It wasn’t just about the money, but about data, or rather the harvesting of data, which, if you want to be a stickler about it, is really also just all about making more money. In an industry that relies on data for much of its product development, digital, pharmaceutical, technical or otherwise, he who holds the most data, calls the shots.

Nowhere is this more true than in the field of genomics. The strides we’ve made in the last 10 years alone have revolutionized our ability to analyze and sequence genetic information, or DNA. DNA is the code to the life that flows through your body and your DNA is unique to you. It is your genetic fingerprint and holds the key to diseases, inherited or otherwise, that you may or still will, suffer from.

With each advance in our ability to decode DNA we move closer and closer to identifying key genes responsible for, well, just about everything that occurs in our bodies. We’ve also discovered that having certain genes misfire can predispose us to certain medical conditions and it is not unlikely that, in the near future, this information will allow us, with a fair degree of accuracy, to determine a person’s life span, and more importantly, invent pathways to intervene around suffering and disease.

So why now and why Covid?

Well, we’re now post pandemic, things have moved on, and Covid tests are now available that can be run at home. All good and well, but what happened to the billions of laboratory run PCR swabs we submitted to earlier in the pandemic? While companies undertook to destroy these, at no point did any testing laboratory issue a clear undertaking to not harvest your DNA from said swab.

During the pandemic, almost every American was subjected to a PCR test, sometimes on multiple occasions. Your details, along with your swab, were sent off to a laboratory for testing. I wrote an article on this topic way back in 2020, warning the public of the potential abuse of their data. You can read that piece here.

To think that an opportunity like this, literally a once in a lifetime present for data harvesting, would have been overlooked, is so preposterously naïve as to be laughable.

Which then raises the following questions;

• Who orchestrated the collection of this data? Was it government based, industry based, or a combined effort.
• Your DNA profile would now reside alongside your personal profile (remember, your details were attached to that swab). Who legally owns this DNA profile?
• Are the companies/government willing to issue an assurance as to the ethical use of this data, thereby ensuring you are not discriminated against, based on your DNA profile?
• As the data would have been illicitly harvested without your informed consent, are these questions simply moot, as no one will publicly acknowledge this?

Make no mistake, this was the DNA jackpot and companies may utilize this data to sell you products, refuse you products, refuse you work, refuse you insurance, withdraw your driving license, confiscate any guns you own (as soon as genes are identified that predispose an individual to violence or mental instability), the list is endless and the data worth an untold fortune.

It is, from a financial standpoint, potentially the biggest haul of the pandemic, a gift that will continue to offer returns to companies and governments until you close your eyes one day for the final time, probably on a predetermined day.

So the issue here isn’t really about “IF” your DNA was harvested from the swab you provided, but rather “WHO” now holds that DNA profile. If you’re considering committing a crime, I’d think twice about it, as that single hair you leave behind at the scene will result in the police knocking on your door. Remember, they don’t have to explain how they found you.

Isn’t this a good thing for our health?

It absolutely should be, if the powers that be could be trusted to act ethically with the data. We could identify individuals who are prone to certain diseases and conditions and intervene at an early stage, potentially saving billions of dollars in healthcare. Sadly, trust and ethics, particularly in the case of healthcare and government, were early victims of the pandemic, as the public was lied to, manipulated and then coerced on multiple levels.

Lets take an example. A gene is identified that can predict with 90% accuracy the onset of Disease X in people over the age of 40. Based on the DNA profiles now on record, filters show that 42 million Americans will contract Disease X in the next ten years. A quick calculation shows that treating, rather than preventing the disease will generate 30 times the profit, versus developing a cure.

Sadly, our healthcare systems are not designed for ethics and philanthropy. For the most part, they are FIAT driven systems that pursue profit as their ultimate goal. Only a naïve, well intentioned simpleton would suggest the above example has anything other than one inevitable outcome and it certainly isn’t cure.

