Dr. Cong Zeng and colleagues in their recent study provide evidence that, SARS-CoV-2 spreads through cell-cell contact in cultures, mediated by the spike glycoprotein, which is promoted by cell-cell fusion. Their study recently appeared in bioRxiv.
Viruses can spread in cultured cells and tissues by two fundamentally distinct modes: cell-free or direct cell-cell contact. The latter mode of viral transmission normally involves tight cell-cell contacts, sometimes forming virological synapses, where local viral particle density increases, resulting in efficient transfer of virus to neighbouring cells. Additionally, this transmission has the ability to evade neutralization, accounting for efficient virus spread and pathogenesis, as has been shown for HIV & HCV.
“In this work, we evaluated cell-to-cell transmission of SARS-CoV-2 in the context of cell-free infection and in comparison to SARS-CoV.”
— wrote authors of the study
They discovered that SARS-CoV-2 spike is more efficient in mediating cell-to-cell transmission than SARS-CoV spike, yet the spike of SARS-CoV is more capable of mediating cell-free infection.
“To our knowledge, this is the first direct comparison of cell-to-cell transmission vs. cell-free infection between SARS-CoV-2 and SARSCoV in cultured cells, and the results provide important insights into two distinct modes of infection and the host-viral factors that regulate these processes.”
— wrote authors of the study
But, why is SARS-CoV-2 spike more efficient than SARS-CoV spike for mediating cell-to-cell transmission in cultured cells? Well, this is in part related to the higher cell-cell fusion activity of SARS-CoV-2 spike compared to SARS-CoV. However, they also recognized that extensive cell-cell fusion by SARS-CoV-2 spike can lead to giant syncytia formation (or you can say black fungus) and cell death, which in turn reduces cell-to-cell transmission. Therefore, fine control of the spike induced cell-cell fusion is important for efficient cell-to-cell transmission and, therefore, the spreading infection of SARS-CoV-2.
In addition, it has been found that, although ACE2 enhances cell-to-cell transmission of SARS-CoV-2 and SARS-CoV, but it is not absolutely required.
Finally, they compared the sensitivity of cell-to-cell transmission vs. cell-free infection of SARS-CoV-2 to treatments by neutralizing monoclonal antibodies and COVID-19 convalescent plasma – both of which have been approved by the FDA for emergency use. They found that while cell-free infection of SARS-CoV-2 was almost completely blocked by these treatments, cell-to-cell transmission of SARS-CoV-2 was, to a large extent, refractory.
“While in this work, we obtained evidence that SARS-CoV-2 spike more efficiently mediates cell-to-cell transmission than the SARS-CoV spike, a direct comparison using authentic viruses of both, especially in primary human lung and airway epithelial cells, is needed. Ultimately, we must determine the role, if any, of cell-to-cell transmission of SARS-CoV-2 in disease progression and pathogenesis in COVID-19 patients.”
Reference: Cong Zeng, John P. Evans, Tiffany King, Yi-Min Zheng, Eugene M. Oltz, Sean P. J. Whelan, Linda Saif, Mark E. Peeples, Shan-Lu Liu, “SARS-CoV-2 Spreads through Cell-to-Cell Transmission”, bioRxiv 2021.06.01.446579; doi: https://doi.org/10.1101/2021.06.01.446579
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The etiology of HPV -HNSCC is linked to expression of the HPV oncoprotein, E6, which influences tumor formation, growth and survival.
E6 effects this oncogenic phenotype in part through inhibitory protein-protein interactions and accelerated degradation of proteins with tumor suppressor properties, such as p53 and caspase 8. Interfering with the binding between E6 and its cellular partners may therefore represent a reasonable pharmacological intervention in HPV tumors.
In this study, the authors probed a small-molecule library using AlphaScreen™ technology to discover novel E6 inhibitors.
Further testing of this analog in a panel of HPV and HPV– cell lines showed good potency and a large window of selectivity as demonstrated by apoptosis induction and significant inhibition of cell growth, cell survival in HPV cells.
