Current Strategies to Tackle COVID-19
Since the pandemic started in 2020, a number of therapies have been developed to combat COVID-19.
The leading options for preventing infection include social distancing, mask-wearing, and vaccination. They are still recommended during the upsurge of the coronavirus’s latest mutation, the Omicron variant.
But in December 2021, The United States Food and Drug Administration (USDA) granted Emergency Use Authorization to two experimental pills for the treatment of new COVID-19 cases.
These medications, one made by Pfizer and the other by Merck & Co., hope to contribute to the fight against the coronavirus and its variants. Alongside vaccinations, they may help to curb extreme cases of COVID-19 by reducing the need for hospitalization.
Despite tackling the same disease, vaccines and pills work differently:
|Taken by injection||Taken by mouth|
|Used for prevention||Used for treatment only|
|Create an enhanced immune system by stimulating antibody production||Disrupt the assembly of new viral particles|
How a Vaccine Helps Prevent COVID-19
The main purpose of a vaccine is to prewarn the body of a potential COVID-19 infection by creating antibodies that target and destroy the coronavirus.
In order to do this, the immune system needs an antigen.
It’s difficult to do this risk-free since all antigens exist directly on a virus. Luckily, vaccines safely expose antigens to our immune systems without the dangerous parts of the virus.
In the case of COVID-19, the coronavirus’s antigen is the spike protein that covers its outer surface. Vaccines inject antigen-building instructions* and use our own cellular machinery to build the coronavirus antigen from scratch.
When exposed to the spike protein, the immune system begins to assemble antigen-specific antibodies. These antibodies wait for the opportunity to attack the real spike protein when a coronavirus enters the body. Since antibodies decrease over time, booster immunizations help to maintain a strong line of defense.
*While different vaccine technologies exist, they all do a similar thing: introduce an antigen and build a stronger immune system.
How COVID Antiviral Pills Work
Antiviral pills, unlike vaccines, are not a preventative strategy. Instead, they treat an infected individual experiencing symptoms from the virus.
These medications disrupt specific processes in the viral assembly line to choke the virus’s ability to replicate.
The Mechanism of Molnupiravir
RNA-dependent RNA Polymerase (RdRp) is a cellular component that works similar to a photocopying machine for the virus’s genetic instructions. An infected host cell is forced to produce RdRp, which starts generating more copies of the virus’s RNA.
Molnupiravir, developed by Merck & Co., is a polymerase inhibitor. It inserts itself into the viral instructions that RdRp is copying, jumbling the contents. The RdRp then produces junk.
The Mechanism of Nirmatrelvir + Ritonavir
A replicating virus makes proteins necessary for its survival in a large, clumped mass called a polyprotein. A cellular component called a protease cuts a virus’s polyprotein into smaller, workable pieces.
Pfizer’s antiviral medication is a protease inhibitor made of two pills:
- The first pill, nirmatrelvir, stops protease from cutting viral products into smaller pieces.
- The second pill, ritonavir, protects nirmatrelvir from destruction by the body and allows it to keep working.
With a faulty polymerase or a large, unusable polyprotein, antiviral medications make it difficult for the coronavirus to replicate. If treated early enough, they can lessen the virus’s impact on the body.
The Future of COVID Antiviral Pills and Medications
Antiviral medications seem to have a bright future ahead of them.
COVID-19 antivirals are based on early research done on coronaviruses from the 2002-04 SARS-CoV and the 2012 MERS-CoV outbreaks. Current breakthroughs in this technology may pave the way for better pharmaceuticals in the future.
One half of Pfizer’s medication, ritonavir, currently treats many other viruses including HIV/AIDS.
Gilead Science is currently developing oral derivatives of remdesivir, another polymerase inhibitor currently only offered to inpatients in the United States.
More coronavirus antivirals are currently in the pipeline, offering a glimpse of control on the looming presence of COVID-19.
Author’s Note: The medical information in this article is an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes. Please talk to your doctor before undergoing any treatment for COVID-19. If you become sick and believe you may have symptoms of COVID-19, please follow the CDC guidelines.
Visualizing the Relationship Between Cancer and Lifespan
New research links mutation rates and lifespan. We visualize the data supporting this new framework for understanding cancer.
A Newfound Link Between Cancer and Aging?
A new study in 2022 reveals a thought-provoking relationship between how long animals live and how quickly their genetic codes mutate.
Cancer is a product of time and mutations, and so researchers investigated its onset and impact within 16 unique mammals. A new perspective on DNA mutation broadens our understanding of aging and cancer development—and how we might be able to control it.
Mutations, Aging, and Cancer: A Primer
Cancer is the uncontrolled growth of cells. It is not a pathogen that infects the body, but a normal body process gone wrong.
Cells divide and multiply in our bodies all the time. Sometimes, during DNA replication, tiny mistakes (called mutations) appear randomly within the genetic code. Our bodies have mechanisms to correct these errors, and for much of our youth we remain strong and healthy as a result of these corrective measures.
However, these protections weaken as we age. Developing cancer becomes more likely as mutations slip past our defenses and continue to multiply. The longer we live, the more mutations we carry, and the likelihood of them manifesting into cancer increases.
A Biological Conundrum
Since mutations can occur randomly, biologists expect larger lifeforms (those with more cells) to have greater chances of developing cancer than smaller lifeforms.
