Herpesyl Review - Does Herpeyl Supplement Prevents Herpes Virus?

Herpesyl Review – Does Herpeyl Supplement Prevents Herpes Virus?

  • April 2, 2021

New York City, NY, April 02, 2021 (GLOBE NEWSWIRE) — Herpes has become one of the severe problems for people of all ages. Studies show that about 25% of Americans have these diseases in one form or the other. This means almost one-fourth of the population is affected by this disease. If this disease is left untreated, it can turn into meningitis, encephalitis and many other dangerous conditions.

But now, the treatment has arrived in the market at a reasonable price in the form of Herpesyl that promises quick relief when used consistently. With the Herpesyl capsule, one can eradicate the harmful herpes virus.

What Is Herpesyl?

Herpesyl is the only natural capsule in the market that can quickly eradicate Herpes and prevent it from spreading. HSV1 and HSV2 both can be treated with these capsules.

Herpes is not a medicine or chemical compound; it is a natural formula developed after a lot of research by leading scientists and their studies.

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Herpesyl ingredients

Vitamin C: Vitamin C is used to ensure that the body is protected from the harmful herpes virus. Herpes supports one’s body in absorbing the nutrients and enhancing immunity so that one can easily fight the virus.

Vitamin E: Vitamin E is considered one of the essential vitamins that enhance skin and hair conditions.

Since the herpes virus can negatively affect areas like genitals, chin or lips, the ingredient helps strengthen the skin’s immunity and helps it heal on a cellular level.

Selenium: The presence of selenium in Herpesyl supports the human brain in eliminating the virus. How it works is that when the virus is closer to the brain, selenium sends signals to the brain, and hence a defense mechanism to destroy the virus is activated.

Graviola Leaf: The other essential ingredient used in Herpesyl is the Graviola leaf, rich in antioxidant herbs that support the human body’s immune system to fight Herpes and keep the body clean.

Graviola leaf transmits the antioxidants in the body and kills the harmful cells of the virus because of the fantastic ingredients allocated where they are hiding.

Shitake: The more robust mushroom supports enhancing the cells of the human brain and immunity.

It stops the brain from damage and enhances cognitive abilities so that the brain signals the cells immediately when the virus is detected.

Burdock: Burdock has excellent nutrients that nourish the human brain and enhance the cells-fighting abilities. Burdock supports the body in fighting the virus, which is not easy at all.

Red Raspberry: This ingredient helps eliminate both the herpes simplex viruses from their hiding place by offering sufficient support to the cells.

Herpesyl maintains the brain cells by enhancing the communication with the other cells to destroy the virus.

Turmeric: Turmeric is a fantastic ingredient that supports the body in boosting its immune system and fighting with the HSV1 and HSV2.

Grape Seed: The ingredient has antiviral properties, which allow the cells to look for both the forms of Herpes virus and flush them out. These ingredients give a further indication to the brain to kill the virus.

Quercetin Seeds: This seed helps in completely removing the virus, its symptoms, and outbreaks.

Pomegranate: Pomegranate is also one of the most vital ingredients that make the Herpesyl effective product to improve the body’s natural ability to destroy the virus.

MUST SEE: “Shocking New Herpesyl Report – This May Change Your Mind”

How does Herpesyl work?

Below is a step by step guide explaining how Herpesyl works:

Step 1: Absorption: Herpesyl’s ingredients quickly get absorbed in the human body and improve the immune system.

The ingredients help in fighting the harmful virus, ensuring that they cannot hide. In this way, this product begins the cleaning process of the virus.

Step 2: Empowering Brain Cells: The nutrients derived from Herpesyl nourish the brain cells that send a signal to the immune system to fight the dangerous virus. This helps the body prepare and kill the virus.

Step 3: Kicking out Herpes: This formula cleans the whole body and starts healing on a cellular level.

The above three steps help clean the body and make sure that the virus doesn’t return.

How to Use Herpesyl

Herpesyl is accessible in the form of capsules. Every bottle of Herpesyl contains 60 capsules, which lasts for a month if consumed daily.

One needs to consume Herpesyl for 90 to 180 days regularly for 3 to 6 months. One should take two capsules daily, either with a glass of water, with meals, or as prescribed by the doctor.

The capsules of Herpesyl are 100% natural and don’t contain any harmful substances.

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Benefits of Herpesyl

One gets multiple benefits by using the Herpesyl; some of them are given below :

Treats Herpes from root: Many prefer Herpesyl as it removes the virus from the root preventing its return. It is the ideal treatment for HSV-2 and HSV-1, well known for eliminating such critical conditions.

Brain Nourishment: Herpesyl comes with a wide range of robust and safe ingredients that enhance brain nerve cells. These essential nutrients function to optimize the proper function of the brain. With the effectiveness of the Herpesyl, the human body gets the power to eliminate the virus, which leads to healthy neurons, allowing the effective transmission of signals.

Boosts immunity: Herpes virus weakens the immune system after the body loses the power to fight diseases. Herpesyl functions excellently to improve the body’s immune system, making it extra secure to any disease. The impressive thing after using the Herpesyl is that after eradicating the virus, it doesn’t return again anytime.

Side effects of Herpesyl

Herpesyl doesn’t have any adverse effects, and yes, it is safe to use and non-addicted as it contains natural ingredients. It has been verified as a dietary supplement by the FDA.

Purchase and Price

Herpesyl is strongly suggested as it is safe and legit to use. The developer has confirmed that this product works effectively. The majority of the consumers are satisfied with this product, which means this product is worth buying. One should purchase this product to protect themselves from the effect of the harmful virus Herpes.

Herpesyl is highly affordable. There is no need to spend extra on any other materials as one can get the fantastic product to flush out the easily affordable herpes virus. Below are some of its pricing packages :

Get one bottle of Herpesyl at $69 per bottle. This can be a slightly expensive package for people looking for a limited dosage.

3 bottles of Herpesyl are available at the cost of $177, which is the same as the $59 per bottle. This means one can get this at an incredible discount when ordering bulk.

One can order six bottles of Herpesyl at $249, which is equal to $49 per bottle, which is the most affordable package. In this package, one can save up to $20 when compared with a single bottle price.

Money-Back Guarantee and Refund Policy

Each order of Herpesyl has a 100% money-back guarantee. Every person has different physiology and it takes considerable time to show its effect. If, due to any reason, any user is unhappy with the results of the product, Herpesyl, they can request a refund from the manufacturer within 60 days of buying. While asking for a refund, one needs to return the products as they will get a refund.

Pros

  • This product doesn’t need any limited diets or workouts.
  • Also, this will indicate the cause of the disease to the brain.
  • Herpesyl is made using top-quality ingredients in an FDA-approved facility.
  • With this product, one can quickly prevent the effect of the virus.
  • It is 100% safe and natural.