The fact that the data has been harvested without your consent is of course, the ultimate red flag. If the public would have stood to only benefit health wise from the sharing of genetic data, don’t you think we would already have volunteered it? No. Deep down inside, we know we can no longer trust the institutions tasked with our wellbeing. They know that we know.

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CAR T therapy, a “living drug,” traditionally involves isolation and purification of T cells outside the body. The cells are then modified with a synthetic receptor and then re-infused into the body for treatment of cancers. Researchers have now successfully demonstrated that T cells can be modified in vivo by mRNA technology, bypassing the need for extraction, chemotherapy and re-infusion. Although this method proves effective in treating mice with scarred hearts, considering fibrosis contributes to over 800,000 deaths worldwide, the study contains great potential for human treatment.

A Damaged Heart 

The heart, flexible yet strong, circulates blood through the body by pumping blood through its chambers. Aging and injury tamper with this function, creating scarred and thickened tissue called fibrosis. Although fibrosis occurs normally when healing, a highly fibrotic heart loses its elasticity; the stiffened tissues and interrupted electrical signaling prevent proper contractions of the heart (see Figure 1). Cardiac fibrosis is highly associated with heart disease and heart failure.

Cardiac fibrosis has no “cure-all” treatment. Early detection improves prognosis, but options dwindle as damage progresses irreversibly. People with advanced cardiac fibrosis may take drugs which antagonize overstimulation of the heart or might even require heart valve replacement.

How CAR T Cells Work

In their study, Rurik et al. explore a new method to directly counter cardiac fibrosis. This method builds upon the basics of CAR T: the use of T cells with a synthetically engineered receptor to target and kill specific cells.

CAR T is approved to treat people with certain lymphomas, leukemias, and multiple myeloma. Figure 2 illustrates this process. In these cases, the desired T cells are extracted from the patient’s body. Synthetic mRNA is inserted into the cell with a retrovirus, a virus commonly used in gene therapy to permanently change other cells’ genomes. The altered and expanded cells are then infused back into the body after preparatory chemotherapy. These T cells target either CD19 or BCMA, two antigens found on malignant B cells.

The benefit of inserting genetic information with a retrovirus lies in its permanence. The CAR T cells can expand and persist in the body for a long time after infusion, continually fighting the cancerous cells they encounter. However, this is of no benefit to researchers hoping to fight cardiac fibrosis. If T cells continuously target fibrotic cells, they would impair normal healing processes and potentially induce autoimmunity. Rurik et al. employ an elegant solution which shortens the CAR T cells’ active duty, thereby circumventing the extraction process altogether.

 New CAR T Cell Design 

The team adapted mRNA delivery technology seen in current COVID-19 vaccines and applied it to basic Chimeric Antigen Receptor design. The mRNA does not integrate into the T cell genome, allowing for temporary transcription of the mRNA and transient expression of the new receptor.

CD5 Lipid Nanoparticles (LNP) 

The authors adopted a strategy to introduce the chimeric receptor to T cells in the body rather than extracting and purifying them outside the body. To accomplish this aim, they first synthesized mRNA that encodes a receptor against fibroblast activation protein (FAP), a protein expressed on activated fibroblasts responsible for fibrosis. They purified the mRNA and packaged the engineered mRNA into standard lipid nanoparticles (LNP).

The team then decorated the lipid nanoparticle surface with CD5 targeting antibodies to direct lipid uptake. The integration of CD5 antibodies allowed the lipid nanoparticles to target antigen CD5 naturally expressed by T cells once injected into the body; the CAR T cells are made after a single shot.

Chimeric Antigen Receptor 

The chimeric antigen receptor contains a single chain variable fragment (scFv) derived from fibroblast activation protein monoclonal antibodies; this recognition domain enables the CAR T cell to target cells which express fibroblast activation protein. The CAR design also includes CD28 and CD3z signaling domains in the cytoplasm. All three components are mouse-specific. Not illustrated in Figure 3 is an added small peptide which prevents immune suppression.

