public is unable to distinguish genuine scholarship and balanced expert advice from snake oil peddled by fraudsters and charlatans.

AM: Can you explain the main causes of false-positive or false-negative results and what can be done to reduce the chances of them occurring?SB: False positive results in a properly validated and CE-marked PCR test are caused by contamination or by inappropriate interpretation of the results. Contamination can be introduced during the sampling procedure, the extraction process or the dispensing of reagents for the PCR test. This is routinely detected by including appropriate negative controls at every stage, i.e., samples that do not contain the target RNA or DNA. These controls must always be negative; if they are and a PCR result is positive, this means that whatever target was being amplified is present. This is especially important when there is very little target present and the analysis generates results near the tests limit of detection. The analytical sensitivity of a PCR test refers to the smallest amount of target in a sample that can be detected and in theory this is a single molecule. It goes hand in hand with its analytical specificity, which describes the ability of the test to detect one specific target, e.g., SARS-CoV-2, as distinct from, say SARS-CoV.

However, both are different from diagnostic sensitivity and specificity, the former referring to the ability of the test to identify individuals who are infectious and the latter to its ability to identify correctly those without the disease. Hence a true PCR positive may well not be detecting infectious virus, for example if the individual has been asymptomatic for a couple of weeks after coming down with a disease and, whilst a few virus particles or nucleic acid fragments are present, they are not clinically relevant. Hence the interpretation of the test was at fault, not the test itself. This is a real problem for two reasons (1) the infectious dose of SARS-CoV-2 is still unknown and (2) the qPCR result output is the quantification cycle (Cq), which is not an objective value but differs with instruments, reagents and operators. Monitoring a combination of parameters that include symptoms, probability of infection and PCR results is the best approach to minimize false clinical positives.

False negatives, on the other hand, can be caused by sample degradation during handling or storage, which can be especially problematic with RNA, the presence of inhibitors, poor testing protocols, inexperienced staff not following proper procedures and, least likely, reagent failure. It may also be that the sample taken from an individual did not contain any virus or so little that it got lost or excessively diluted during the extraction procedure. This is of course why a negative test result is really a presumptive negative and a second test a day or so later could well result in a positive result, if the individual is in the early stages of infection.

AM: In 2009, you published the MIQE guidelines, with the aim of encouraging better experimental practice and more reliable interpretation of qPCR results. Have COVID-19 tests been developed using these guidelines? How could the guidelines be applied to improve the use of qPCR testing?SB: The MIQE guidelines were aimed at the research community, where new tests targeting a multitude of targets are being constantly developed and where it is difficult to compare the results generated in one laboratory with those obtained in another one. Furthermore, they deal with quantitative testing, which is somewhat different from testing for SARS-CoV-2.

However, the guidelines are relevant as they call for transparency with regards to assay design, reporting of test performance and interpretation of results. Researchers and companies have done a sterling job in developing a range of tests that are sensitive and specific and continue to monitor the emergence of new strains to ensure that their tests continue to generate reliable results. There should be more openness with regards to sharing the sequence details of the various tests in use, but the information provided is generally sound and informative.

However, the main issue that has caused some problems with the reliability of testing is the sampling, transport and extraction workflow, which is far from optimal. There are numerous different reagents and protocols, variable skill levels of those taking the samples, different time lines within the transport practice and inconsistent storage conditions as well as different RNA extraction and concentration procedures that all combine to increase the variability of test results, especially when comparing different test centres within or between different countries. There is an urgent need to develop a clear set of guidelines for optimal sample collection, which should be from saliva for SARS-CoV-2 as well as for RNA extraction, which would help standardize and so make the whole process more reliable.

AM: The use of qPCR to quantitate viral load is a particular area of concern. What are the main challenges of using the technique for this purpose? Are there any steps that can be taken to reduce the ambiguity of results?SB: First of all it is important to distinguish between infectious dose and viral load. It is still unknown what the infectious dose is for SARS-CoV-2, i.e., the amount of virus required to make a person sick. Its ease of transmission suggests that it may be quite low, but this might be 100, 1,000 or 10,000 viral particles. A higher infectious dose could result in a higher viral load, which describes the amount of virus replicating within the cells of an infected individual. There is evidence that higher viral loads result in more severe symptoms and may be associated with a worse outcome as well as lead to more shedding of whole virus by the infected individual.

A standard qPCR test cannot record exact viral copy numbers, as the test result for a positive sample only records a PCR cycle number, e.g., 25.5. This means that the instrument first detected the presence of a target after 25.5 cycles, and whilst a lower Cq value suggests that there is more target present, without additional information it is impossible to tell how much more. This requires knowledge of the amplification efficiency, since it is obvious that a more efficient test will record a lower Cq earlier than a less efficient test.

Quantification also requires the addition of standards, ideally certified reference RNA of known copy number, that amplify at specific PCR cycle numbers. The cycle number of the virus can then be related directly to that standard and give a measure of quantity. Unfortunately, such standard still do not exist. There is a related technology, called digital PCR, which can provide absolute counts of viral copy number. However, this technology is not suited to mass testing and it is expensive. The best solution, for the time being is to record a test result as positive or negative and interpret that result within the individual clinical context and, if in doubt, repeat a day or so later.

AM: In what ways do you think the pandemic has shaped the future of PCR?SB: Undoubtedly there will be a huge demand for continued, rapid testing at hospitals, care homes, nurseries, airports, cruise liners etc, initially for SARS-CoV-2 but extending to other respiratory viruses as well as fungal and bacterial pathogens. This will drive the development of easy-to-use sampling, extraction and testing devices that can rapidly test multiple samples with little or no operator intervention.

At the same time there will be an increasing demand for more personal devices, such as hand-held microfluidics-based systems where you can add a small amount of saliva, blood, urine or faecal matter and get a rapid test result in the privacy of your own home, at the GPs surgery or even at the chemists. The speed potential of the PCR and its ability to detect numerous targets all at the same time are still largely unexplored and the focus on improving current protocols and introducing new instrumentation and improved reagents will only serve to make PCR even more ubiquitous than it is now.

Reference: Bustin S, Mueller R, Shipley G, Nolan T. COVID-19 and diagnostic testing for SARS-CoV-2 by RT-qPCRfacts and fallacies. Int J Mol Sci. 2021;22(5):2459. doi:10.3390/ijms22052459

Professor Stephen Bustin was speaking to Anna MacDonald, Science Writer for Technology Networks.

Continued here:
RT-qPCRFacts and Fallacies: An Interview With Professor Stephen Bustin - Technology Networks