Cons

  • This natural formula is only available on the internet at their official website, and only limited stocks are available.
  • People who are 18 years or older are allowed to use these capsules. It gives the best result if used for at least 180 days.

ALSO READ: Herpesyl Customer Reviews and Testimonials: Does It Work For Everyone?

FAQs

Who can take Herpesyl?

Herpesyl is a natural ingredient product for adults only; it is not for children.

Is Herpesyl a Miracle Product?

The thing that should be kept in mind is that this product can’t work miracles if the user does not take it regularly.

Must one have a prescription for purchasing Herpesyl?

Most of the medications for Herpes are available only with a prescription, but in the case of Herpesyl, one does not require any prescription as it is a dietary supplement and not a drug.

From where can one buy Herpesyl?

Herpesyl is not available in pharmacies, drug stores, and consumers can obtain it directly from its official website, which will undoubtedly be an original product at affordable deals.

Conclusion

There are many supplements available for treating several health situations. Among those

thousand products, Herpesyl has gained importance and popularity because of its unique ingredients that seek work effectively to quickly flush out the herpes virus. Thus, it seems a legit product that can be used by people with Herpes, trying to get rid of the disease by failing to do so. Herpesyl definitely promises to cure the disease from the root, so that it never returns again.

Official Website: https://herpesyl.com 

Email: support@herpesyl.com 

Telephone number: (889) 995-1512

About 72hours.org

This review, published by 72hours, is a well-researched assessment made by a group of experts in the health industry committed to bringing only the highest quality products and health programs. Although efforts have been made to ascertain the product’s information, the purchase is at the buyer’s risk. The publisher does not assume liability for any inaccuracies. It is recommended to consult a physician before placing an order. All orders placed will be subject to the terms and conditions available on the product’s website.

Media Contact – info@72hours.org

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This product review includes relevant affiliate links, which can result in commissions from qualifying purchases without any additional cost to the reader. The affiliate commission earned helps keep the site running so that our research team can review and recommend the best quality products.

Disclaimer

Any recommendations and advice given here are the opinions of 72hours and should be implemented only after consultation with a licensed healthcare professional. If you use any medications, you must consult your physician before placing an order for the product.

Results may vary from person to person. The FDA has not evaluated this product, and it is not meant to diagnose, treat or cure any medical ailment.

Content Disclaimer: The information does not constitute advice or an offer to buy. Any purchase made from the above press release is made at your own risk. Consult an expert advisor/health professional before any such purchase. Any purchase made from this link is subject to the final terms and conditions of the website’s selling as mentioned in the above as source. The content publisher and its downstream distribution partners do not take any responsibility directly or indirectly. If you have any complaints or copyright issues related to this article, kindly contact the company this news is about. 

Could a common cold virus help fight COVID-19?

Could a common cold virus help fight COVID-19?

  • March 29, 2021

Image of a rhinovirusShare on Pinterest
A recent study asks whether a common virus might help fight COVID-19. Photo edited by Stephen Kelly; Photography courtesy of Thomas Splettstoesser/Wikimedia
  • A lab-based study has found that a virus that causes the common cold can trigger an innate immune response against SARS-CoV-2, the virus responsible for COVID-19.
  • In theory, infections with the common cold virus could inhibit the transmission of SARS-CoV-2 among members of a population and reduce the severity of infections.
  • Further research could lead to control strategies or treatments that exploit such interactions between viruses.

For decades, scientists have been hunting for a cure for the common cold, with little success.

However, recent research hints that this bothersome — though usually mild — infection may be a hidden ally in the fight against pandemic viruses such as influenza and SARS-CoV-2.

Human rhinoviruses (HRVs), which cause more than half of all common colds, are the most widespread respiratory viruses in humans.

Previous research suggests that HRVs may have inhibited the spread of the influenza A virus subtype H1N1 across Europe during the 2009 flu pandemic.

Experts believe that the HRVs did this by inducing human cells to produce interferon, which is part of the body’s innate immune defenses against viral infection.

Research has shown that SARS-CoV-2 is susceptible to the effects of interferon.

This finding led scientists at the MRC-University of Glasgow Centre for Virus Research in the United Kingdom to speculate whether HRVs could help combat the spread of SARS-CoV-2 and limit the severity of infections.

To find out, the researchers infected cultures of human respiratory cells in the lab with either SARS-CoV-2, an HRV, or both viruses at the same time.

The cultures closely mimicked the outer layer of cells, called the epithelium, that lines the airways of the lungs.

SARS-CoV-2 steadily multiplied in the cells that the team had infected with this virus alone. However, in cells also infected with HRV, the number of SARS-CoV-2 virus particles declined rapidly until they were undetectable just 48 hours after the initial infection.

In further experiments, the scientists found that HRV suppressed the replication of SARS-CoV-2, regardless of which virus infected the cells first.

Conversely, SARS-CoV-2 had no effect on the growth of HRV.

To test their hunch that HRV was inhibiting SARS-CoV-2 by triggering the cells’ innate immune response, the researchers repeated their experiments in the presence of a molecule that blocks the effects of interferon.

Sure enough, the molecule restored the ability of SARS-CoV-2 to replicate in cells infected with HRV.

“Our research shows that human rhinovirus triggers an innate immune response in human respiratory epithelial cells, which blocks the replication of the COVID-19 virus, SARS-CoV-2,” says senior author Prof. Pablo Murcia.

“This means that the immune response caused by mild, common cold virus infections could provide some level of transient protection against SARS-CoV-2, potentially blocking transmission of SARS-CoV-2 and reducing the severity of COVID-19,” Prof. Murcia adds.

The researchers used a mathematical simulation to predict how different numbers of HRV infections of varying lengths might affect the spread of SARS-CoV-2 through a population.

The results showed that the number of new SARS-CoV-2 infections in a population is inversely proportional to the number of HRV infections.

The model predicts that if the common cold virus were to become sufficiently widespread and persistent, it could temporarily prevent SARS-CoV-2 from spreading.

“The next stage will be to study what is happening at the molecular level during these virus-virus interactions to understand more about their impact on disease transmission,” says Prof. Murcia.

“We can then use this knowledge to our advantage, hopefully developing strategies and control measures for COVID-19 infections,” he adds.

The research appears in The Journal of Infectious Diseases.

In their paper, the researchers speculate that mild HRV infections might be mutually beneficial for the virus and its human hosts.

They write that the immune system may have evolved to allow HRV to replicate and transmit to new hosts. In return, the virus keeps more severe and potentially lethal viral infections at bay.

At the Science Media Centre in London in the United Kingdom, other scientists welcomed the research but flagged some potential limitations.