Dr. Penelope J. Duerksen-Hughes from The Loma Linda University said, “Head and neck squamous cell carcinomas (HNSCC) are heterogeneous tumors that arise in the upper respiratory tract and are the 6th most common cancer worldwide by incidence.“
“Head and neck squamous cell carcinomas (HNSCC) are heterogeneous tumors that arise in the upper respiratory tract and are the 6th most common cancer worldwide by incidence.“
In parallel, HPV -HNSCC, which is caused by HPV, has risen dramatically within the same period.
Compared to its HPV- counterpart, HPV -HNSCC carries a more favorable prognosis and is more prevalent in younger and otherwise healthier patients.
HPV oncoproteins, particularly E6, represent a unique and potentially therapeutically favorable strategic approach for targeted HPV -HNSCC treatment.
These findings are corroborated by findings that have shown that the absence of p53 and caspase 8 in HNSCC is correlated with attenuation of sensitivity of HPV -HNSCC to chemotherapy and radiation.
Consistent with this, genetic tools such as CRISPER, TALEN gene knockouts, RNAi and other agents that indirectly knock down E6 mRNA have demonstrated that depleting the protein abundance of E6 leads to anti-proliferative effects and enhances the response of HPV cells to chemotherapy agents and radiation.
The Duerksen-Hughes Research Team concluded in their OncotargetResearch Output, “the evidence we have gathered suggests that GA-OH can serve as a basis for better understanding the mechanism of E6 inhibition, and has the potential for further development to improve potency and drug-likeness. Tools such as computational modelling and medicinal chemistry can utilize this inhibitor as a good starting point for optimization and in understanding important interactions between E6 and its inhibitors.“
Reference Chitsike L., Yuan C., Roy A., Boyle K., Duerksen-Hughes P. J. A high-content AlphaScreen™ identifies E6-specific small molecule inhibitors as potential therapeutics for HPV+ head and neck squamous cell carcinomas. Oncotarget. 2021; 12: 549-561. Retrieved from https://www.oncotarget.com/article/27908/text/
Aging published “Cdkn1a transcript variant 2 is a marker of aging and cellular senescence” which reported that cellular senescence is a cell fate response characterized by a permanent cell cycle arrest driven primarily the by cell cycle inhibitor and tumor suppressor proteins p16Ink4a and p21Cip1/Waf1. In mice, the p21Cip1/Waf1 encoding locus, Cdkn1a, is known to generate two transcripts that produce identical proteins, but one of these transcript variants is poorly characterized.
The authors show that the Cdkn1a transcript variant 2, but not the better-studied variant 1, is selectively elevated during natural aging across multiple mouse tissues.
Importantly, mouse cells induced to senescence in culture by genotoxic stress upregulated both transcripts, but with different temporal dynamics: variant 1 responded nearly immediately to genotoxic stress, whereas variant 2 increased much more slowly as cells acquired senescent characteristics.
Upon treating mice systemically with doxorubicin, which induces widespread cellular senescence in vivo, variant 2 increased to a larger extent than variant 1. Variant 2 levels were also more sensitive to the senolytic drug ABT-263 in naturally aged mice.
Upon treating mice systemically with doxorubicin, which induces widespread cellular senescence in vivo, variant 2 increased to a larger extent than variant 1.
Thus, variant 2 is a novel and more sensitive marker than variant 1 or total p21Cip1/Waf1 protein for assessing the senescent cell burden and clearance in mice.
Dr. Judith Campisi from The Buck Institute for Research on Aging as well as The University of California said, “The stringent cell growth arrest associated with cellular senescence is determined, among other mechanisms, by activities of cyclin-dependent kinase inhibitor proteins p16Ink4a and p21Cip1/Waf1, encoded by the Cdkn2a and Cdkn1a loci, respectively.”
