COVID-19 re-infection re-infection risk is relatively low, but not zero. Studies suggest that people who have had COVID-19 may have some level of immunity to the virus, at least for a certain period. However, this immunity may not be long-lasting and may vary depending on a person’s age, overall health, and other factors.

The risk of re-infection also depends on the prevalence of the virus in a person’s community and their level of exposure to it. If someone is exposed to the virus again, their immune system may be able to recognize and fight off the virus more quickly, potentially resulting in milder symptoms.

Several studies have reported cases of COVID-19 re-infection, although these cases appear relatively rare. The Centers for Disease Control and Prevention (CDC) has stated that re-infection with COVID-19 is uncommon within 90 days of the initial infection.

However, it is still important to follow public health guidelines to prevent the spread of the virus, even if you have previously been infected. Mitigation strategies include wearing a mask, practicing physical distancing, and getting vaccinated when a vaccine is available to you.

Let’s explore the most comprehensive data compiled to analyze national immunity protection against the virus. The researchers recently published their findings in The Lancet.

“I didn’t expect to recover from my second operation but since I did, I consider that I’m living on borrowed time. Every day that dawns is a gift to me and I take it in that way. I accept it gratefully without looking beyond it. I completely forget my physical suffering and all the unpleasantness of my present condition and I think only of the joy of seeing the sun rise once more and of being able to work a little bit, even under difficult conditions.”
― Henri Matisse

Covid-19 infection and future risk reduction

Researchers analyzed 65 studies from 19 countries. Let’s get right to the bottom-line conclusion of the study authors:

[The] meta-analyses showed that protection from past infection and any symptomatic disease was high for (COVID-19) ancestral, alpha, beta, and delta variants but were substantially lower for the Omicron BA.1 variant. A Covid infection provided some protection against re-infection from the original (ancestral), alpha, and delta variants. While the risk reduction diminished over time, it remained at 79 percent at 40 weeks.

Protection against re-infection by the Omicron BA.1 variant diminished more quickly, reaching 36 percent at 40 weeks.

Protection from re-infection from ancestral, alpha, and delta variants declined over time but remained 78.6 percent at 40 weeks (around ten months).

The report notes that protection against re-infection by the Omicron BA.1 variant declined more rapidly and was estimated at 36 percent over that same 40-week period.

Covid infection and future severe infection

What about severe infection? Having an infection protects against severe infections from future infections. More specifically, the protection was 90.2 percent for the original, alpha, and delta variants and 88.9 percent for Omicron BA.1 at 40 weeks (about ten months).

As protection appears to wane over time, even individuals with natural immunity will likely still need an annual COVID booster shot to maximize risk reduction for severe illness.

The post Got Covid? How Long Do You Have Protection After Catching the Virus? appeared first on Medika Life.

Using the body’s own immune cells as anticancer agents has long been part of this dream. I was an early pioneer in creating one of the first proven cell therapies using dendritic macrophages to treat prostate cancer. Today, immune cell therapy offers hope to people with cancer and other previously untreatable diseases.

This series will explain a recent and revolutionary cell therapy called CAR T, delving into current successes and future opportunities.

The “T’ of CAR “T” 

CAR T is short for Chimeric Antigen Receptor T cells. Essential to understanding this therapy is an understanding of T cells and cell-mediated immunity.

Adaptive Immunity 

Adaptive immunity allows humans to form a tailored defense to foreign invaders. Adaptive immune cells memorize the telltale signs of enemies and trigger defensive mechanisms if the signs are detected in the future. This branch of immunity concerts two separate arms—humoral immunity driven by antibody-producing B cells, and cell-mediated immunity driven by “helper” T cells and “killer” T cells.

CAR T technology alters the typical functioning of cytotoxic cells. Instead of indirectly aiding antiviral processes as CD4+ helper T cells do, CAR T borrows the cytotoxic power of CD8+ killer T cells to destroy infected or abnormal host cells, thus transforming into a “living drug.” A typical cytotoxic T cell eliminates threats using the following process:

WIKIPEDIA Link Added

The process (as illustrated in Figure 1) begins with the differentiation of an inactive T cell—in essence, any T cell without a specified purpose. As if waiting for the right key, a T cell does not activate unless it encounters an antigen presenting cell (APC) with its corresponding antigen. In order for an interaction between the two cells to occur, several steps must occur.