Gary McLean, who is a professor in molecular immunology at London Metropolitan University in the U.K., said that the major limitation was that the study involved just one of the 160 or more possible strains of rhinovirus.

He said there was no guarantee that each strain would have the same effect on SARS-CoV-2 infections.

He added that translating results from a lab experiment to real life is “very tricky,” saying:

“Although it is likely that a common cold virus, such as rhinovirus, would induce a strong innate immune response that could block SARS-CoV-2 infections, it would still require both infections to occur at a similar time.”

In addition, he pointed out that intensive infection control measures over the past year have made the common cold less prevalent, reducing the potential for HRV-triggered innate immunity to combat the spread of SARS-CoV-2.

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

(image: Korea Bizwire/Kobiz Media)

Researchers Develop Fake RNA Virus to Boost Vaccine Efficacy

  • March 26, 2021

(image: Korea Bizwire/Kobiz Media)

(image: Korea Bizwire/Kobiz Media)

DAEJEON, March 26 (Korea Bizwire) – A South Korean research team has developed an adjuvant that can help vaccines work better.

The Korea Research Institute of Chemical Technology said Thursday that researchers had developed an adjuvant that acts as a fake RNA virus to make it easier for the vaccine to penetrate the cell and invigorate the immune system.

A vaccine antigen refers to a piece of the crushed virus or a dead virus that is deprived of RNA virus.

When injecting a live virus, there is a risk in which the RNA virus actually penetrates into the cell, allowing the virus to proliferate therein.

However, when injecting an antigen that is deprived of RNA virus, the immune system does not function properly, thereby reducing the effect of the vaccine.

The newly-developed fake RNA virus compound enables the receptor of the cell to misunderstand it as a real one and activate the body’s immune system to secrete immune materials such as interferon and cytokine.

Real RNA virus is a high molecule compound that is difficult to produce. The cost of producing RNA virus is very high.

The research team succeeded in developing and mass-producing the fake RNA virus at a low cost. When tested in mice, its superior effect in improving influenza and foot-and-mouth disease vaccines was confirmed.

J. S. Shin (js_shin@koreabizwire.com)


Freiburg researchers receive ERC funding to develop and test immunostimulatory drug candidates

New study shows how the immune system relates to cancer

  • March 22, 2021

Three University of Colorado Cancer Center researchers are part of a team that recently published a paper offering new insight into how the immune system relates to cancer. Quentin Vicens, PhD, Jeffrey Kieft, PhD, and Beat Vögeli, PhD, are authors on the paper, which looks at how an enzyme called ADAR1 operates in pathways associated with cancer.

“In a cell, ADAR1 edits native RNA — or self-RNA — so that the cell recognizes it as its own. It’s a key protection against autoimmune disorders,” Kieft says. “But if a virus infects, viral RNA isn’t edited by ADAR1, so the cell can recognize that and react. The cell knows it has foreign RNA, and it activates immune responses to fight off that infection.”

For their paper published last month in the journal Nature Communications, Kieft, Vögeli, Vicens, and the rest of the team — including Parker Nichols, a graduate student in the Structural Biology and Biochemistry program in the CU School of Medicine who works jointly in the Kieft and Vögeli labs — looked at where specifically the ADAR1 binds to RNA to perform the editing process. They already knew a domain of ADAR1 known as Z-alpha binds to a form of RNA called Z-RNA, but they found that Z-alpha ADAR1 can bind to other RNA forms as well.

The team asked, ‘How are all these locations in RNA being recognized by Z-alpha if they supposedly don’t form Z-RNA? One of the take-home messages is that other forms of RNA can bind to Z-alpha ADAR1 and can even partially form Z-RNA. That was a surprise because it shows that RNA can form this specific Z structure in places we didn’t recognize before.”


Jeffrey Kieft, PhD, Study Author, CU School of Medicine

The team is now proposing a model for how Z-alpha ADAR1 is able to bind to different types of RNA. It’s an important finding in cancer research because of the role of ADAR1 in cancer regulation. A normally functioning immune system oftentimes can detect cancerous cells as being dangerous and then eliminate them, but if there’s too much ADAR1 editing happening, a cell could be tamping down the immune response in an effort to protect itself.

“In a lot of cancers, there is upregulation of ADAR1; it is doing more than it should,” Kieft says. “The excess ADAR1 presumably is leading to more RNA editing than is normal. This is going to misregulate things, affecting specific regions of RNA or types of RNA.

The excess editing is going to throw off the normal immune response, but it probably has a lot of other affects in the cell as well. Cancer is a disease where gene regulation has gone awry, so if an important regulatory pathway like editing by ADAR has gone haywire, that can contribute to the cancer.”

Knowing all the targets of ADAR1 in a cell is also a step toward more effective therapies, Kieft says. If researchers understand the pathways, they may be able to find a way to disrupt the overactive editing process and boost the immune response. It’s a finding applicable to many other diseases as well — Vögeli says since the paper was published, the researchers have heard from other scientists around the country interested in ADAR1.

“We have gotten a lot of feedback on the paper,” he says. “There is a lot of interest in this field right now, and other people are interested in how they could use our structural information.”

Vögeli and Vicens are now organizing a meeting focused on ADAR1 function and putting together special issues of the journals Molecules and International Journal of Molecular Sciences.

Vicens says the research project also illustrates the importance of collaborative work and being open to new directions. “I basically brought a new project and direction to the Kieft lab when I joined,” Vicens says. “Both labs were open to supporting it intellectually and financially, and the resultant team effort enabled research that would not otherwise have been done.”

Source:

Journal reference:

Nichols, P. J., et al. (2021) Recognition of non-CpG repeats in Alu and ribosomal RNAs by the Z-RNA binding domain of ADAR1 induces A-Z junctions. Nature Communications. doi.org/10.1038/s41467-021-21039-0.

Study: What level of neutralising antibody protects from COVID-19? Image Credit: Juan Gaertner / Shutterstock

What is a protective neutralizing antibody titer against SARS-CoV-2 infection?

  • March 15, 2021

Caused by the worldwide spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus disease 2019 (COVID-19) pandemic continues to damage global public health and economic vitality. The only hope of returning to any semblance of normalcy lies with the achievement of population immunity, either by natural infection or by vaccination.

A new preprint, released on the medRxiv* server, describes a predictive model of protective immunity against SARS-CoV-2 infection that could help evolve optimal vaccination strategies to maintain protection and reduce the death rate.

Study: What level of neutralising antibody protects from COVID-19? Image Credit: Juan Gaertner / Shutterstock

As natural infection is associated with a frighteningly high loss of life (over 2.6 million deaths and counting), vaccine-elicited immunity is the only viable way out. Active immunity has been observed to set in following the vast majority of infections.