The increased expression of these proteins is a major hallmark of senescence in most cells, and therefore have become markers of senescence both in culture and in vivo.
Consistent with the fact that senescent cells increase with age in many mouse and human tissues, Cdkn2a mRNA levels also increase with age in these tissues.
To date, possible changes in the expression of Cdkn1a transcript-specific variants during age or cellular senescence have not been explored.
The authors also analyze expression levels in a cell culture model of mouse cells subjected to genotoxic stress-induced senescence to evaluate their relative utility as senescence markers both in culture and in vivo.
The Campisi Research Team concluded in their AgingResearch Output that it remains unexplored the possibility that the different transcript variants are preferentially associated with one or other cell fate.
Human cells also express several Cdkn1a transcript variants.
Among the ten human transcript variants currently annotated, at least one shares translational regulatory mechanisms with the murine p21var2.
Interestingly, even though murine variant 2 and human variant 4 do not appear to share sequence homology, the translational regulation in both transcripts is driven by the integrated stress response and results in cell cycle arrest.
The potential relevance of this mechanism for cellular senescence in humans remains unknown, and the functions and interrelations of the different Cdkn1a transcript variants have not been studied in depth.
Positively charged atoms steady the machinery that the virus uses to trick the system
Scientists from The University of Texas Health Science Center at San Antonio have discovered a mechanism by which SARS-CoV-2 exploits changes in metal ion concentrations to disguise itself in the body. Varying concentrations of metal ions — positively charged atoms such as magnesium, manganese and calcium — are observed in hospitalized COVID-19 patients.
“This is a newly described metal-dependent mechanism by which these ions help the virus to evade immune surveillance,” said Yogesh Gupta, PhD, senior author of the research published June 2 in the journal Nature Communications. Dr. Gupta is assistant professor of biochemistry and structural biology at the UT Health Science Center San Antonio and investigator with its Greehey Children’s Cancer Research Institute.
Dr. Gupta and colleagues captured atomic-level snapshots during various stages of camouflaging activity of the coronavirus. It turns out metal ions have an architectural purpose — they form a bridge between viral messenger RNA (which are instructions for encoding the virus) and a protein complex consisting of viral proteins nsp16 and nsp10. The activity is sort of like a scaffold swaying in the wind and workers laying hands on it to steady it.
With the scaffold stabilized, the virus then uses nsp16 to modify its messenger RNA cap into a Trojan horse unrecognizable to the immune system. This tricks the defenses, protects the RNA code from being degraded and enhances viral growth in the body. This activity is required each time the virus multiplies.
The nsp16/nsp10 protein complex stretches itself when the RNA cap is modified, which is a second finding the scientists reported. The stretching is facilitated by metal ion binding.
The understandings gleaned in this research can eventually aid treatment of all coronaviruses.
“The next step is to use this structural knowledge to develop novel therapies to treat COVID-19 and emerging coronavirus infections,” Dr. Gupta said. “We are already studying how imbalances in metal concentrations regulate the host immune response to these infections.”
This research was made possible by the San Antonio Partnership for Precision Therapeutics, the Institute for Integration of Medicine and Science, the Max and Minnie Tomerlin Voelcker Fund, the Cancer Prevention and Research Institute of Texas, UT Health San Antonio and the Greehey Children’s Cancer Research Institute.
Reference: Viswanathan, T., Misra, A., Chan, SH. et al. A metal ion orients SARS-CoV-2 mRNA to ensure accurate 2′-O methylation of its first nucleotide. Nat Commun 12, 3287 (2021). https://doi.org/10.1038/s41467-021-23594-y
Researchers at the Francis Crick Institute have identified a protein that helps tumours evade the immune system and, in certain types of cancers, is linked to a poorer chance of survival. The protein could become a target for future cancer treatments.
A crucial part of the immune system’s response to cancer is a group of white blood cells, called CD8+ T-cells, which kill tumour cells. Before they launch their anti-tumour response, these cells must be told who to attack by another immune cell, called a dendritic cell.
