mRNA Breakthrough Offers a Potential Heart Attack Cure

King’s College London researchers are turning to the same technology behind the mRNA COVID-19 vaccines to develop the first damage-reversing heart attack cure. They used mRNA to deliver the genetic instructions for specific proteins to damaged pig hearts, sparking the growth of new cardiac muscle cells. “The new cells would replace the dead ones and instead of forming a scar, the patient has new muscle tissue,” lead researcher Mauro Giacca said. Researchers are turning to the same technology behind Pfizer and Moderna’s vaccines to develop the first damage-reversing heart attack cure.

Diseases of the heart are the leading cause of death around the world; the WHO estimates that 17.9 million people died from cardiovascular disease in 2019, representing almost a third of all deaths. Of those, 85% are ultimately killed by heart attacks and strokes. Heart attacks occur when blood flow to parts of the heart is blocked, often due to fat or cholesterol build up. The cardiac muscle cells — marvelous little powerhouses that keep you beating throughout your entire life — are starved of oxygen and can be damaged or killed. Left in its wake is not the smoothly pumping cardiac muscle, but instead scar tissue.

We are all born with a set number of muscle cells in our heart and they are exactly the same ones we will die with. The heart has no capacity to repair itself after a heart attack,” explained Giacca.

At least, until now. To develop their heart attack cure, the researchers turned to mRNA, which delivers the instructions for protein creation to cells. Whereas the Pfizer and Moderna vaccines instruct cells to make the spike protein of SARS-CoV-2, priming the immune system against the virus, the same technology can deliver a potential heart attack cure by carrying the code for proteins that stimulate the growth of new heart cellsPharmaTimes reported. In an experiment with pigs (a close match for the human heart), the mRNA treatment stimulated new heart cells to grow after a heart attackregenerating the damaged tissues and creating new, functional muscle rather than a scar.

According to BioSpace, harnessing mRNA in this way has been dubbed “genetic tracking,” named for the way the mRNA’s progress is tracked via the new proteins it is creating. The technique is being explored to create vaccines for pathogens like HIV, Ebola, and malaria, as well as cancers and autoimmune and genetic diseases. While thus far their heart attack cure has only been successfully tested in porcine pumpers, the team hopes to begin human clinical trials within the next couple years. “Regenerating a damaged human heart has been a dream until a few years ago,” Giacca said, “but can now become a reality.”


Can Plasma From Recovered Covid-19 Patients Cure Infected Others?

US Food and Drug Administration (FDA) officials announced today they have approved plans for nationwide trials of two treatments for Covid-19, the global pandemic disease caused by the new coronavirus—and for their simultaneous use in perhaps hundreds of hospitals.

The therapeutic agents—convalescent plasma and hyperimmune globulin—are both derived from the blood of people who have recovered from the disease, decoctions of the antibodies that the human immune system makes to fight off germs.


This is an important area of research—the use of products made from a recovered patient’s blood to potentially treat Covid-19,” said FDA commissioner Stephen Hahn in a release announcing the trials. “The FDA had played a key role in organizing a partnership between industry, academic institutions, and government agencies to facilitate expanded access to convalescent plasma. This is certainly a great example of how we can all come together to take swift action to help the American people during a crisis.”

Physicians are already using a somewhat haphazard collection of antiviral and other drugs for people critically ill with Covid-19, because they don’t have any other options. Nothing—no drug, no vaccine—is approved for use specifically against Covid-19 in the United States, so any new possibility is a hopeful one. Convalescent plasma and hyperimmune globulin join the rarified group of therapeutics that scientists are testing, including a trial of the Ebola drug remdesivir and the much-hyped antimalarial/immune suppressants chloroquine and hydroxychloroquine.

Using blood products from people who’ve already beaten a disease is a century-old approach, predating vaccines and antibiotics. Inspired by its use against polio, two physicians at a Naval hospital in Massachusetts tried it on people who had pneumonia as a result of influenza in 1918, with enough success to warrant more tests. The quality of actual studies of efficacy has varied over the decades, but health care workers used convalescent plasma against SARS, MERS, and Ebola. And a couple of studies—small and preliminary—have shown convalescent plasma having some promise against SARS-CoV-2 as well.