Researchers estimate that convalescents with antibodies against the virus (seropositive convalescents) are protected against reinfection by 90%, while vaccine antibodies do the job of reducing reinfection by 50-85%. The duration for which protective immunity lasts is unknown, but the immune response is known to wane rapidly.

Also, new variants have rapidly emerged that could be resistant to antibodies specific to the antigens of the older strains.

The current study aims to identify the factors that predict adequate protection against SARS-CoV-2 infection so that it becomes possible to predict how the changes in immunity levels will affect the clinical outcomes of the individual patient. This would help to tailor vaccination and immunotherapy protocols so as to ensure this level of immunity is created and maintained – and, in turn, this would help economic activity to begin again with confidence.

In early influenza pandemics, a hemagglutination inhibition (HAI) titer of 1:40 is correlated with 50% protection from infection. This level results from analyzing data on standardized HAI tests carried out on serum from individuals challenged with the influenza virus vs controls.

The lack of similar assays for immunity to SARS-CoV-2 has made it difficult to compare the level of immunity in a susceptible population to that in a resistant one, and human challenge models are impossible with the current death rate.

Immunological mechanisms associated with protection from infection include neutralizing antibodies, as well as memory T and B cells. The use of convalescent serum and therapeutic antibodies (such as the Regeneron cocktail) has proved the major role played by neutralizing antibodies.

The current study used neutralization titers obtained during in vitro studies with sera from vaccinated and convalescent individuals. The neutralization capacity of standardized convalescent serum has been suggested to be more comparable to the results from a variety of assays, and so the sera were normalized against this standard.

Neutralization titers were averaged, and the log standard deviation was also determined in each study for the sake of achieving comparable values. The normalized mean convalescent neutralizing titer was calculated for the same assay in the same study, and values from different studies were compared against the reported phase 3 vaccine efficacy.

The authors thus obtained a strong linear relationship between the mean neutralization level and the protective efficacy for different vaccines. The results show that a 50% protective neutralization level is achieved at about a fifth of the antibody titer found in convalescent plasma, on average.

That is, the level of neutralizing antibodies required to protect against 50% of infection is one-fifth of the mean neutralizing antibody titer found in convalescent serum. Again, when adjusted to prevent false results due to a normal distribution of data, they found that the estimated protective level was about 29% of the mean convalescent level, slightly higher than the earlier estimation. However, the latter figure represents the titer needed to ensure 100% protection.

This demonstrates the ability to predict the correlation between the average level of protection and the observed efficacy of protection if the level of neutralization titers and their distribution is known.

To test the utility of this approach in arriving at the protective efficacy of a new vaccine, the researchers analyzed the data against all possible groups of vaccinated or convalescent subjects, apart from one, to predict the efficacy of the last group.

They tested the predictive accuracy against a new vaccine with phase 3 efficacy results recently released, at around 81%. The researchers found that, with the mean observed neutralization level of around 79% of the convalescent titer measured in that study, the new vaccine had a predicted efficacy of around 79%, which is close to the reported figure.

This study can be carried forward with access to more standardized assay and trial results, which would yield more homogeneous data. The researchers caution that the association of neutralization with protective efficacy in these studies does not imply that such antibodies mediate protection against infection.

Instead, other immune responses leading to protection could be correlated with neutralizing titer, and thus create an apparent association. Thus, examining the predictive value of other serological and cellular immune markers is necessary to identify the best predictive marker, compared to neutralization.

Nonetheless, the rapid decline of neutralization titers after natural infection and vaccination has been observed. The mean neutralization titer wanes by half over the first eight months following infection. However, the decline likely slows down over time.

The researchers compared the neutralization titer decay in convalescent sera and in vaccine recipient sera. They found that when measured at 26-115 days from vaccination or from the onset of symptoms, the titers appeared to decline at almost the same rate.

The researchers assumed that neutralization is the major mechanism of protection against infection or at least the major correlate; that both vaccine-induced and natural antibodies decay at the same rate; and that the rate of decay is unrelated to the initial titer. The researchers then constructed a model of neutralization and protection over the first 250 days after vaccination, using the half-life of the 90-day neutralization titer from convalescent sera.

This showed that decreasing neutralization titers affect protection from infection in a non-linear fashion, with the drop being proportional to the initial vaccine efficacy.

For example, a vaccine starting with an initial efficacy of 95% would be expected to maintain 58% efficacy by 250 days. However, a response starting with an initial efficacy of 70% would be predicted to drop to 18% efficacy after 250 days.”

This approach would also allow an estimation of the time taken for the initial efficacy to drop to 50% or 70%, thus helping to determine the interval necessary before a boost will be needed to maintain minimal neutralization efficacy levels.

The model also shows that a lower neutralization titer against a variant of concern (VOC) will have a greater impact on vaccines with lower protective titers against the wildtype virus. If the vaccine has high efficacy (95%) against the latter, for instance, a five-fold drop in efficacy would reduce the efficacy against the VOC to 67%.

Conversely, if the vaccine has only 70% efficacy at first, the efficacy against the VOC at five-fold lower levels will be only 25%. Such figures are of concern in the light of recent research, which shows that the neutralization titer against the South African VOC B.1.351 is 7.6-9-fold lower than for the earlier variants.

Protection from severe infection.

Protection from severe infection. (A) The predicted relationship between efficacy against mild (any) SARS-CoV-2 infection (x-axis) versus efficacy against severe infection (y-axis). The black line indicates the best fit model for the relationship between protection against any versus severe SARS-CoV-2 infection. Shaded areas indicate 95% confidence intervals. Efficacy against severe infection was calculated by using a severe threshold that was a factor of 0.16 smaller than mild infection (CI = 0.039 to 0.66). (B) Extrapolating the decay of neutralisation titres over time. This model assumes a half-life of SARS-CoV-2 neutralisation titre of 90 days over the first 250 days 5, after which the decay decreases (at rate 0.01d-1) until a 10-year half-life is achieved 33,34. For different initial starting levels the model projects the decay in level over the subsequent 1000 days. The green line indicates the predicted 50% protective titre from mild SARS-CoV-2 infection, and the purple line indicates the 50% protective titre from severe SARS-CoV-2 infection. The model illustrates that, depending on the initial neutralisation level, individuals may maintain protection from severe infection whilst becoming susceptible to mild infection (ie: with neutralisation levels remaining in the green shaded region). (C) Extrapolating the trajectory of protection for groups with different starting levels of protection. The model uses the same assumptions on the rate of immune decay discussed in panel B. Note: The projections beyond 250 days rely on an assumption of how the decay in SARS-CoV-2 neutralisation titre will slow over time. In addition, the modelling only projects how decay in neutralisation is predicted to affect protection. Other mechanisms of immune protection may play important roles in providing long-term protection that are not captured in this simulation.