Genetic Integration In Vivo

The team found that lipid nanoparticles could successfully deliver the mRNA package to T cells, as seen in Figure 4. The killer T cell absorbs the lipid nanoparticle by endocytosis. The lipid particle then degrades and the synthetic mRNA releases into the cell. Finally, the cellular machinery reads the genetic instruction and briefly produces the receptor against fibroblast activation protein. This is possible with both animal and human T cell cultures.

Transitory CAR Expression 

Unlike traditional CAR T cells that carry a chimeric receptor encoded by DNA inserted into the genome, these CD5+ T cells carry mRNA only transiently. The mRNA is not integrated into the cell’s genome and remains stuck in the T cell cytoplasm before degrading. This is ideal; fibroblast activation protein receptors must be expressed briefly as longer expression may harm other tissues.

 Results 

The research team assessed the efficacy of the CAR T cells in different conditions. When they treated the cells in tissue culture, more than 80% of T cells expressed the chimeric antigen receptor and could effectively kill target cells with fibroblast activation protein.

The team then tested this model on mice with cardiac fibrosis. The mice received medication to injure the heart and induce scarring. After one week, the team administered the lipid-mRNA injection. Consistent CAR expression was noted 48 hours after injection, and disappeared after one week.

The results were impressive. The function of the heart’s largest chamber improved, in some cases returning to uninjured levels. Similarly, the amount of blood filling the heart normalized to safe volumes. The therapy notably reduced the thickness of the heart. Finally, although the mass of the largest chamber did not normalize, it trended towards improvement.

One caveat in lipid-CAR T cell delivery is that some cells, perivascular fibroblasts, do not express fibroblast activation protein. In consequence, these cells were not impacted by CAR T cells and some fibrosis persisted. No overly toxic side effects were noted.

Trogocytosis

A key observation of effective CAR T therapy is the ability of the modified T cells to take small bites of the target cell—a phenomenon known as trogocytosis. Deriving “trogo” from the Greek word “to bite,” trogocytosis entails one cell nibbling another and, in the process, transferring the surface molecules from one to the other. The researchers found evidence of CAR T cells “nibbling” the activated fibroblasts and retaining the stolen antigens (illustrated in Figure 5), suggesting that the T cells successfully adopted the chimeric antigen receptors in vivo.

Future Implications

CAR T therapy revolutionized cancer treatment with its efficacy and innovation. Combining mRNA technology to this therapy creates a temporary version of this “living drug” that does not sacrifice on quality. The therapy is well tailored to heal mice with damaged and scarred hearts, and widens the possibilities to treat other non-cancerous human ailments. If translated to clinical settings, transient CAR T therapy may be less expensive and more readily available than its traditional counterpart

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Can viruses alter our very genetic code, effectively hijacking and hiding in our cells for generations and how does this affect the health of future generations? Could viruses be mutating us, cell by cell? Sounds like science fiction, doesn’t it?

To answer these questions conclusively, we need to first go back to 1918 and the greatest killer of all time. I’m not referring to the First World War, but rather the Spanish Influenza.

The 1918 Spanish Flu Pandemic

It killed between 50 and 100 million people in three pandemic waves between 1918 and 1919. The chart below shows death rates in a some of the affected areas.

As with other 20th-century epidemics and pandemics, such as HIV/Aids, Africa, and Asia suffered proportionately more than Europe and North America.

Whilst the average case mortality in the developed world was about 2%, in India, where 18.5 million perished, it was 6%, and in Egypt, where 138,000 died, it was 10%. If we adjust for population growth, in today’s world the Spanish Flu would have claimed between 200 million and 425 million people.

So-called, not because it originated in Spain, but because Spain was the only country to openly speak about the pandemic, the Spanish Flu was unusual. Unlike traditional influenza outbreaks, it targeted healthy individuals between the ages of 15 and 40, sparing the aged.