Firstly, the antigen presenting cell must process the antigen, the enemy components, into smaller peptides. Then, these peptides must be carried to the antigen presenting cell’s surface by major histocompatibility complexes (MHC). Immature CD8+ T cells require MHC Class I molecules to facilitate this translocation. Around this time, a secondary signal such as CD80 or CD86 must also be received by the T cell. In the final step, the antigen presenting cell releases a protein signal called CD40 and cooperates with helper T cells to finalize the differentiation process.

How Killer T Cells Kill 

DANANGUYEN DERIVATIVE: NAGUALDESIGN

Killer T cells destroy infected and abnormal cells by inducing apoptosis, a form of controlled cell death which does not spark inflammation. Pockets of enzyme within the T cell must make contact with the target cell to trigger its death.

When a cytotoxic T cell recognizes its target, it binds to the class I MHC molecule on the surface of the target cell (see Figure 3) to create a bridge. With the bridge completed, the T cell can then release the enzymes. One enzyme drills pores in the target cell’s membrane, thus ruining its integrity. The other travels through these newly made tunnels, tipping an enzyme cascade inside the target cell which accelerates its degradation.

The crumbling target cell mimics the imagery of bricks falling from castle walls. Nearby phagocytes recognize the “crash of bricks”—more accurately, sense a change in membrane—and begin ingesting the target cell. The target cell breaks down to nothing inside the phagocyte without stimulating inflammation or other side effects.

Construction of a Chimeric Antigen Receptor 

Killer T cells are clearly useful in clearing irregular host cells. Researchers recognized this and sought to harness this natural design to eliminate cancer cells through CAR T. Chimeric antigen receptors are engineered to detect a specific antigen and trigger the destruction of a target cell. The most basic CAR T design accomplishes this by manipulating antigen binding sites normally intrinsic to antibodies—single chain variable fragments (scFV)—to lend cytotoxic T cells higher antigen specificity. The CAR T cell recognizes specific antigens thanks to this domain.

Next comes the flexible hinge region. This region simultaneously stabilizes the CAR while its length provides grants easier access to specific antigens. The transmembrane domain anchors the antibody and hinge structure.

The intracellular domain describes receptors lying within the T cell. Basic CAR T design employs CD3 here, a T cell receptor needed for T cell differentiation (see Figure 4). Second and third generation CAR models included secondary signal receptors such as CD28 to improve target cell elimination and cell signaling (Figure 5).

More recent research developments in CAR design deviate from this foundational model to finetune precision and function. For example, T cell receptor fusion construct (TRuC) CAR tethers the scFV region to the several intracellular CD3 subunits, thereby reducing secondary signaling hypothesized to be unnecessary.

Universal CAR (uCAR), on the other hand, augments antibody specification by fusing biotin to the transmembrane domain and the endodomain. Other research efforts incorporate cytokines (signaling molecules) and other molecules to improve T cell expansion and persistence, as well as synthetic control switches to minimize the therapy’s toxic side effects. The groundwork model inspires many alternative CAR designs beyond those demonstrated here.

The beauty of this science lies in the melding of two previously separate abilities. CAR T therapy replaces the T cell receptor with an antibody-like structure, all while maintaining the transduction machinery of a T cell. Like this, MHC class I binding becomes irrelevant and a response can be immediately triggered.

The CAR T Therapy Process 

What does the CAR T therapy process look like?

Figure 2 illustrates the progression clearly. For a patient receiving CAR T therapy, the process may begin with a medical professional drawing their blood and separating T cells from that sample using apheresis; this would be an autologous treatment, as the cells used originate from the same patient. T cells can also be isolated from a healthy donor’s blood sample, otherwise known as allogeneic transplantation.

The cells must then be genetically altered to recognize a particular target in a cell processing center. To do this, the cells are “expanded”—a process which stimulates T cell proliferation. The new plethora of T cells must be purified and then genetically modified with a gene that encodes the desired chimeric antigen receptor. CRISPR technology can be used here to accomplish the task.

The cells are now ready for infusion. The cells are frozen and sent back to the treatment center. The patient preps for infusion with a lymphocyte-depleting chemotherapy; the chemotherapy reduces the number of white blood cells in the blood to reduce competition for the CAR T cells, thus helping them multiply. With success, the engineered T cells will recognize the antigen on cancerous cells, bind to it, and mark it for destruction via apoptosis. The infusion takes between 30 to 90 minutes to complete, but the patient will be closely monitored for days, weeks or months to watch for any adverse side effects and to receive additional treatments.