In their study, published in Cell today (2 June), the scientists identified a protein that is present in blood plasma and is also secreted by cancer cells, secreted gelsolin, which interferes with this relay process by blocking a receptor inside dendritic cells. With no instruction passed to the T-cells, the tumours avoid their killer response.
The team analysed clinical data and samples from cancer patients with 10 different types of the disease and found that individuals with liver, head and neck and stomach cancers, who have lower levels of this protein in their tumours had higher chances of survival.*
They also found that blocking the action of this protein in mice with cancer increased their response to treatments including checkpoint inhibitors, a major immunotherapy.
Caetano Reis e Sousa, author and group leader of the Immunobiology Laboratory at the Crick, says: “The interaction between tumour cells, the surrounding environment and the immune system is a complex picture. And although immunotherapies have revolutionised the way certain cancers are treated, there’s still a lot to understand about who is most likely to benefit.
“It’s exciting to find a previously unknown mechanism for how our body recognises and tackles tumours. This opens new avenues for developing drugs that increase the number of patients with different types of cancer who might benefit from innovative immunotherapies.”
This work builds on the team’s research into dendritic cell biology. These cells absorb debris from dead cancer cells and hold them internally in pockets called phagosomes. Binding to a protein on the debris, F-actin, triggers these pockets to burst, releasing the debris into the cell where they can be processed and moved to the surface to signal the presence of a tumour to nearby T-cells.
When the researchers examined the activity of secreted gelsolin, they found the protein outcompetes a key dendritic cell receptor, blocking its ability to bind to F-actin and therefore the ability of the dendritic cells to initiate a T-cell response.
“Dendritic cells play a vital role in the immune system and our body’s response to cancer,” says Evangelos Giampazolias, author and postdoc in the Immunobiology Laboratory at the Crick. “Understanding this process in more detail will enable us to identify how cancers are able to hide and how we might remove their disguise.”
Oliver Schulz, author and research scientist in the of the Immunobiology Laboratory at the Crick says, “While secreted gelsolin circulates in healthy blood plasma, some cancer cells secrete really high levels of it – so these tumours are launching an anti-immune defence which helps them avoid killer T-cells.
“Reducing levels of this protein will help alleviate the competition for binding to F-actin and allow dendritic cells to communicate their vital message.”
The researchers will continue this work, trying to develop a potential therapy that targets the secreted gelsolin in the tumour without affecting the activity of this protein in other parts of the body.
Reference: Giampazolias, E. et al. (2021). Secreted gelsolin inhibits DNGR-1-dependent crosspresentation and cancer immunity. Cell. 10.1016/j.cell.2021.05.021
Some Covid-19 patients develop diabetes in the course of their infection. An international study with participation by the University of Basel has mapped how coronavirus attacks and destroys insulin-producing pancreatic cells. The researchers also identified a way to protect these cells.
Diabetes is considered a risk factor in contracting a severe bout of coronavirus SARS-CoV-2. That a severe Covid-19 infection can, conversely, lead to diabetes is less well known. Yet a number of studies have shown that roughly 15% of hospitalized Covid-19 patients are newly diagnosed with diabetes.
An international research team led by the Stanford University School of Medicine, including participation by researchers from the University of Basel and the University Hospital of Basel, has now been able to show that coronavirus can actually infect pancreatic beta cells. The scientists report their findings in the journal Cell Metabolism. Beta cells produce the hormone insulin, which stimulates tissue cells to absorb sugar from the blood, thus lowering blood sugar.
Alternative entry point
Unlike lung tissue, where coronavirus primarily uses a protein called ACE2 as a portal of entry into the cells, the beta cells of the pancreas have only low quantities of ACE2. For this reason, it has been unclear until now whether and how the virus enters these cells. To answer this question, the researchers analyzed tissue samples from seven deceased Covid-19 ‑patients in Basel.