Thanks in no small part to people like Jeffrey Taubenberger, a molecular pathologist at the National Institute of Allergy and Infectious Diseases who has been studying the 1918 virus for nearly thirty years, we now have a much better idea of exactly what the world was dealing with.

In the late 1990s, he succeeded in retrieving fragments of viral RNA from stored pathology specimens taken from American soldiers who had died of flu at a US army camp in 1918 and an Inuit woman who’d been buried on a beach in Alaska, where the permafrost had preserved her lung tissue from decay.

The discovery of H1N1

In 2005, Taubenberger and his colleague, Anne Reid published the virus’s genetic sequence. Their findings were a shock. Previously, epidemiologists had observed that flu pandemics were preceded or followed by outbreaks of influenza-like illnesses in dogs, cats, and horses. It was also known that from time to time flu viruses could infect pigs and, of course, humans, and that wild flu virus circulated in migratory waterfowl.

When Taubenberger analyzed the genome of the Spanish flu, he found that most of its genes were derived from a bird flu virus. Taubenberger considered the H1N1 virus so ‘avian-like’ he could not discount the possibility that it had transmitted directly from birds to humans shortly before 1918 and perhaps as early as 1916.

The source of the outbreak is still a matter of debate. The genes map most closely to wild waterfowl from North America but, despite examining the Smithsonian Institute’s extensive bird collections, Taubenberger was not able to find viable autopsy remains from before 1918.

One theory suggests ‘spillover’ may have occurred in early 1918, not far from an army camp in Kansas that supplied soldiers to the American Expeditionary Force. Another option favored by British virologist John Oxford is that the pandemic began at Étaples, a huge British military camp an hour south-west of Boulogne.

Why does all of this matter?

Why should we be concerned with these facts? After all, the virus did not survive, did it?

It has survived. We simply did not know what to look for before it was correctly identified. Genes from the Spanish flu continue to circulate in both human and pig populations to this day. Some of these genes are direct descendants of the 1918 virus whilst others have reassorted with other pandemic viruses, such as the 1968 Hong Kong flu and the hybrid H1N1 virus responsible for the 2009 swine flu pandemic which originated in the USA.

This matters because, in mice, the H1N1 Spanish flu is extremely virulent, generating 39,000 times more virus particles than a modern flu strain. Research has shown that by targeting the immune response in infected mice they can be protected but humans still remain at risk.

How is it possible though that the virus continues to be carried by human hosts a hundred years later? How has this happened and what mechanisms have enabled this. Has it become a part of our genetic code and if so, how does this process occur? More importantly, what have the consequences been to the carriers and their descendants?

Are we carrying the seeds for future epidemics in our own genes and has the viral world discovered the perfect hiding place whilst it waits? Inside its hosts?

To understand the processes at work here we first need a little basic science on human genes, chromosomes, and how our DNA functions. It might get a little hairy here, but I’ve tried to simplify this as much as possible.

Understanding Cells, Chromosomes, Genes and DNA.

This topic gets complicated really quickly so for ease of understanding, here’s the simple version and if you keep to the ordering above, it will help you understand how they tie together.

All life is made up of cells. All cells in the human body, except red blood cells, contain chromosomes.

The word ‘chromosome’ comes from the Greek words khroma meaning “color” and soma meaning “body”. Laboratory experiments in the 1880s revealed chromosomes could be easily stained with dyes, thus making studying them easier. Hence the name.

Let’s recap. Cells, and inside these, chromosomes. On each of these chromosomes, we find a gene. You know genes as the traits you pass on to your children. These are unique instructions for hair color, height, and all the other features that make you, well, you.

Every factor in inheritance is due to a particular gene. Genes specify the structure of particular proteins that make up each cell. Gene comes from the Greek word genea meaning generation, origin, beginning, kin, or sometimes race. Gene was shortened from “pangene” which means “all-generation”.

