The summer surge of COVID-19 cases in Orange County and across the nation is being fueled by the delta variant, which is proving more than twice as contagious and capable of producing more severe illness than the original SARS-CoV-2 coronavirus.
Q. How does the delta variant differ from the original form of the pandemic virus?
A. The form of the original coronavirus is really not clear. If, as we think, SARS-CoV-2 appeared in humans after jumping from an animal host, such as a bat, then the sequence may have already contained mutations in its genome that allowed that species jump.
Many of the so-called emerging diseases represent jumps from an animal host to humans.
The power of this genetic flexibility is characteristic of RNA viruses. This flexibility results in the production of a swarm of related viral “offspring” at each round of replication, allowing the virus to select a genetic makeup best adapted to a given host in the form of the variant viruses we’re now experiencing. Mutations are always present in the progeny viruses and may be selected for replication if they offer an advantage in a new host species.
The current variants of SARS-CoV-2 — which include the B.1.1.7 (alpha), B.1.351 (beta), B.1.617.2 (delta) and P.1 (gamma) variants circulating in the United States — are classified as variants of concern. Beta, delta and gamma are derived from the alpha virus, which was first described in the United Kingdom in 2020.
Q. What makes the delta variant more contagious and virulent?
A. Current research, based on observation of patients infected with the delta variant, shows that the delta strain may produce as much as 1,000 times more virus in the nasal passages and upper respiratory tract early in the infection, when people may not exhibit overt symptoms.
This combination leads to a high proportion of asymptomatic carriers who can spread the infection to others. Vaccinated individuals are protected from a severe reaction to the disease, which could require hospitalization and may result in death. Recent data indicates that less than 1% of newly hospitalized COVID-19 patients have been fully vaccinated.
This offers two advantages for viral spread: First, the spread of the virus in droplets from the upper respiratory tract is facilitated by the larger amount of infectious virus in the nasal secretions; and second, the immune response is not as robust in that location as it is in the lower respiratory tract.
Q. Can vaccines reduce the delta variant’s spread?
A. Vaccines are not designed to prevent infection but to prevent disease. The evidence with the delta variant shows that vaccines are very effective at preventing severe disease and hospitalization.
The question I’m often asked is how the vaccines work. They “educate” the immune system by exposing it to critical viral proteins made during the life cycle of a virus. In the case of SARS-CoV-2 and COVID-19, the protein spike that allows the virus to enter cells is the protein targeted by the vaccines, which introduce a viral RNA message that directs the body to make a synthesis of the spike protein in the absence of the actual virus. The result of this exposure is a robust immune response.
In this way, the vaccines “prime” the immune response to combat the virus with antibodies and T-cells at the time of infection without the normal delay. In this case, the vaccination is designed to quell any new infection, usually without symptoms. Each viral exposure serves to restimulate, or boost, the immune response protection it affords. The net result is to mitigate, or reduce, the spread of infection.
Q. Will the COVID-19 virus circulate like influenza each year?
A. It appears that the SARS-CoV-2 virus has been established as part of the human virome — which is the total collection of viruses in and on the human body — and will persist. The virus has spread rapidly among widely dispersed human populations.
It has shown the ability to mutate, to fine-tune and sustain the infectious cycle through several cycles of infection in humans and animals. Viral variants have arisen and will continue to appear. Some of these will be more capable of spreading. It’s possible that the virus may become less virulent for humans but, like the common cold coronaviruses, still persist.
Finally, precursors of SARS-CoV-1 and SARS-CoV-2 still exist in bats and may provide a reservoir for future cycles of human infection.
Research efforts will continue to find ways to control this virus, as we have done for polio and smallpox, both of which were controlled in the 1950s and 1970s. The principal difference with SARS-CoV-2 is that the virus has an animal reservoir in the Asian horseshoe bat and is capable of reemergence.
This is also the case with influenza, which persists in waterfowl and is amplified in swine. The genetics of influenza are dictated by the host, with mammalian strains emerging by passage through pigs. If it’s shown that the SARS-CoV-2 virus — like the flu virus — requires an intermediate host to make the jump from bat to human, then immunizing that host may be effective.