The analysis found evidence of SARS-CoV-2 in the pancreatic beta cells of the victims. These cells also contained large quantities of a protein that the virus uses as an alternative entry point to ACE2: neuropilin-1 (NRP1). Laboratory tests on cultured beta cells further showed that infected cells produced less insulin and exhibited signs of die-off. When the researchers used an inhibitor to block neuropilin-1, the virus was much less successful at penetrating the cells.
The fact that infection of beta cells could be reduced in this way, at least in lab tests, shows that it might also be possible to protect these cells in patients with a severe case of Covid-19.
“Current research cannot say for sure whether sugar metabolism normalizes again in all Covid-19 patients after an infection, or whether and how often permanent diabetes may develop,” explains pathologist Dr. Matthias Matter of the University of Basel and the University Hospital Basel. Dr. Matter lead the parts of the study that were conducted in Basel. He says there is evidence that patients with “long Covid” – i.e. symptoms that persist after the infection has cleared – have signs of diabetes several weeks to months afterwards. It would therefore be extremely useful to develop a way to prevent lasting damage to the pancreas.
Featured image: Fluorescent microscopic image of cells: When SARS-CoV-2 (red) infects beta cells, they produce less insulin (green) and show signs of death. The cell nuclei are stained blue. (Fluorescent microscopic image: Chien-Ting Wu et al., Cell Metabolism)
Original publication: Chien-Ting Wu, Peter V. Lidsky, Yinghong Xiao, Ivan T. Lee, Ran Cheng, Tsuguhisa Nakayama, Sizun Jiang, Janos Demeter, Romina J. Bevacqua, Charles A. Chang, Robert L. Whitener, Anna K. Stalder, Bokai Zhu, Han Chen, Yury Goltsev, Alexandar Tzankov, Jayakar V. Nayak, Garry P. Nolan, Matthias S. Matter, Raul Andino, Peter K. Jackson, SARS-CoV-2 infects human pancreatic Î² cells and elicits Î² cell impairment, Cell Metabolism, 2021, , ISSN 1550-4131, https://doi.org/10.1016/j.cmet.2021.05.013. (https://www.sciencedirect.com/science/article/pii/S1550413121002308)
Metastases can develop in the body even years after apparently successful cancer treatment. They originate from cancer cells that migrated from the original tumor to other organs, and which can lie there inactive for a considerable time. Researchers have now discovered how these “sleeping cells” are kept dormant and how they wake up and form fatal metastases. They have reported their findings in the journal Nature.
A tumor can leave behind an ominous legacy in the body: cancer cells can migrate from the tumor to other tissues in the body, where they survive after treatment in a kind of hibernation called dormancy. Currently, cancer medicine relies on monitoring cancer patients after their initial treatment in order to detect the awakening of these cells to form metastases. One of the biggest questions in cancer research is what exactly causes this transition.
“This dormancy period offers an important therapeutic window in which the number of cancer cells and their heterogeneity are still manageable,” says Professor Mohamed Bentires-Alj, group leader at the Department of Biomedicine at the University of Basel and University Hospital Basel. “Understanding the cellular and molecular mechanisms underlying tumor dormancy is therefore crucial to preventing the recurrence of cancer.” His team has made an important step in this direction.
First author Dr. Anna Correia and her co-authors used mouse models and human tissue samples, and were able to determine how cancer cells, which had originally migrated from a mammary tumor to the liver, remained dormant or awoke to form metastases.
Guardians of dormancy
Two cell types play a key role in this transition. One of these cell types is the natural killer cell, i.e. a type of immune cell that traditionally kills abnormal or infected cells, but can also slow down their proliferation. As the researchers found, this is exactly what they appear to do to control dormant cancer cells. The natural killer cells secrete a messenger substance called interferon gamma, which keeps the cancer cells in hibernation.