Finally, Genes contain DNA (deoxyribonucleic acid). DNA is the chemical basis of heredity.

Again, for clarity. DNA is in genes, genes are on chromosomes and live in our cells. You’ve probably heard of the Human Genome Project. This was a project undertaken to map all genes and chromosomes in a human. The combination of gene and chromosome gives it its name – Genome.

For those of you who wish to explore the topic in more depth, here is an excellent and still reasonably easy to follow article from Nature on DNA structure. We’re going to head off now on what may appear at first to be a tangent, but the reason for this will become clearer as you read.

Genetic conditions and Gene Therapy

Gene therapy is an experimental technique that uses genes to treat or prevent disease. In the future, this technique may allow doctors to treat a disorder by inserting a gene into a patient’s cells instead of using drugs or surgery. Researchers are testing several approaches to gene therapy, including:

• Replacing a mutated gene that causes disease with a healthy copy of the gene.
• Inactivating, or “knocking out,” a mutated gene that is functioning improperly.
• Introducing a new gene into the body to help fight a disease.

Gene therapy is currently only considered as a treatment for diseases or conditions that do not respond to conventional medicine.

Several inherited immune deficiencies have been treated successfully with gene therapy. Most commonly, blood stem cells are removed from patients, and retroviruses are used to deliver working copies of the defective genes. After the genes have been delivered, the stem cells are returned to the patient.

Because the cells are treated outside the patient’s body, the virus will infect and transfer the gene to only the desired target cells.

The conditions where gene treatment is offering the most hope include Fat metabolism disorder, Parkinson’s, Auto-Immune disorders, Cancer, Blood Disease, Hemophilia, Hereditary Blindness, and others. For a more detailed overview consult this article from the Genetics department at the University of Utah

So now you’re probably wondering why viruses feature in gene therapy and what exactly are retroviruses? Let’s examine that in a little more depth.

Viruses and Retroviruses

Viruses, or more accurately retroviruses, play an essential role in gene therapy. This is because of a virus’s ability to penetrate cells and affect changes on a cellular level within the human body.

Viruses are tiny microbes that can infect cells. Once in a cell, they use cellular components to replicate. They can be classified according to several factors, including:

• the type of genetic material they use (DNA or RNA)
• the method they use to replicate within the cell
• their shape or structural features

Retroviruses are a type of virus that use RNA as their genetic material and a special enzyme called reverse transcriptase to translate the virus’s genetic information into DNA.

That DNA can then integrate into the host or your cell’s DNA. At this point, the retrovirus can replicate itself using your cell’s resources.

Hold up, what is RNA?

RNA is similar to DNA in lots of ways. The really crucial difference is that RNA has an extra oxygen molecule. This makes RNA less stable than DNA. If it’s less stable, why do viruses choose to rely on it?

Here are the advantages. Organisms that need to change rapidly tend to use RNA as their genetic material. Viruses, such as influenza and HIV, choose RNA rather than the more stable alternative of DNA so they can change and keep one step ahead of the immune system of their hosts.

RNA has another critical function in virtually all organisms. It acts as a messenger; a short-lived intermediate communicating the information contained in our genes to the rest of the cell.

RNA acts as a messenger in the process of ensuring genes are translated into proteins, the tools of the cell, things such as haemoglobin to carry oxygen around the body.

Why can RNA trigger chemical reactions but DNA doesn’t seem to? The reasons are two-fold. Firstly RNA possesses the extra oxygen molecule, DNA doesn’t. Secondly, the special ability of RNA to fold up into complex shapes allows it to form tools that can do things inside the cell, The DNA double helix holds information securely but doesn’t do much else.

If you want to manipulate and control a cell and its genetic material, RNA is the way to go. This is why it’s the virus’s tool of choice.

How Retroviruses work

To better understand the difference between the two types of virus, let’s use the example of the life cycle of AIDS or Acquired Immunity Deficiency Syndrome Virus. This example focuses on how retroviruses (the AIDS virus) replicate within a cell, the main distinctive feature that separates them from viruses.