Side effects can occur if the “living drug” multiplies too actively, the most common being cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Also commonly known as “cytokine storm,” CRS occurs when proteins called cytokines flood the immune system and send it into overdrive. Symptoms tend to be mild—fever, nausea, headache, rash, and more—and resolve within a couple of days, but they can also be severe or life threatening. ICANS refers to a neurotoxic condition that appears within one to three weeks after T cell infusion. Early signs, such as tremor and lethargy, can lapse into stupor, seizures or coma if untreated. More on managing side effects to come in later installments in this series.

The long term side effects of CAR T are unknown. As a result, the FDA stipulates that gene editing treatments such as CAR T therapy should be monitored for up to 15 years—five years of annual follow ups, followed by ten years of questionnaires and/or other queries.

What Illnesses Can CAR T Treat?

CAR T therapy is FDA approved to treat B cell-derived lymphomas—cancers caused when B cells (not T cells) grow too rapidly—as well as multiple myeloma, cancer of plasma cells found in the bone marrow. These treatments tailor chimeric antigen receptors to target an antigen called CD19 found only on the tumor cells of lymphoma patients. Another target is BCMA, a B cell maturation antigen specific to multiple myeloma.

CAR T therapies may be federally approved, but they are not used as first or second line cancer treatments; usually CAR T therapy is considered after receiving standard chemotherapy treatment and other alternatives. And as a newer treatment, it may be more expensive than other therapies or may not be fully covered by health insurance.

But this field is ever growing. Several hundred clinical trials are in progress to test the boundaries of this mechanism and enhance its design. The next installations in this series will cover some of the most recent discoveries in the CAR T circuit, such as treatment advances in B cell lymphomas, lupus and heart disease, as well as innovations in CAR T precision.

The post From Lymphoma To Lupus And Beyond: The Remarkable Research Of CAR T Therapy appeared first on Medika Life.

But what bout when your immune system mistakes your tissues for a threat? You may develop an autoimmune disorder.

Autoimmune conditions include type 1 diabetes, rheumatoid arthritis, multiple sclerosis, Crohn’s disease, lupus, psoriasis, certain thyroid problems, and more. Women are more likely to develop such problems.

Autoimmunity: Definition

An aberrant immune response directed at a normal body entity characterizes autoimmune diseases. The immune system’s B or T cells (or both) get revved up without an ongoing infection or other detectable cause. This unwanted response leads to cell injury and inflammation.

Autoimmune diseases can be generalized or tissue- or organ-specific. They can be acute or chronic.

With the exceptions of autoimmune thyroiditis and rheumatoid arthritis, autoimmune diseases are fortunately relatively rare. Still, autoimmune diseases, in aggregate, strike five percent of the population in Western countries.

Autoimmune mechanisms

Autoimmunity affects targets such as proteins, carbohydrates, and nucleic acids. We call such targets self-antigens or autoantigens. On the other hand, a molecule from an infecting organism that stimulates an immune response is a foreign antigen or non-self.

While autoimmune diseases are the product of a pathologic state, autoimmunity is based on mechanisms that underlie normal immune responses to foreign substances.

We may divide immune responses into two categories, including innate and adaptive. The former is a rapid, non-specific response to stress, trauma, or an infection. On the other hand, an adaptive immune response is slow (days to weeks). We make B- or T-cell antigens targeting a foreign invader for an adaptive response.

So here’s the thing: An adaptive immune response can be persistent and retain memory. In this context, autoimmune disease is the product of a specific autoimmune response to an autoantigen. There is a system failure, as normally, the immune system should prevent this kind of hyper-reactivity to self-antigens.

Autoimmune disease treatment

Autoimmune disease treatment requires substances that lower immune system activity or block the inflammation that causes tissue injury. Sometimes, treatment targets a specific infection. Other approaches aim at a functional disturbance (for example, replacing insulin for those with type 1 diabetes).

Let’s turn to some ways to protect your body from itself.

1. Autoimmune: Get a team

Gather a team that takes a whole-person approach. Members may include:

• Rheumatologists treat joint diseases such as rheumatoid arthritis and other autoimmune diseases like lupus or Sjögren’s syndrome.
• Gastroenterologists treat diseases of the GI tract, such as celiac and Crohn’s disease.
• Endocrinologists treat conditions of the glands, including Graves’ disease, Hashimoto’s thyroiditis, and Addison’s disease.
• Dermatologists treat skin conditions, such as psoriasis.
• Others. Nutritionists, physical therapists, and others can provide significant value.

2. Autoimmune: Complementary approaches

Writing in the August 2022 issue of Prevention, Dr. Andrew Weil explains that while there is generally no cure for autoimmune conditions, many are manageable with prescription medications. In addition, lifestyle and natural remedies may help, too.