The other cell type, the hepatic stellate cell, influences the natural killer cells. When these liver cells are activated, they inhibit the immune cells, which in turn allows the cancer cells to awaken from hibernation. “There can be various reasons why hepatic stellate cells are activated; for example, chronic inflammation in the body or persistent infection,” Correia explains. The researchers will now investigate the exact causes in further studies.
The published results indicate several possible methods of preventing metastasis: immunotherapy based on interleukin-15, which increases the number of natural killer cells in the tissue; interferon gamma therapy, which maintains the dormant state of the cancer cells; and inhibitors of the mechanism through which the hepatic stellate cells paralyze the natural killer cells. Appropriate therapies already exist for all these approaches, but they still need to be clinically tested.
Natural barriers against metastasis
“Our findings raise the hope of immunotherapies that focus on natural killer cells as a preventive strategy for patients with dormant cancer cells at risk of developing metastases,” says Bentires-Alj. “The next stage on the long road to an established treatment will be to show that stimulating natural killer cells prevents metastasis in human patients. We are currently looking for ways to finance this next step and are already in discussion with our clinical collaborators at the University Hospital Basel.”
“These cells are a natural barrier against metastasis in the liver,” Correia explains. If they could be used to prevent the development of metastases in other parts of the body, too, it might be possible to permanently prevent the recurrence of cancer. “My team is already studying such mechanisms in other metastatic sites and the results are promising,” concludes Bentires-Alj.
ICFO researchers report in Nature on having achieved, for the first time, entanglement of two multimode quantum memories located in different labs separated by 10 meters, and heralded by a photon at the telecommunication wavelength.
The scientists implemented a technique that allowed them to reach a record in the entanglement rate in a system that could be integrated into the fibre communication network, paving the way to operation over long distances.
The results are considered a landmark for quantum communications and a major step forward in the development of quantum repeaters for the future quantum internet.
During the 90s, engineers made major advances in the telecom arena spreading out the network to distances beyond the cities and metropolitan areas. To achieve this scalability factor, they used repeaters, which enhanced attenuated signals and allowed these to travel farther distances with the same features such as intensity or fidelity. Now, with the addition of satellites, it is completely normal to be in the middle of a mountain in Europe and talk with your loved ones living in the other part of the world.
In the road towards building the future Quantum internet, quantum memories play the same role. Together with sources of qubits, they are the building blocks of this novel internet, acting as quantum repeaters of data operations and using superposition and entanglement as the key ingredients of the system. But to operate such system at a quantum level, the entanglement between quantum memories had to be created over long distances and maintained as efficiently as possible.
All together in one
In a recently published study in Nature, ICFO scientists Dario Lago, Samuele Grandi, Alessandro Seri and Jelena Rakonjac, led by ICREA Prof at ICFO, Hugues de Riedmatten, have achieved scalable, telecom-heralded matter-matter entanglement between two remote, multimode and solid-state quantum memories. In simpler words, they were able to store, for a maximum of 25 microseconds, one single photon in two quantum memories placed 10m apart.
The researchers knew that the photon was in one of the two memories, but they did not know in which one, which emphasized this counter-intuitive notion that we have of nature, which allows the photon to be in a quantum superposition state in the two quantum memories at the same time but, amazingly, 10 meters apart. The team also knew that the entanglement was created with the detection of a photon at telecom wavelength, and it was stored in the quantum memories in a multiplexed fashion, “a feature akin to allowing several messages to be sent at the same time in a classical channel”. These two key features have been achieved together for the first time and define the stepping stone in extending this scheme to much longer distances.
As Dario Lago, a PhD student at ICFO and first author of the study, enthusiastically pinpoints “So far, several of the milestones achieved in this experiment were done by other groups, like entangling quantum memories or achieving storage of the photons in quantum memories with a very high efficiency and high rates. But, the uniqueness about this experiment is that our techniques achieved very high rates and can be extended to longer distances.”
