APU Health & Fitness Infectious Diseases Original

From Delta to Omicron: How Coronavirus Variants Behave

By Daniel G. Graetzer, Ph.D.
Faculty Member, School of Health Sciences

The Delta variant of SARS-CoV-2 was first detected in late 2020 in India, and it became the dominant global coronavirus strain in June 2021. Many reports indicate the Delta mutation spread on average from one person to about six people. This is approximately twice the original SARS-CoV-2 virus infection rate, which spread to only about two or three other people on average.

Delta’s Incubation Period Is Short, Increasing Its Community Spread

Delta appears to have an incubation period of only about four days, which fuels its spread faster than the estimated six days of the original coronavirus. As a result, the Delta variant’s transmission and community spread were faster. Delta caused more hospitalizations and deaths than earlier variants, primarily because it was able to infect many more people.

Related link: The Coronavirus Omicron Variant: Its Evolution and Future

Omicron Cases Are Rising Due to Its High Number of Mutations and Ability to Evade the Immune System

Omicron variant cases are currently rising faster than hospital admissions, probably due to the Omicron variant’s high number of mutations that enable it to evade the human immune response. Fortunately, the Omicron variant seems to be milder and causes less severe short-term disease. However, it is too early to know much about the long-term effects of any variant, if later “breakthrough” infections will increase or what the effectiveness of current vaccines will be.

Related link: How to Get and Stay Motivated to Build a Healthy Lifestyle

Delta and Omicron Mutations

Delta has about 13 mutations with about nine mutations of the spike protein (the protrusion on the outer surface of the virus that enables it to latch onto human cells). Two proteins can form a molecular hook (receptor-binding domain), which enable the virus to cling to cells more tightly.

Omicron is considered a “monster mutation.” It has over 30 mutations in the spike protein region and about 10 mutations in the receptor-binding domain, which has also contributed to increased transmission and community spread. Variants acquire mutations that allow them to evade vaccine-induced antibodies, which explains why there have been “breakthrough” infections in persons who were previously vaccinated or were infected with previous strains.

When someone with a severely compromised immune system (such as from HIV/AIDS) gets infected, a coronavirus can potentially stay within the patient’s body for a longer period of time. The longer it stays within human cells, the more time it has to make more copies of itself and the greater the chance of making copying errors (mutations), which possibly explains Omicron’s large number of mutations.

Fortunately, the risk of reinfection with the Delta variant is low, as antibodies currently seem to be effective at protecting most people. Omicron shares similar mutations with the earlier Beta and Gamma variants, which appeared to be more resistant to vaccination than Delta.

Virologists Are Monitoring Coronavirus Variants

Virologists are continually monitoring data on coronavirus variants. They are comparing Delta and Omicron variant success against the antibodies made by persons who only got two doses of the COVID-19 vaccine versus persons who got a booster after their initial two vaccine doses.

Coronavirus variants can be likened to cat burglars who sneak into your house, consume your food and make millions of babies on your couch. These babies then spread rapidly to your other furniture to make more children and eventually destroy almost everything inside your home. The term “cat burglar” is somewhat ironic as one leading theory proposes that COVID-19 spread from bats to cats to humans in a public market selling wildlife in Wuhan, China.

Prescribing the Right Amount of Medication to Combat the Virus Is Tricky

Clinicians are worth their money if they can prescribe the absolute minimum dose of the correct medication within the right timeframe after someone’s initial contact with the coronavirus, so they can both defeat the virus and prevent side effects. If the medication dose is too high, that can cause considerable collateral damage to the body.

Viruses have differing rates of replication within different humans. Also, once a virus enters different cells within the same person, it has the potential to duplicate itself – tens of thousands of copies – within just a few hours. Under certain conditions, it only takes a few days for an infected person to get loaded with millions of viral particles within each teaspoon of blood!

Because viral proteins come from human proteins, the medications to fight viruses must be very specific to prevent them from doing as much damage as a virus – or more damage – to otherwise healthy body cells. Many patients are given a “cocktail” of antiviral medications because a group of antiviral medicines are more difficult for a given family of rapidly mutating viruses to resist.

Unfortunately, some virus families mutate too quickly for even a large cocktail of antiviral medications to defeat. Viruses have the potential to mutate faster than bacteria. They are also less likely to mutate into versions that are so riddled with errors that they can no longer continue replicating, which is likely one reason why some variants have fizzled out on their own.

Antibodies block viruses primarily within the bloodstream before they can get inside body cells, whereas most T-cells fight the virus once it passes into cells from blood. The effectiveness of antibodies (stimulated within the body from prior virus exposure or vaccines) and other virus fighters such as T-cells contributes to the range of signs and symptoms of a given virus strain.

The Difference between Disease Signs and Symptoms

Disease signs and symptoms often describe the same medical condition, but these terms differ from a biomedical perspective. Signs are numerically measurable indicators of illness (often verified by a formal diagnosis from a healthcare provider), but symptoms are what a potentially soon-to-be-diagnosed patient is personally feeling.

Signs can be felt, heard or seen. Some examples of disease signs in a patient would be:

  • A measurement of body temperature in degrees Fahrenheit/Celsius
  • The heart rate in beats per minute
  • Blood pressure in millimeters of mercury
  • The size of a bruise or open wound in inches/centimeters
  • Abnormal heart rhythms measured in millimeters by an electrocardiogram (ECG) machine

Symptoms are subjective and often not outwardly visible to other people. For instance, a patient may experience feelings of chills, nausea and dizziness, which are not objective, measurable external signs that can be documented.

The signs and symptoms for influenza often happen suddenly with no prior warning. However, a COVID-19 infection often causes a “slow burn” after which the infected person briefly feels better before “crashing.”

Most COVID-19 patients with mild to moderate signs and symptoms recover in about two weeks, and patients with severe symptoms generally recover in about six weeks. By definition, a carrier is an infected person who currently has no signs or symptoms. That carrier is probably not aware that he or she is shedding a virus and potentially spreading it to others.

Scientists are continually documenting COVID-19 cases and hospitalizations caused by all coronavirus variants. Countries differ by vaccination rates, however. The U.S. has a relatively medium vaccination rate; the UK has a relatively high initial vaccination rate; and Israel has one of the world’s highest vaccination and booster rates.

Omicron Could Potentially Stimulate Antibodies to Prevent Reinfections

There is potentially one piece of good news about the emerging Omicron variant. If Omicron quickly spreads around the world but causes much less severe illness and deaths, it could potentially stimulate antibodies that might protect people from reinfection by other coronavirus strains in the future. Healthcare data in the coming years will hopefully help to further assess this possibility.

Daniel G. Graetzer, Ph.D., received his B.S. from Colorado State University/Fort Collins, a M.A. from the University of North Carolina/Chapel Hill, and a Ph.D. from the University of Utah/Salt Lake City and has been a faculty member in the School of Health Sciences, Department of Sports and Health Sciences, since 2015. As a regular columnist in encyclopedias and popular magazines, Dr. Graetzer greatly enjoys helping bridge communication gaps between recent breakthroughs in biomedical knowledge, practical application of developing scientific theories and societal well-being.

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