• Lower your stress
• Consider an anti-inflammatory diet. This approach includes more fruits and vegetables (preferably organic) and the replacement of meat with plant-based protein. Dr. Weil also recommends increasing omega-3 fatty acids (such as salmon or sardines). These maneuvers may tamp down inflammation.
• Consider supplements. Tumeric and omega-3 fatty acids may be helpful, but check in with your doctor before considering them.

More than 80 autoimmune diseases exist. I hope we can find better solutions soon. Thank you for joining me.

The post When Immunity Goes Rogue appeared first on Medika Life.

What is Colostrum?

Colostrum is a form of milk produced by the mammary glands in late pregnancy and the few days after giving birth.

Human and bovine (cows)colostrums are thick, sticky, and yellowish. In humans, it has high concentrations of nutrients and antibodies, but it is small in quantity. Colostrum is high in carbohydrates, high in protein, high in antibodies, and low in fat (as human newborns may find fat difficult to digest).

Newborns have very small digestive systems, and colostrum delivers its nutrients in very concentrated low-volume doses.

It has a mild laxative effect, encouraging the passing of the baby’s first stool, which is called meconium. This clears excess bilirubin, a waste product of dead red blood cells which is produced in large quantities at birth due to blood volume reduction, from the infant’s body and helps prevent jaundice.

Colostrum contains large numbers of antibodies called “secretory immunoglobulin” (IgA) that help protect the mucous membranes in the throat, lungs, and intestines of the infant. Leukocytes are also present in large numbers; these begin protecting the infant from harmful viruses and bacteria.

Ingesting colostrum establishes beneficial bacteria in the infant’s digestive tract. Premature babies tend to fare better on human colostrum than commercial infant formulas. Human milk contains special components, called growth modulators, that help the premature baby’s digestive system adjust to oral feedings.

Research indicates that premature babies fed formula tend to vomit more and continue tube feeding longer than babies fed human colostrum and breast milk.

Breastmilk’s magical ingredient

Colostrum is packed into your first few day’s supply of breastmilk. It’s like nature’s version of baby “vaccine” specifically designed to boost your baby’s immunity.

One of the major immune boosters in colostrum is called secretory immunoglobulin A (SIgA), which coats the internal organs and lining of the digestive, respiratory and reproductive tracts. SIgA doesn’t let bacteria and pathogens get in through the gut, so it protects your baby from the inside out. Colostrum is lower in some nutrients (such as lactose and fat) than mature breastmilk and higher in others (such as protein and potassium) and is designed to suit your newborn’s growing body.

The post Colostrum, Breastmilk’s Magical Ingredient and What it Contains appeared first on Medika Life.

Hope is on the horizon.

But Covid-19 is a novel virus with new vaccines and treatments, so it is not a surprise that many people have questions, especially about what to do after getting vaccinated. My mother, who qualified for vaccination in category 1B, prompted this story the morning after her second vaccine dose when she sent me this text:

Like millions of senior citizens, my mother is anxious to get out of the house and hug her grandchildren. Many others may be feeling the same way: Senior citizens and those with medical conditions are classified as 1B. Qualifications vary state by state but generally include those greater than 65 years old or with chronic medical conditions.

One important thing for vaccinated people to understand is that immunity does not come immediately after vaccination. It takes time for your body to build up protection. The two mRNA vaccines approved in the U.S. both require two doses. The first shot primes the immune system to produce protective antibodies. The second dose kicks it into high gear.

Here is what we know about post-vaccine immunity with the two Covid-19 vaccines currently available in the U.S.: In phase 3 clinical trials, the Pfizer vaccine showed a 95% efficacy seven days after the second dose. The Moderna vaccine offers 94% immunity at least 14 days after dose number two.

Two weeks after completing the vaccination course, recipients can breathe a sigh of relief. Their risk of severe disease from Covid-19 is very low. But we must remember that the risk is not zero.

The Covid-19 vaccine protects us from getting the disease, but we do not yet know if the vaccine prevents transmission. There is a growing amount of encouraging evidence regarding the protective effect of the vaccine against transmission, but at this moment, we don’t currently know whether a vaccinated person can still transmit the SARS-CoV-2 virus to others.

No vaccine is 100% effective, and according to the current data, 5% of those getting a Covid-19 mRNA vaccine may still be at risk. Vaccine recipients should continue to wash their hands, wear a face mask in public, and practice social distancing.