It was all promising enough that the FDA wanted to make sure current patients could have access to the plasma at the same time that researchers were starting a more rigorous investigation. “This seems like ancient history, but maybe it isn’t. There have been niche uses of it for a while,” says Michael Joyner, a physiologist at the Mayo Clinic who in March spearheaded the creation of an ad hoc coalition of researchers interested in pursuing the therapy. Joyner is facilitating the 40-center trial of the new therapies approved today by the FDA, with researchers at Johns Hopkins leading the science. (Joyner himself received gamma globulin, a variant of the treatment, as a preventative against hepatitis B in the 1980s, when he was a medical student.)

At Houston Methodist Hospital, James Musser, the chair of Pathology and Genome Medicine, is a friend of Arturo Casadevall, the Johns Hopkins University immunologist who proposed using convalescent serum early in the pandemic. Musser pushed to get his hospital involved, putting out a call for donors—people who had confirmed positive tests for the virus and had gone at least 14 days without symptoms. His hospital is already doing compassionate-use transfusions. “So far, as of yesterday, we’ve transfused four patients,” Musser said on Thursday. He expected a fifth to receive plasma today. And how’d it work?The truth is, it’s far too early,” Musser says. “We, nationally, need to do controlled trials and understand, first and foremost, is this a safe therapeutic? There’s lots of reasons to think it will be, but you never know.”


A Promising Antiviral Is Being Tested for the Coronavirus

As the coronavirus outbreak continues to spread worldwide and more people become critically ill, scientists are racing to find a treatment that will help turn the tide. Dozens of medicines are in clinical trials in China—and now in the U.S.—to treat the disease, officially named COVID-19. Some are antiviral drugs that are already used to narrowly target other viruses. Experts say these medications are unlikely to do much against the novel coronavirus. Other drugs being tested—such as the broad-spectrum antiviral remdesivir, developed by Gilead Sciences—could prove quite effective, some evidence suggests. But only the rigorous, controlled clinical studies now underway will be able to confirm this possibility.

At the time of this writing, the COVID-19 outbreak has sickened more than 82,000 people globally and killed more than 2,800 of them. No vaccine or direct treatment currently exists. The more than 80 clinical trials being conducted in China involve drugs that were developed to treat illnesses such as HIV/AIDS, malaria and Ebola. These candidates include HIV antivirals called protease inhibitors, which work by blocking enzymes the virus needs to replicate, and a malaria drug called chloroquine, which is not an antiviral but has shown some efficacy against COVID-19 in a lab dish. Yet experts say drugs that specifically target other pathogens are unlikely to work well enough.

The mistake generally made these days is to think that [just] any antiviral would be effective against [the coronavirus]. This is, of course, not true,” says Erik De Clercq, an emeritus professor of medicine at KU Leuven in Belgium, who helped discover the HIV antiviral tenofovir. De Clercq believes scientists should focus on developing compounds tailored to the new virus.

Instead of being in a hurry [to test] all known compounds—what they now call ‘repurposing a compound,’—we really need new compounds that are specific for [the coronavirus] and would be the subject of clinical trials,” he says. But until such compounds can be developed and tested, De Clercq says he is hopeful that remdesivir—an experimental drug that was originally developed to treat Ebola and has also proved effective against the SARS and MERS viruses in vitro—could be effective. (Gilead, which manufactures remdesivir, developed tenofovir and other antiviral drugs based on compounds De Clercq co-discovered.)


Why Are HIV Drugs Being Used to Treat the Coronavirus?

On Tuesday, the Japanese government announced it will begin clinical trials to test treatments for the deadly new coronavirus that’s engulfed China and spread to over two dozen countries. Rather than new drugs, they’ll be studying existing medications already used to treat HIV and other viral diseases. But why exactly are researchers hopeful that these drugs can be repurposed for the new coronavirus, and how likely are they to work?