• Attachment. The virus binds to a receptor on the surface of the host cell. In the case of HIV, this receptor is found on the surface of immune cells called CD4 T cells.
• Entry. The envelope surrounding the HIV particle fuses with the membrane of the host cell, allowing the virus to enter the cell.
• Reverse transcription. HIV uses its reverse transcriptase enzyme to turn its RNA genetic material into DNA. This makes it compatible with the host cell’s genetic material, which is vital for the next step of the life cycle.
• Genome integration. The newly synthesized viral DNA travels to the cell’s control center, the nucleus. Here, a special viral enzyme called integrase is used to insert the viral DNA into the host cell’s DNA.
• Replication. Once its DNA has been inserted to the host cell’s genome, the virus uses the host cell’s machinery to produce new viral components, such as viral RNA and viral proteins.
• Assembly. The newly made viral components combine close to the cell surface and begin to form new HIV particles.
• Release. The new HIV particles push out from the surface of the host cell, forming a mature HIV particle with the help of another viral enzyme called protease. Once outside the host cell, these new HIV particles can go on to infect other CD4 T cells.

So if retroviruses are able to interfere with our genes and hijack our cell mechanisms, what about a normal virus? In particular, what about our pesky neighborhood pandemics, The H1N1 strains, and novel Coronavirus? I’ve examined results from SARS-CoV, the 2002 virus, and not SARS-CoV2 (COVID19) as we do not as yet have sufficient reliable clinical data on the latest outbreak. Sequence homology (a process to assess similarities) of SARS-CoV-2 with SARS-CoV and MERS-CoV was 77.5% and 50%, respectively.

The information contained below is from this article in the American Journal of Pathology. Please refer for sources.

The novel Coronavirus (SARS-CoV) belongs to a family of large, positive, single-stranded RNA viruses. Genomic characterization shows that the SARS-CoV is only moderately related to other known coronaviruses.

ACE2, a metallopeptidase, was identified as the functional receptor for SARS-CoV. (COVID19 is assumed to also utilize ACE2 as its functional receptor)

Recently, human autopsy studies have shown that SARS-CoV S protein and its RNA could be detected in ACE2-positive cells and not in ACE2-negative cells. This implies that only ACE2-positive cells are susceptible to SARS-CoV infection. This finding contradicts existing research and requires further investigation.

Genetic factors also seem to play a causative role in the pathogenesis of SARS. For a group of Taiwanese patients, the HLA-B*4601 haplotype was associated with the severity of SARS infection.

As far as viruses are concerned, our genes really do matter.

What the virus does inside our bodies

COVID19 is different from the 2002 SARS-COV virus. It is far more infectious and researchers now think they’ve figured out why. Spike proteins are what coronaviruses use to bind to the membranes of human cells they infect. The binding process is activated by certain cell enzymes.

COVID19 is different. It has a specific structure that allows it to bind at least 10 times more tightly than the corresponding spike protein of SARS-CoV to their common host cell receptor. This is in part due to the fact that the spike protein contains a site that recognizes and becomes activated by an enzyme called furin.

This matters as furin is a host-cell enzyme in various human organs. It is found in the liver, the lungs, and the small intestines, allowing the virus to potentially attack several organs at once.

According to researchers, the “furin-like cleavage site” recently discovered in SARS-CoV-2 spike proteins may explain the viral life cycle and pathogenicity of the virus. Studies are now confirming that these ‘furin-like cleavage sites’ are what makes COVID19 so infectious.

Worryingly, researchers have drawn parallels between SARS-CoV-2 and the avian influenza viruses. They note that a protein called haemagglutinin in influenza is the equivalent of the SARS-CoV-2 spike protein. Furin activation sites may be what make these viruses so highly pathogenic.

What happens once the COVID19 virus gains access to your cells? Here is the latest research from the University of California SAN Francisco, summarised below.