The study also shows that the 50% neutralization level that confers protection against severe infection was 3% of the average convalescent level, assuming that neutralization and not cellular responses are important in this protection.

This six-fold difference in the protective titer against severe infection relative to that against any infection will probably be reflected at all levels of vaccine efficacy against mild infection with SARS-CoV-2. If so, and if it does not change over time, individuals with protective immunity are far more likely to remain protected against severe disease for far longer, even with waning neutralization titers, than to be protected against infection per se.

The researchers project an exponential decay rate after eight months until a ten-year half-life. Against this background, they predict that even without a boost to the immune system, a large percentage of individuals will remain protected against severe infection with a similar strain, requiring only 3% of the initial mean neutralization titer in convalescent patients, even if mild or asymptomatic infection occurs as the titer drops below 20% of the mean convalescent titer.

This study provides a model to use the available limited data on convalescent and vaccination antibody studies in order to predict the course of immunity to the virus.

*Important Notice

medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

New SARS-CoV-2 vaccine candidate produces strong immune response, prevents SARS-CoV-2 infection

New SARS-CoV-2 vaccine candidate produces strong immune response, prevents SARS-CoV-2 infection

  • March 10, 2021

A new SARS-CoV-2 vaccine candidate, developed by giving a key protein’s gene a ride into the body while encased in a measles vaccine, has been shown to produce a strong immune response and prevent SARS-CoV-2 infection and lung disease in multiple animal studies.

Scientists attribute the vaccine candidate’s effectiveness to strategic production of the antigen to stimulate immunity: using a specific snippet of the coronavirus spike protein gene, and inserting it into a sweet spot in the measles vaccine genome to boost activation, or expression, of the gene that makes the protein.

Even with several vaccines already on the market, researchers say this candidate may have advantages worth exploring – especially related to the measles vaccine’s established safety, durability and high-efficacy profile.

The measles vaccine has been used in children since the 1960s, and has a long history of safety for children and adults.”


Jianrong Li, Study Senior Author and Professor of Virology, Department of Veterinary Biosciences, Ohio State University

“We also know the measles vaccine can produce long-term protection. The hope is that with the antigen inside, it can produce long-term protection against SARS-CoV-2. That would be a big advantage, because right now we don’t know how long protection will last with any vaccine platforms.”

The Ohio State Innovation Foundation has exclusively licensed the technology to Biological E. Limited (BE), a Hyderabad, India-based vaccine & pharmaceutical company.

The research is published online today (March 9, 2021) in the journal Proceedings of the National Academy of Sciences.

The coronavirus that causes COVID-19 uses the spike protein on its surface to bind to its target cells in the nose and lungs, where it makes copies of itself and releases them to infect other cells. Like all vaccines, this candidate initiates the production of antibodies that recognize the new protein as foreign, training the immune system to attack and neutralize the spike protein if SARS-CoV-2 ever enters the body.

Li created the COVID-19 vaccine using a live attenuated measles virus as a vehicle with colleagues Mijia Lu, a postdoctoral researcher in Li’s laboratory and first author on the paper, and co-authors Stefan Niewiesk, Ohio State professor of veterinary biosciences, and Mark Peeples, professor of pediatrics at Ohio State and a researcher at Nationwide Children’s Hospital in Columbus.

For this work, the researchers tested seven versions of the spike protein to find the most effective antigen. They landed on a stabilized “prefusion” version of the protein – the shape the protein is in before it infects a cell.

The scientists inserted the prefusion spike protein gene containing manufacturing instructions into a segment of the measles vaccine genome to generate high expression of the protein, reasoning that the more SARS-CoV-2 spike protein produced, the better the immune response.

The team tested the vaccine candidate in several animal models to gauge its effectiveness, and found that the vaccine induced high levels of neutralizing antibodies against SARS-CoV-2 in all of the animals.

Some may think most humans’ immunity to measles, thanks to decades of widespread vaccination, would render its status as a coronavirus vaccine vehicle useless. To quell those concerns, researchers gave cotton rats a measles vaccine and showed that a second immunization with the measles-based SARS-CoV-2 vaccine candidate could induce a strong neutralizing antibody response to the coronavirus.

Genetically modified mice produced helper T cells – a type of white blood cell – in response to the vaccine, another important way the body fights infection, and severe disease in particular.

“The orientation of T helper cells induced by a vaccine is an important predictor of protection, and this vaccine mainly induces Th1 cells, which enhances the safety and efficacy of the vaccine,” said co-author Amit Kapoor, associate professor of pediatrics at Ohio State and a researcher at Nationwide Children’s Hospital.

Golden Syrian hamsters, which are susceptible to contracting COVID-19, received the vaccine and were then injected with the coronavirus. The vaccinated hamsters were protected from lung infection and other sickness symptoms indicated through weight loss.

“When we looked at the amount of neutralizing antibody induced in the hamster, it was actually higher than from people who had been infected with COVID, suggesting the vaccine may be better than SARS-CoV-2 infection in inducing protective immunity. That was our goal,” Peeples said.

The researchers have confidence in the platform not only because the measles vaccine is safe, effective and affordable to produce, but because several experimental measles-based vaccines against other viruses are in development. A vaccine against chikungunya virus, spread by mosquitos, has been shown to be safe, well-tolerated and good at provoking an immune response in a Phase 2 clinical trial.

And even with a variety of COVID-19 vaccines now available in the United States and other countries, there is still a lot to learn about which are the safest and most effective for specific populations, such as children and pregnant women, and which vaccines are the most economical to produce.

“We can make vaccines much more quickly now than in the past. But if we had to do it the traditional way this time, we wouldn’t have a vaccine protecting us in this short amount of time,” Niewiesk said. “The mRNA vaccines in use now were made in record time. And they protect against disease and are safe. Although not quite as fast, we were able to make this vaccine much more quickly than the original measles vaccine.

“We don’t yet know how long the mRNA vaccines will protect or how much they will cost. In the meantime, an alternative vaccine that should protect for a long time, is easy to manufacture and cheap seems like a good idea.”

Source:

Journal reference:

Lu, M., et al. (2020) A safe and highly efficacious measles virus-based vaccine expressing SARS-CoV-2 stabilized prefusion spike. Proceedings of the National Academy of Sciences. doi.org/10.1073/pnas.2026153118.

Children's immune response more effective against COVID-19 -- ScienceDaily

Tackling tumors with two types of virus — ScienceDaily

  • March 6, 2021

An international research group led by the University of Basel has developed a promising strategy for therapeutic cancer vaccines. Using two different viruses as vehicles, they administered specific tumor components in experiments on mice with cancer in order to stimulate their immune system to attack the tumor. The approach is now being tested in clinical studies.