Setting up the experiment
Achieving this landmark took its effort and time. During the course of several months, the team setup the experiment, where they used a rare-earth doped crystal as a quantum memory for the basis of their test.
Then, they took two sources generating correlated pairs of single photons. In each pair, one photon, named idler, is at a 1436nm (telecom wavelength), and the other, named signal, is at a wavelength of 606nm. The single signal photons, were sent to a quantum memory, made up of millions of atoms all randomly placed inside a crystal, and stored there via a protocol called atomic frequency comb. Alongside, the idler photons, also called heralding or messenger photons, were sent through an optical fiber to a device called beam-splitter, where the information about their origin and path was completely erased. Samuele Grandi, postdoctoral researcher and co-first author of the study, comments, “We erased any sort of feature that would tell us where the idler photons were coming from, let it be source 1 or 2, and we did this because we did not want to know any information about the signal photon and in which Quantum Memory it was being stored in”. By erasing these features, the signal photon could have been stored in any of the quantum memories, which means that entanglement was created between them.
Every time that the scientists saw on the monitor a click of an idler photon arriving at the detector, they were able to confirm and verify that there was, in fact, entanglement. This entanglement consisted in a signal photon in a superposition state between the two quantum memories, where it was stored as an excitation shared by tens of millions of atoms for up to 25 microseconds.
As Sam and Dario mention, “The curious thing about the experiment is that it is not possible to know if the photon was stored in the quantum memory in the lab 1 or in Lab 2, which was more than 10 meters away. Although this was the principal feature of our experiment, and one that we kind of expected, the results in the lab were still counter-intuitive, and even more peculiar and mind-blowing to us is that we were capable of controlling it!”
The importance of heralded photons
Most of the previous studies that have experimented with entanglement and quantum memories used herald photons to know whether or not the entanglement between quantum memories had been successful. A heralding photon is like a messenger dove and the scientists can know upon its arrival that the entanglement between the quantum memories has been established. When this happens, the entanglement attempts stop and the entanglement is stored in the memories before being analyzed.
In this experiment, the scientists used a heralding photon in the telecom frequency, confirming that the entanglement being produced could be established with a photon that is compatible with existing telecom networks, an important feat since it allows entanglement to be created over long distances and, even more so, enables these quantum technologies to be easily integrated into the existing classical network infrastructures.
Multiplexing is key
Multiplexing is the capability of a system to send several messages at the same time through only one channel of transmission. In classical telecommunications, this is a frequent tool used to transmit data over the internet. In quantum repeaters, such technique is slightly more complex. With standard quantum memories, one has to wait for the message heralding the entanglement to come back to the memories, before one can try again to create entanglement. But with the use of the atomic frequency comb protocol, which allows this multiplexing approach, the researchers were able to store the entangled photons at many different times in the quantum memory, without having to wait for a successful heralding event before generating the next entangled pair. This condition, called “temporal multiplexing” is a key feature that represents a major increase in the operational time of the system, leading to an increment in the final entanglement rate.
As Prof. ICREA at ICFO Hugues de Riedmatten enthusiastically remarks “This idea was conceived more than 10 years ago and I am thrilled to see that it has now succeeded in the lab. The next steps are to bring the experiment outside of the lab, to try and link different nodes together and distribute entanglement over much larger distances, beyond what we currently have now. In fact, we are in the midst of achieving the first quantum link of 35km, which will be done between Barcelona and ICFO, in Castelldefels”.
It is clear that the future quantum network will bring many applications in the near future. This achieved landmark proves and confirms that we are in the correct pathway towards developing these disruptive technologies and beginning to deploy them into what will be a new way of communicating, the Quantum Internet.
This study has received partial funding from the Quantum Flagship research project Quantum Internet Alliance (QIA), by the Gordon and Betty Moore foundation, as well as the Fundació Cellex, Fundació Mir-Puig, Generalitat de Catalunya, and the Spanish government, among other entities.