To infect us, the SARS-CoV-2 virus gets its genetic material into our cells and then co-opts our own proteins, reassigning them to the task of making millions of copies of itself.

This tsunami of copied viruses ultimately kills cells, releasing virus particles that travel through the body to infect more cells or be spread to new human hosts, perpetuating the outbreak.

Scientists have identified the proteins in our body the virus uses and now hope to identify drugs to combat or halt the virus’s ability to replicate using these proteins.

You should now have a much clearer understanding of the mechanisms at play when viruses attack our cells.

We can now focus on the original questions we raised. Do viruses encode themselves into our genes? Do those who survive them transmit copies of the virus to their children through their DNA and can viruses mutate our cells, and by association our genetic codes.

An entwined viral and genetic history

If you escape the COVID19 virus or don’t develop serious symptoms it could be thanks to your parents and their ancestors. All of them.

According to an article from the National Institute of General Medical Sciences (NIGMS) viruses have been engaged in genetically engineering their hosts (read us) since the dawn of mankind.

Now, nearly 10 percent of the human genome is made of bits of virus DNA. For the most part, this viral DNA is not harmful. In some cases, scientists are finding, it actually has a beneficial impact.

When viruses infect us, they can embed small chunks of their genetic material in our DNA. Although infrequent, the incorporation of this material into the human genome has been occurring for millions of years. As a result of this process, nearly 10 percent of the modern human genome comprises viral genetic material.

Over time, most of the viral invaders populating our genome have mutated to the point that they no longer lead to active infections.

Occasionally, these stowaway sequences of viral genes, called “endogenous retroviruses” (ERVs), can contribute to the onset of diseases such as cancer. They can also make their hosts susceptible to infections from other viruses.

However, some of our viral hitchhikers bestow crucial benefits to their human hosts. They offer protection against disease and have shaped important aspects of human evolution, such as our ability to digest starch.

So the definitive answer to the question as to whether viruses can alter our genetic structure is a resounding yes. The relationship is complex and these viral passengers come with advantages and disadvantages.

It’s an incredibly difficult field to study as is explained in the following article. Studies cannot be conducted in human subjects but model organisms are proving a powerful experimental platform.

In terms of the advantages and disadvantages we acquire from our viral passengers, we have no way of knowing how these impact us and how they will impact future generations. Scientists are only now unravelling the complexities of ERV’s.

What we do know for sure is that although your flu symptoms may abate as you get over the infection, the virus you contracted will remain with you as part of your genetic makeup to be passed on to future generations.

As to these future generations paying the price for their ancestors exposure, the following story offers an interesting perspective.

South Africa and the Spanish Flu

Time to head back to 1918 and the Spanish Flu for a telling example afforded us by the passage of time.

South Africa was seriously affected by the 1918 pandemic. Nearly 500 000 people or 8% of its population died. Of these deaths, nearly 80% were of black African decent. Also particularly hard hit were the white Afrikaners, predominantly Dutch families living in the country.

Separated from their European ancestors by two or three generations, the Dutch represented a unique demographic in South Africa and their survivors of the pandemic suffered an unusual consequence of their infection.

Today, a large percentage of their direct descendants give birth to children with really poor eyesight. A statistically significant segment of their children require glasses at an early age, some as early as three.

The genetic cause has been traced back to the effects of the 1918 viral infection on their ancestors. One hundred years later, the H1N1 strain is still with us and we feel its effects in ways we may not be aware of. How this gene manipulation will play out in future generations remains to be seen.

Sadly, I have been unable to track down the relevant data referencing the research for the above, perhaps a South African medical student or doctor would be kind enough to provide the reference?

There is a lot of evidence to suggest that the 1918 pandemic would have claimed far fewer lives had people not been subjected to cramped conditions towards the end of the war. The lesson is a clear one.

Stay home, stay safe, wear a mask and help flatten the curve.

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