Making use of the immune system as an ally in the fight against cancer forms the basis of a wide range of modern cancer therapies. One of these is therapeutic cancer vaccination: following diagnosis, specialists set about determining which components of the tumor could function as an identifying feature for the immune system. The patient is then administered exactly these components by means of vaccination, with a view to triggering the strongest possible immune response against the tumor.

Viruses that have been rendered harmless are used as vehicles for delivering the characteristic tumor molecules into the body. In the past, however, many attempts at creating this kind of cancer therapy failed due to an insufficient immune response. One of the hurdles is that the tumor is made up of the body’s own cells, and the immune system takes safety precautions in order to avoid attacking such cells. In addition, the immune cells often end up attacking the “foreign” virus vehicle more aggressively than the body’s own cargo. With almost all cancer therapies of this kind developed so far, therefore, the desired effect on the tumor has failed to materialize. Finding the appropriate vehicle is just as relevant in terms of effectiveness as the choice of tumor component as the point of attack.

Arenaviruses as vehicles

The research group led by Professor Daniel Pinschewer of the University of Basel had already discovered in previous studies that viruses from the arenavirus family are highly suitable as vehicles for triggering a strong immune response. The group now reports in the journal Cell Reports Medicine that the combination of two different arenaviruses produced promising results in animal experiments.

The researchers focused on two distantly related viruses called Pichinde virus and Lymphocytic choriomeningitis virus, which they adapted via molecular biological methods for use as vaccine vectors. When they took the approach of administering the selected tumor component first with the one virus and then, at a later point, with the other, the immune system shifted its attack away from the vehicle and more towards the cargo. “By using two different viruses, one after the other, we focus the triggered immune response on the actual target, the tumor molecule,” explains Pinschewer.

Tumor eliminated or slowed down

In experiments with mice, the researchers were able to measure a potent activation of killer T cells that eliminated the cancer cells. In 20% to 40% of the animals — depending on the type of cancer — the tumor disappeared, while in other cases the rate of tumor growth was at least temporary slowed.

“We can’t say anything about the efficacy of our approach in humans as yet,” Pinschewer points out. However, ongoing studies with a cancer therapy based on a single arenavirus have already shown promising results. The effects on tumors in animal experiments cannot be assumed to translate directly into the effect on corresponding cancer types in humans. “However, since the therapy with two different viruses works better in mice than the therapy with only one virus, our research results make me optimistic,” Pinschewer adds.

The biotech company Hookipa Pharma, of which Pinschewer is one of the founders, is now investigating the efficacy of this novel approach to cancer therapy in humans. “We are currently exploring what our approach by itself can actually achieve,” the researcher says. “If it proves successful, a wide range of combinations with existing therapies could be envisaged, in which the respective mechanisms would join forces to eliminate tumors even better.”

Story Source:

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

watercolor illustration of coronavirus cells

Coronavirus Deranges the Immune System in Complex and Deadly Ways

  • March 4, 2021


This story also ran on USA Today. It can be republished for free.

There’s a reason soldiers go through basic training before heading into combat: Without careful instruction, green recruits armed with powerful weapons could be as dangerous to one another as to the enemy.

The immune system works much the same way. Immune cells, which protect the body from infections, need to be “educated” to recognize bad guys — and to hold their fire around civilians.

In some covid patients, this education may be cut short. Scientists say unprepared immune cells appear to be responding to the coronavirus with a devastating release of chemicals, inflicting damage that may endure long after the threat has been eliminated.

“If you have a brand-new virus and the virus is winning, the immune system may go into an ‘all hands on deck’ response,” said Dr. Nina Luning Prak, co-author of a January study on covid and the immune system. “Things that are normally kept in close check are relaxed. The body may say, ‘Who cares? Give me all you’ve got.’”

While all viruses find ways to evade the body’s defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized.

Some covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus. Doctors in Italy first noticed a pattern in March 2020, when several covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis. As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke.

All these conditions can be triggered by “autoantibodies” — rogue antibodies that target the patient’s own proteins and cells.

In a report published in October, researchers even labeled the coronavirus “the autoimmune virus.”

“Covid is deranging the immune system,” said John Wherry, director of the Penn Medicine Immune Health Institute and another co-author of the January study. “Some patients, from their very first visit, seem to have an immune system in hyperdrive.”

Although doctors are researching ways to overcome immune disorders in covid patients, new treatments will take time to develop. Scientists are still trying to understand why some immune cells become hyperactive — and why some refuse to stand down when the battle is over.

Key immune players called “helper T cells” typically help antibodies mature. If the body is invaded by a pathogen, however, these T cells can switch jobs to hunt down viruses, acting more like “killer T cells,” which destroy infected cells. When an infection is over, helper T cells usually go back to their old jobs.

In some people with severe covid, however, helper T cells don’t stand down when the infection is over, said James Heath, a professor and president of Seattle’s Institute for Systems Biology.

About 10% to 15% of hospitalized covid patients Heath studied had high levels of these cells even after clearing the infection. By comparison, Heath found lingering helper T cells in fewer than 5% of covid patients with less serious infections.

In affected patients, helper T cells were still looking for the enemy long after it had been eliminated. Heath is now studying whether these overzealous T cells might inflict damage that leads to chronic illness or symptoms of autoimmune disease.

“These T cells are still there months later and they’re aggressive,” Heath said. “They’re on the hunt.”

Friendly Fire

Covid appears to confuse multiple parts of the immune system.

In some patients, covid triggers autoantibodies that target the immune system itself, leaving patients without a key defense against the coronavirus.

In October, a study published in Science led by Rockefeller University’s Jean-Laurent Casanova showed that about 10% of covid patients become severely ill because they have antibodies against an immune system protein called interferon.

Disabling interferon is like knocking down a castle’s gate. Without these essential proteins, invading viruses can overwhelm the body and multiply wildly.

New research shows that the coronavirus may activate preexisting autoantibodies, as well as prompt the body to make new ones.

In the January study, half of the hospitalized covid patients had autoantibodies, compared with fewer than 15% of healthy people. While some of the autoantibodies were present before patients were infected with SARS-CoV-2, others developed over the course of the illness.

Other research has produced similar findings. In a study out in December, researchers found that hospitalized covid patients harbored a diverse array of autoantibodies.

While some patients studied had antibodies against virus-fighting interferons, others had antibodies that targeted the brain, thyroid, blood vessels, central nervous system, platelets, kidneys, heart and liver, said Dr. Aaron Ring, assistant professor of immunology at Yale School of Medicine and lead author of the December study, published online without peer review. Some patients had antibodies associated with lupus, a chronic autoimmune disorder that can cause pain and inflammation in any part of the body.