At your vaccination appointment, you will receive a copy of your vaccination record. Apps and digital documents are coming, but for now, your safest move is to keep the vaccine record in a safe place where it won’t get lost. I recommend taking a picture for storage on your phone.

Here is what it looks like:

The waitlists for Covid-19 vaccination vary across the country. The Centers for Disease Control and Prevention provide an up-to-date resource to help people find a vaccine hub here. The waitlists are long, even for those who currently qualify. I recommend taking proactive measures and signing up now.

If you are feeling nervous about getting the vaccine, here is what it was like for me. The process was simple, painless, and life-saving.  

If you want to see what getting vaccine looks like, here you go.

The post You Got the Second Dose of the Covid-19 Vaccine. Now What? appeared first on Medika Life.

This morning my Twitter feed blessed me with an outstanding video from Raven Baxter AKA Raven the Science Maven. Her video provides a fantastic explanation of immunology. The best part is she teaches us through rap music.

She walks us through the various types of antibodies and explains B cells as “B cells know the haters when they see them, so it’s fight night.” And how can you not love a lyric like “NK natural killers makin’ haters going night night”?

Baxter is an American molecular biologist and science communicator. She is a doctoral student at the University of Buffalo and the founder of STEMbassy, an organization dedicated to high-level science and technology discussions in politics, culture, and social issues. She is also the founder of Black In Science Communication.

We need more scientific leaders using social media tools and creative approaches to educate the public.

Science is fun!

Thank you for reminding us Raven the Maven.

The post A Biologist Explains Antibodies through Rap Music appeared first on Medika Life.

We still don’t know.

Enter this important study published in Nature Medicine. Researchers from China studied 37 asymptomatic individuals in the Wanzhou District who were diagnosed with confirmed SARS-CoV-2 infections but had no relevant clinical symptoms in the preceding 14 days and during hospitalization.

They found that IgG levels and neutralizing antibodies — the antibodies that are much longer-lasting and are protective against further infection — started to decrease within 2–3 months after infection. 40% of patients with asymptomatic infection had no antibodies detected within 8 weeks of the initial infection. And, it seemed that those who had no symptoms had a weaker immune response to the virus.

On the one hand, this makes some sense. If you didn’t develop any symptoms, your immune response may not have been as robust as someone else who had a fever, chills, body aches, and other symptoms. Many of those symptoms are as a result of the immune response to the virus itself.

On the other hand, just because it seemed that those patients who had an asymptomatic infection with SARS-CoV-2 had decreased antibodies after 2–3 months, it does not mean that they will get the virus again and again and again. This is because of the nature of the adaptive immune response to infection.

When we first get an infection — any infection — we develop an initial immune response with antibodies called IgM. Then, later, the body develops IgG antibodies, which more protective and longer-lasting. When we take vaccines, we are coaxing the immune system to develop those IgG antibodies.

Some immune responses, like that to Measles or the Measles vaccine, are life-long. Others, like that to influenza, do not last our entire lives. We still don’t know exactly what kind of immune response is generated to SARS-CoV-2. Still, even if the initial immune response doesn’t last very long, the body usually keeps a memory of the previous infection. And so, if and when we get infected with SARS-CoV-2 again, the body’s immune system should remember the previous infection, and it should develop a very robust secondary immune response.

The key word is “should.” If the virus mutates, then all bets are off, as the body has not seen this new mutated version of the virus. Further, what this study does not answer — and it cannot answer unless researchers deliberately infect these individuals with SARS-CoV-2 — is if these individuals with asymptomatic infection become symptomatic if re-exposed to the same virus again.

Still, the implications of this research are significant.

If immunity doesn’t last very long, then having antibodies doesn’t mean we are free to disregard social distancing requirements. And, if a vaccine is developed, perhaps it may need to be taken every year — like the influenza vaccine — and not once in our lifetimes, like the measles vaccine.

In addition, if it is true that 40% of individuals who had asymptomatic infection don’t have detectable antibodies 8 weeks after infection, if they test negative for the antibodies, it does not mean that they never had Covid-19.

This will make it harder to determine the true extent of viral infection in the community.

As I have written before, this virus and the infection it causes is so new, there is so much that we don’t know. Every bit of information adds to the larger body of evidence.

True, there is so much out there that it is overwhelming at times. That said, it is still important to gather that information. This is because, the more we know, the better equipped we will be to fight this horrible scourge.

The post Antibodies to SARS-CoV-2 May Only Last 2–3 Months, Study Says appeared first on Medika Life.