Strangely, no association exists.
It is one of biology’s biggest mysteries as to why massive creatures like whales or elephants rarely seem to experience cancer. This is called Peto’s Paradox. Even stranger: some smaller creatures, like the naked mole rat, are completely resistant to cancer.
This phenomenon motivates researchers to look into the genetics of naked mole rats and whales. And while we’ve discovered that special genetic bonuses (like extra tumor-suppressing genes) benefit these creatures, a pattern for cancer rates across all other species is still poorly understood.
Cancer May Be Closely Associated with Lifespan
Researchers at the Wellcome Sanger Institute report the first study to look at how mutation rates compare with animal lifespans.
Mutation rates are simply the speed at which species beget mutations. Mammals with shorter lifespans have average mutation rates that are very fast. A mouse undergoes nearly 800 mutations in each of its four short years on Earth. Mammals with longer lifespans have average mutation rates that are much slower. In humans (average lifespan of roughly 84 years), it comes to fewer than 50 mutations per year.
The study also compares the number of mutations at time of death with other traits, like body mass and lifespan. For example, a giraffe has roughly 40,000 times more cells than a mouse. Or a human lives 90 times longer than a mouse. What surprised researchers was that the number of mutations at time of death differed only by a factor of three.
Such small differentiation suggests there may be a total number of mutations a species can collect before it dies. Since the mammals reached this number at different speeds, finding ways to control the rate of mutations may help stall cancer development, set back aging, and prolong life.
The Future of Cancer Research
The findings in this study ignite new questions for understanding cancer.
Confirming that mutation rate and lifespan are strongly correlated needs comparison to lifeforms beyond mammals, like fishes, birds, and even plants.
It will also be necessary to understand what factors control mutation rates. The answer to this likely lies within the complexities of DNA. Geneticists and oncologists are continuing to investigate genetic curiosities like tumor-suppressing genes and how they might impact mutation rates.
Aging is likely to be a confluence of many issues, like epigenetic changes or telomere shortening, but if mutations are involved then there may be hopes of slowing genetic damage—or even reversing it.
While just a first step, linking mutation rates to lifespan is a reframing of our understanding of cancer development, and it may open doors to new strategies and therapies for treating cancer or taming the number of health-related concerns that come with aging.
Explainer: What to Know About Monkeypox
What is monkeypox, and what risk does it pose to the public? This infographic breaks down the symptoms, transmission, and more.
Explainer: What to Know About Monkeypox
The COVID-19 pandemic is still fresh in the minds of the people around the world, so it comes as no surprise that recent outbreaks of another virus are grabbing headlines.
Monkeypox outbreaks have now been reported in multiple countries, and it has scientists paying close attention. For everyone else, numerous questions come to the surface:
- How serious is this virus?
- How contagious is it?
- Could monkeypox develop into a new pandemic?
Below, we answer these questions and more.
What is Monkeypox?
Monkeypox is a virus in the Orthopoxvirus genus which also includes the variola virus (which causes smallpox) and the cowpox virus. The primary symptoms include fever, swollen lymph nodes, and a distinctive bumpy rash.
There are two major strains of the virus that pose very different risks:
- Congo Basin strain: 1 in 10 people infected with this strain have died
- West African strain: Approximately 1 in 100 people infected with this strain died
At the moment, health authorities in the UK have indicated they’re seeing the milder strain in patients there.
Where did Monkeypox Originate From?
The virus was originally discovered in the Democratic Republic of Congo in monkeys kept for research purposes (hence the name). Eventually, the virus made the jump to humans more than a decade after its discovery in 1958.
It is widely assumed that vaccination against another similar virus, smallpox, helped keep monkeypox outbreaks from occurring in human populations. Ironically, the successful eradication of smallpox, and eventual winding down of that vaccine program, has opened the door to a new viral threat. There is now a growing population of people who no longer have immunity against the virus.
Now that travel restrictions are lifting in many parts of the world, viruses are now able to hop between nations again. As of the publishing of this article, a handful of cases have now been reported in the U.S., Canada, the UK, and a number of European countries.
On the upside, contact tracing has helped authorities piece together the transmission of the virus. While cases are rare in Europe and North America, it is considered endemic in parts of West Africa. For example, the World Health Organization reports that Nigeria has experienced over 550 reported monkeypox cases from 2017 to today. The current UK outbreak originated from an individual who returned from a trip to Nigeria.
Could Monkeypox become a new pandemic?
Monkeypox, which primarily spreads through animal-to-human interaction, is not known to spread easily between humans. Most individuals infected with monkeypox pass the virus to between zero and one person, so outbreaks typically fizzle out. For this reason, the fact that outbreaks are occurring in several countries simultaneously is concerning for health authorities and organizations that monitor viral transmission. Experts are entertaining the possibility that the virus’ rate of transmission has increased.
Images of people covered in monkeypox lesions are shocking, and people are understandably concerned by this virus, but the good news is that members of the general public have little to fear at this stage.
I think the risk to the general public at this point, from the information we have, is very, very low.
–Tom Inglesby, Director, Johns Hopkins Center for Health Security
» For up-to-date information on monkeypox cases, check out Global.Health’s tracking spreadsheet
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