In his study, Ring and his colleagues found autoantibodies against proteins that help coordinate the immune system response. “These are the air traffic controllers,” Ring said. If these proteins are disrupted, “your immune system doesn’t work properly.”

Covid patients rife with autoantibodies tended to have the severest disease, said Ring, who said he was surprised at the level of autoantibodies in some patients. “They were comparable or even worse than lupus,” Ring said.

Although the studies are intriguing, they don’t prove that autoantibodies made people sicker, said Dr. Angela Rasmussen, a virologist affiliated with Georgetown’s Center for Global Health Science and Security. It’s possible that the autoantibodies are simply markers of serious disease.

“It’s not clear that this is linked to disease severity,” Rasmussen said.

The studies’ authors acknowledge they have many unanswered questions.

“We don’t yet know what these autoantibodies do and we don’t know if [patients] will go on to develop autoimmune disease,” said Dr. PJ Utz, a professor of immunology and rheumatology at Stanford University School of Medicine and a co-author of Luning Prak’s paper.

But recent discoveries about autoantibodies have excited the scientific community, who now wonder if rogue antibodies could explain patients’ differing responses to many other viruses. Scientists also want to know precisely how the coronavirus turns the body against itself — and how long autoantibodies remain in the blood.

‘An Unfortunate Legacy’

Scientists working round-the-clock are already beginning to unravel these mysteries.

A study published online in January, for example, found rogue antibodies in patients’ blood up to seven months after infection.

Ring said researchers would like to know if lingering autoantibodies contribute to the symptoms of “long covid,” which afflicts one-third of covid survivors up to nine months after infection, according to a new study in JAMA Network Open.

“Long haulers” suffer from a wide range of symptoms, including debilitating fatigue, shortness of breath, cough, chest pain and joint pain, according to the Centers for Disease Control and Prevention. Other patients experience depression, muscle pain, headaches, intermittent fevers, heart palpitations and problems with concentration and memory, known as brain fog.

Less commonly, some patients develop an inflammation of the heart muscle, abnormalities in their lung function, kidney issues, rashes, hair loss, smell and taste problems, sleep issues and anxiety.

The National Institutes of Health has announced a four-year initiative to better understand long covid, using $1.15 billion allocated by Congress.

Ring said he’d like to study patients over time to see if specific symptoms might be explained by lingering autoantibodies.

“We need to look at the same patients a half-year later and see which antibodies they do or don’t have,” he said. If autoantibodies are to blame for long covid, they could “represent an unfortunate legacy after the virus is gone.”

Widening the Investigation

Scientists say the coronavirus could undermine the immune system in several ways.

For example, it’s possible that immune cells become confused because some viral proteins resemble proteins found on human cells, Luning Prak said. It’s also possible that the coronavirus lurks in the body at very low levels even after patients recover from their initial infection.

“We’re still at the very beginning stages of this,” said Luning Prak, director of Penn Medicine’s Human Immunology Core Facility.

Dr. Shiv Pillai, a Harvard Medical School professor, notes that autoantibodies aren’t uncommon. Many healthy people walk around with dormant autoantibodies that never cause harm.

For reasons scientists don’t completely understand, viral infections appear able to tip the scales, triggering autoantibodies to attack, said Dr. Judith James, vice president of clinical affairs at the Oklahoma Medical Research Foundation and a co-author of Luning Prak’s study.

For example, the Epstein-Barr virus, best known for causing mononucleosis, has been linked to lupus and other autoimmune diseases. The bacteria that cause strep throat can lead to rheumatic fever, an inflammatory disease that can cause permanent heart damage. Doctors also know that influenza can trigger an autoimmune blood-clotting disorder, called thrombocytopenia.

Researchers are now investigating whether autoantibodies are involved in other illnesses — a possibility scientists rarely considered in the past.

Doctors have long wondered, for example, why a small number of people — mostly older adults — develop serious, even life-threatening reactions to the yellow fever vaccine. Three or four out of every 1 million people who receive this vaccine — made with a live, weakened virus — develop yellow fever because their immune systems don’t respond as expected, and the weakened virus multiplies and causes disease.

In a new paper in the Journal of Experimental Medicine, Rockefeller University’s Casanova has found that autoantibodies to interferon are once again to blame.

Casanova led a team that found three of the eight patients studied who experienced a dangerous vaccine reaction had autoantibodies that disabled interferon. Two other patients in the study had genes that disabled interferon.

“If you have these autoantibodies and you are vaccinated against yellow fever, you may end up in the ICU,” Casanova said.

Casanova’s lab is now investigating whether autoantibodies cause critical illness from influenza or herpes simplex virus, which can cause a rare brain inflammation called encephalitis.

Calming the Autoimmune Storm

Researchers are looking for ways to treat patients who have interferon deficiencies — a group at risk for severe covid complications.

In a small study published in February in the Lancet Respiratory Medicine, doctors tested an injectable type of interferon — called peginterferon-lambda — in patients with early covid infections.

People randomly assigned to receive an interferon injection were four times more likely to have cleared their infections within seven days than the placebo group. The treatment, which used a type of interferon not targeted by the autoantibodies Casanova discovered, had the most dramatic benefits in patients with the highest viral loads.

Lowering the amount of virus in a patient may help them avoid becoming seriously ill, said Dr. Jordan Feld, lead author of the 60-person study and research director at the Toronto Centre for Liver Disease in Canada. In his study, four of the placebo patients went to the emergency room because of breathing issues, compared with only one who received interferon.

“If we can bring the viral levels down quickly, they might be less infectious,” Feld said.

Feld, a liver specialist, notes that doctors have long studied this type of interferon to treat other viral infections, such as hepatitis. This type of interferon causes fewer side effects than other varieties. In the trial, those treated with interferon had similar side effects to those who received a placebo.

Doctors could potentially treat patients with a single injection with a small needle — like those used to administer insulin — in outpatient clinics, Feld said. That would make treatment much easier to administer than other therapies for covid, which require patients to receive lengthy infusions in specialized settings.

Many questions remain. Dr. Nathan Peiffer-Smadja, a researcher at the Imperial College London, said it’s unclear whether this type of interferon does improve symptoms.

Similar studies have failed to show any benefit to treating patients with interferon, and Feld acknowledged that his results need to be confirmed in a larger study. Ideally, Feld said, he would like to test interferon in older patients to see whether it can reduce hospitalizations.

“We’d like to look at long haulers, to see if clearing the virus quickly could lead to less immune dysregulation,” Feld said. “People have said to me, ‘Do we really need new treatments now that vaccines are rolling out?’ Unfortunately, we do.”