Reference: Telecom-heralded entanglement between multimode solid-state quantum memories, Dario Lago-Rivera, Samuele Grandi, Jelena V. Rakonjac, Alessandro Seri, and Hugues de Riedmatten, Nature, 2021, https://www.nature.com/articles/s41586-021-03481-8
Chinese researchers realized an elementary link of a quantum repeater based on absorptive quantum memories (QMs) and demonstrated the multiplexed quantum repeater for the first time. On June 2nd the work is published in Nature.
The fundamental task of a quantum network is to distribute quantum entanglement between two remote locations. However, the transmission loss of optical fiber has limited the distance of entanglement distribution to approximately 100 km on the ground. Quantum repeaters can overcome this difficulty by dividing long-distance transmission into several short-distance elementary links. The entanglement of two end nodes of each link is created firstly. Then the entanglement distance is gradually expanded through entanglement swapping between each link.
Previously, an elementary link of a quantum repeater has been realized in cold atomic ensembles and single quantum systems. These demonstrations are all based on emissive QMs, in which the entangled photons are emitted from QMs. Quantum repeaters constructed by emissive QMs have simple structures, but poor compatibilities. It is of great challenge to support deterministic entanglement sources and multiplexed operations simultaneously, which are two key technologies to enhance the entanglement distribution rate. Quantum repeaters based on absorptive QMs can overcome such limitation because they separate the quantum memories and the entangled photon sources.
The research team, led by Prof. LI Chuanfeng and Prof. ZHOU Zongquan from University of Science and Technology of China (USTC), focuses on the research of absorptive QMs based on rare-earth-ion-doped crystals. For this kind of QMs, the entanglement source can be flexibly selected, including deterministic entanglement sources, while remaining the capability of multiplexed operations, and therefore should be more efficient for quantum repeater applications. In this work, they used external entangled photon-pair sources (EPPSs) based on spontaneous parametric down-conversion and achieved heralded entanglement distribution between two absorptive QMs for the first time.
They built an elementary link with an intermediate station and two nodes at the ends. Each node contains an absorptive QM with a bandwidth of 1GHz and a bandwidth-matched EPPS. In each node, one entangled photon of each photon pair was stored in the “Sandwich-like” QM while the other was transmitted to the middle station for joint Bell-state measurement (BSM). A successful entanglement swapping operation was heralded by the successful click of BSM. The entanglement between two QMs 3.5 meters apart was established with a fidelity of approximately 80.4%, although there weren’t any direct interactions between two remote QMs. Four temporal modes were employed in this demonstration of an elementary link of a quantum repeater, accelerating the entanglement distribution rate by four times.
Prof. ZHOU Zongquan said: “The use of absorptive quantum memory is expected to achieve high efficiency quantum repeater and quantum network in the future, and further promote the communication between ‘Cowherd and Weaver Girl’ in the quantum world.”
This work provides a feasible roadmap for the development of practical quantum repeaters and lays the foundation for the construction of high-speed quantum networks. Reviewers pointed out”The present work focuses on the ensemble approach, which has a number of advantages in the context of quantum repeater applications, multiplexing for instance”. They highly recommend this work as”a significant accomplishment that will form the basis for further research” and “a major step forward in the development of a practical quantum repeater”.
Prof. LI Chuanfeng said that the team will continue to improve the indicators of absorptive QM, ” we will use deterministic entanglement source to greatly improve the entanglement distribution rate, and to achieve practical quantum repeaters beyond direct transmission of optical fiber.”
LIU Xiao and HU Jun from CAS Key Laboratory of Quantum Information and CAS Center for Excellence in Quantum Information and Quantum Physics are the co-first authors. The corresponding authors are Prof. LI Chuanfeng and Prof. ZHOU Zongquan.
For future developments, the research team will continue to improve the performances of the absorptive QMs, and adopt deterministic entanglement sources, so as to greatly enhance the entanglement distribution rate, and to achieve a practical quantum repeater that outperform the direct transmission of photons.