Tags: covid | virus | cells | antibody

Let's Hope This Pandemic Isn't a New Abnormal

coronavirus covid nineteen mutation

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By Friday, 22 May 2020 12:41 PM Current | Bio | Archive

As I expect with many others of you, the COVID-19 pandemic brought lots of questions to mind about how viral invasions occur, how our bodies fight back, and what determines which side wins.

So I did some research, and have briefly summarized a truly amazing, albeit also very scary, saga that is more far more complex, yet also more routine, than we may ever have imagined.

Here’s what I learned.

Viruses are an enigma that exist at the boundary of life with only one purpose – to replicate more of themselves in a captured host cell.

Unlike bacteria which are fully alive with a metabolism that requires food, produces waste, and reproduces by division, viruses do none of this. Instead, they survive and multiply by invading and stealing energy from animal cells, then like a puppet master, subvert them, take them over, and force them to clone thousands or hundreds of thousands of themselves.

The secret power viruses possess to accomplish this lies in specific genomes that define each of their special identities and actions. The genes, analogous to software codes that tell computers what to do, tell the invaded cells what to do. However, while computer codes use a binary language, genetic codes use four "letters," each representing the chemicals adenine, guanine, cytosine, and thymine (or sometimes uracil).

Apart from their genes, viruses are essentially membranes — typically spherical, about 1/10,000 of a millimeter in diameter — that look something like a dandelion with a forest of two different-shaped protuberances — one roughly like a spike, the other like a tree —jutting out from their surfaces.

It’s those protuberances that provide viral weapons for invasion that collide, brush against, and snugly bond with sialic acid receptors of certain shapes and structures jutting from target cells much like a hand fitting into a glove. As a virus sits against the cell membrane, such as surface cells in a respiratory tract, more spikes bind to other receptors.

A pit soon forms in the cell membrane beneath the virus, allowing the attacker to slip in through in a kind of bubble called a "vesicle."

All viruses use the same basic mechanism: They inject bits of themselves into healthy cells of the host they’re attacking, and then trick the cells into turning their genetic material against themselves into making duplicate copies of the invaders which are released in massive chain reactions against new victim cells.

The host cells almost always die, usually when the new viral particles burst out to spread the invasions. In humans, viruses directly attack only the respiratory system. This becomes increasingly dangerous as they penetrate deeper into lungs.

Our bodies’ immune systems have extraordinarily intricate and interwoven arsenals containing a great variety of defensive white blood cells, antibodies, enzymes, toxins, and other proteins. The systems also possess a remarkable ability to distinguish between what naturally "belongs," and what does not.

As components of the immune system – various white blood cells, antibodies and other elements circulate everywhere throughout our bodies. As they do so, they collide with other cells or proteins or organisms and "read" physical markings and structures — the "stereochemistry" — of everything they connect with. Anything carrying a "self" marking is left alone. Those that aren’t recognized as belonging, including diseased cells, are attacked.

Virus recognition and identification is based on a "language" written in an alphabet of pyramids, cones, spikes, mushrooms, blocks, hydras, umbrellas, spheres, and ribbons that are twisted into every imaginable shape. Each form conveys a precise message and response.

Foreign physical markings that a defensive component feels, reads, and then binds to are called "antigens" that stimulate the immune system to respond. Antibodies recognize or bind only to a virus bearing that specific antigen.

Detection and recognition of alien antigens sets off a chain of events as the body releases enzymes. Some affect the entire body, such as raising its temperature and causing fever.

Others directly attack and kill the target. Still others serve as chemical messengers, summoning white blood cells to areas of invasion, or dilating capillaries so that killer cells can exit the bloodstream at the point of attack.

Our bodies’ immune defenses react to infections in two surges.

The first, an "innate" response occurs within minutes to hours, triggering alarms that produce effects across the body, such as fever. Tissues and cells produce "interferons," molecules that incapacitate many viruses and recruit white blood cells. For mild infections, this is typically sufficient to defeat the foe.

Some infections, however, require a second wave of "adaptive" immune responses that arrive four or five days after infection. In this case, molecular bits of the offending pathogen, (antigens), are brought to the lymph nodes, where white blood cells called "T" and "B" lymphocytes head out to the front lines — the infected tissues such as the lung, for COVID-19.

The wave of T cells that arrive at the battlefront deploys the principal weapon in their arsenal, the release of cytotoxins, to kill virally infected cells. Over-aggressive immune responses cause much of the devastation in severe cases where the cure can be worse than the disease.

Meanwhile, the B cells pump out antibodies that over several weeks, adapt to the pathogen.

After a successful war is over, a few T and B cells linger in the lymph nodes and in the mucosa of the airways, forming an "immunological memory" that is programmed to fight faster and stronger the next time that pathogen shows up. This is referred to as "protective immunity."

No one can yet be certain whether or not protective COVID-19 immunity from recovered individuals will be permanent. One reason is because the virus has already mutated into two strains: the older "S" type, and a newer, more aggressive "L" type.

More encouraging news is that while all viruses mutate, most don’t persist in subsequent generations.

The purpose of vaccines is to arm T and B cells so they can fight quickly when exposed to the virus. But since antibody levels fall over time, it is also unknown whether COVID-19 immunity will last a lifetime, or like tetanus, will require a booster a decade later.

In any case, let’s hope that this current pandemic is a freak, once-in-a-generation anomaly, not a "new abnormal."

Larry Bell is a senior visiting scholar at the Texas Public Policy Foundation. He is also an endowed professor of space architecture at the University of Houston where he founded the Sasakawa International Center for Space Architecture (SICSA) and the graduate program in space architecture. Larry has written more than 600 articles for Newsmax and Forbes, and is the author of several books. Included are: "Cyberwarfare: Targeting America, Our Infrastructure and Our Future" (2020), "The Weaponization of AI and the Internet: How Global Networks of Infotech Overlords are Expanding Their Control Over Our Lives" (2019), "Reinventing Ourselves: How Technology is Rapidly and Radically Transforming Humanity" (2019), "Thinking Whole: Rejecting Half-Witted Left & Right Brain Limitations" (2018), "Reflections on Oceans and Puddles: One Hundred Reasons to be Enthusiastic, Grateful and Hopeful" (2017), "Cosmic Musings: Contemplating Life Beyond Self" (2016), "Scared Witless: Prophets and Profits of Climate Doom" (2015) and "Climate of Corruption: Politics and Power Behind the Global Warming Hoax" (2011). He is currently working on a new book with Buzz Aldrin, "Beyond Footprints and Flagpoles." Read Larry Bell's Reports — More Here.

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The purpose of vaccines is to arm T and B cells so they can fight quickly when exposed to the virus. But since antibody levels fall over time, it is also unknown whether COVID-19 immunity will last a lifetime, or like tetanus, will require a booster.
covid, virus, cells, antibody
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2020-41-22
Friday, 22 May 2020 12:41 PM
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