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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Freiburg researchers receive ERC funding to develop and test immunostimulatory drug candidates

Using two different viruses to tackle tumors

  • March 4, 2021

An international research group led by the University of Basel has developed a promising strategy for therapeutic cancer vaccines. Using two different viruses as vehicles, they administered specific tumor components in experiments on mice with cancer in order to stimulate their immune system to attack the tumor. The approach is now being tested in clinical studies.

Making use of the immune system as an ally in the fight against cancer forms the basis of a wide range of modern cancer therapies. One of these is therapeutic cancer vaccination: following diagnosis, specialists set about determining which components of the tumor could function as an identifying feature for the immune system. The patient is then administered exactly these components by means of vaccination, with a view to triggering the strongest possible immune response against the tumor.

Viruses that have been rendered harmless are used as vehicles for delivering the characteristic tumor molecules into the body. In the past, however, many attempts at creating this kind of cancer therapy failed due to an insufficient immune response. One of the hurdles is that the tumor is made up of the body’s own cells, and the immune system takes safety precautions in order to avoid attacking such cells.

In addition, the immune cells often end up attacking the “foreign” virus vehicle more aggressively than the body’s own cargo. With almost all cancer therapies of this kind developed so far, therefore, the desired effect on the tumor has failed to materialize. Finding the appropriate vehicle is just as relevant in terms of effectiveness as the choice of tumor component as the point of attack.

Arenaviruses as vehicles

The research group led by Professor Daniel Pinschewer of the University of Basel had already discovered in previous studies that viruses from the arenavirus family are highly suitable as vehicles for triggering a strong immune response. The group now reports in the journal Cell Reports Medicine that the combination of two different arenaviruses produced promising results in animal experiments.

The researchers focused on two distantly related viruses called Pichinde virus and Lymphocytic choriomeningitis virus, which they adapted via molecular biological methods for use as vaccine vectors. When they took the approach of administering the selected tumor component first with the one virus and then, at a later point, with the other, the immune system shifted its attack away from the vehicle and more towards the cargo.

By using two different viruses, one after the other, we focus the triggered immune response on the actual target, the tumor molecule.”


Daniel Pinschewer, Professor, University of Basel

Tumor eliminated or slowed down

In experiments with mice, the researchers were able to measure a potent activation of killer T cells that eliminated the cancer cells. In 20% to 40% of the animals – depending on the type of cancer – the tumor disappeared, while in other cases the rate of tumor growth was at least temporary slowed.

“We can’t say anything about the efficacy of our approach in humans as yet,” Pinschewer points out. However, ongoing studies with a cancer therapy based on a single arenavirus have already shown promising results. The effects on tumors in animal experiments cannot be assumed to translate directly into the effect on corresponding cancer types in humans. “However, since the therapy with two different viruses works better in mice than the therapy with only one virus, our research results make me optimistic,” Pinschewer adds.

The biotech company Hookipa Pharma, of which Pinschewer is one of the founders, is now investigating the efficacy of this novel approach to cancer therapy in humans. “We are currently exploring what our approach by itself can actually achieve,” the researcher says. “If it proves successful, a wide range of combinations with existing therapies could be envisaged, in which the respective mechanisms would join forces to eliminate tumors even better.”

Source:

Journal reference:

Bonilla, W.V., et al. (2021) Heterologous arenavirus vector prime-boost overrules self-tolerance for efficient tumor-specific CD8 T cell attack. Cell Reports Medicine. doi.org/10.1016/j.xcrm.2021.100209.

New therapy extends breast cancer survival rate, prevents reoccurrence

Tackling tumors with two types of virus

  • March 3, 2021

An international research group led by the University of Basel has developed a promising strategy for therapeutic cancer vaccines. Using two different viruses as vehicles, they administered specific tumor components in experiments on mice with cancer in order to stimulate their immune system to attack the tumor. The approach is now being tested in clinical studies.

Making use of the immune system as an ally in the fight against cancer forms the basis of a wide range of modern cancer therapies. One of these is therapeutic cancer vaccination: following diagnosis, specialists set about determining which components of the tumor could function as an identifying feature for the immune system. The patient is then administered exactly these components by means of vaccination, with a view to triggering the strongest possible immune response against the tumor.

Viruses that have been rendered harmless are used as vehicles for delivering the characteristic tumor molecules into the body. In the past, however, many attempts at creating this kind of cancer therapy failed due to an insufficient immune response. One of the hurdles is that the tumor is made up of the body’s own cells, and the immune system takes safety precautions in order to avoid attacking such cells. In addition, the immune cells often end up attacking the “foreign” virus vehicle more aggressively than the body’s own cargo. With almost all cancer therapies of this kind developed so far, therefore, the desired effect on the tumor has failed to materialize. Finding the appropriate vehicle is just as relevant in terms of effectiveness as the choice of tumor component as the point of attack.

Arenaviruses as vehicles

The research group led by Professor Daniel Pinschewer of the University of Basel had already discovered in previous studies that viruses from the arenavirus family are highly suitable as vehicles for triggering a strong immune response. The group now reports in the journal Cell Reports Medicine that the combination of two different arenaviruses produced promising results in animal experiments.

The researchers focused on two distantly related viruses called Pichinde virus and Lymphocytic choriomeningitis virus, which they adapted via molecular biological methods for use as vaccine vectors. When they took the approach of administering the selected tumor component first with the one virus and then, at a later point, with the other, the immune system shifted its attack away from the vehicle and more towards the cargo. “By using two different viruses, one after the other, we focus the triggered immune response on the actual target, the tumor molecule,” explains Pinschewer.

Tumor eliminated or slowed down

In experiments with mice, the researchers were able to measure a potent activation of killer T cells that eliminated the cancer cells. In 20% to 40% of the animals – depending on the type of cancer – the tumor disappeared, while in other cases the rate of tumor growth was at least temporary slowed.

“We can’t say anything about the efficacy of our approach in humans as yet,” Pinschewer points out. However, ongoing studies with a cancer therapy based on a single arenavirus have already shown promising results. The effects on tumors in animal experiments cannot be assumed to translate directly into the effect on corresponding cancer types in humans. “However, since the therapy with two different viruses works better in mice than the therapy with only one virus, our research results make me optimistic,” Pinschewer adds.

The biotech company Hookipa Pharma, of which Pinschewer is one of the founders, is now investigating the efficacy of this novel approach to cancer therapy in humans. “We are currently exploring what our approach by itself can actually achieve,” the researcher says. “If it proves successful, a wide range of combinations with existing therapies could be envisaged, in which the respective mechanisms would join forces to eliminate tumors even better.”

###

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