The new coronavirus, recently named SARS-CoV-2 due to its close genetic ties to the SARS coronavirus, is made out of RNA. Other RNA viruses include the ones that cause Ebola, hepatitis C, and yes, HIV/AIDS.

RNA viruses come in all shapes and sizes, and those that infect humans can do so in different ways. But many of the drugs that go after HIV and the hepatitis C virus broadly target weaknesses found in all sorts of viruses. The approved hepatitis C drug ribavirin, for instance, interferes with something called the RNA-dependent RNA polymerase, an enzyme essential for many virusesincluding coronaviruses—to produce more of themselves inside a cell. HIV drugs like lopinavir inhibit other enzymes that allow viruses to break down certain proteins, which cripples their ability to infect cells and replicate.

Broad antiviral drugs like lopinavir should be able to work against SARS-CoV-2scientists theorize. And there’s already some circumstantial evidence they do. Some of these drugs have been successfully tested out for SARS and MERS, for instance, two other nasty coronaviruses that have emerged in recent years.

In January, the Chinese government announced a trial of 41 patients in Wuhan that would use a combination therapy of lopinavir and another HIV drug, ritonavir. In February, the Chinese government also began a trial using an experimental drug that’s been tested out for Ebola, called remdesivir.

Remdesivir has already been deployed during this outbreak, with seemingly impressive results so far. Last month, the first documented U.S. patient with the virus was treated with remdesivir, following a week of worsening symptoms that had developed into full-blown pneumonia. Within a day of receiving the drug through an IV, though, the man’s symptoms started to improve, and he was eventually released from the hospital.

But one case does not a surefire treatment make. And even if remdesivir or other drugs do prove effective against SARS-CoV-2, they’ll only play a small part in stopping this current outbreak from getting worse. Most cases of COVID-19 (the official name of the disease caused by SARS-COV-2) are still mild and won’t be helped much by antiviral drugs. In terms of preventing the next pandemic, it’s more important to keep people from getting the virus at all, rather than finding drugs to treat them once they do.


How To Stop Influenza Virus

The critical, structural changes that enveloped viruses, such as HIV, Ebola and influenza, undergo before invading host cells have been revealed by scientists using nano-infrared spectroscopic imaging, according to a study led by Georgia State University and the University of Georgia. The researchers found that an antiviral compound was effective in stopping the influenza virus from entering host cells during lower pH exposure, the optimal condition for the virus to cause infection.

Enveloped viruses are among the most deadly known viruses. These viruses have an outer membrane covering their genetic material, and to invade host cells enveloped viruses must first attach to a cell and then open their membrane to release genetic material. Originally, scientists believed this mechanism was controlled by the host cell. In this study, which focused on influenza virus, the researchers examined the structural changes that occur for the virus to open and release its genetic material. They conducted the experiment in the absence of cells and instead simulated the cell environment. When influenza virus infects a person’s body, it goes from a neutral environment outside the cell to a more acidic environment (a lower pH) inside the cell. To simulate the cell environment for this study, the researchers made the environment more acidic. The researchers exposed influenza virus particles to the lower pH and monitored structural changes in the virus.

What we saw is that even without the cell, if we change the environment, the virus particle will break and release the genetic material,” said Dr. Ming Luo, a senior author of the study and professor in the Department of Chemistry at Georgia State. “So it has a proactive mechanism built into the virus particle. Once the virus particle finds that the environment has changed, it will itself release the material. It doesn’t need the help of the cell membrane. It has to find a sweet spot to release the genetic material, and that sweet spot happens to have a low pH.”

The researchers used nano-infrared spectroscopy, a microscopic imaging system, to observe how influenza virus particles change when their environment changes. During his work at Georgia State, Dr. Yohannes Abate, now at the University of Georgia, adapted the imaging technology to have a new, unique function that allowed them to study virus particles in more detail.

The findings are published in the journal PLoS One.