Berkeley, CA

‘very sneaky virus’: UC Berkeley researchers discuss pandemic

Eric Rogers

The coronavirus continues to claim lives as we approach the anniversary of the first pandemic lockdowns in the United States.

As of press time nearly 2.5 million people have died worldwide with more than 48,000 Californians among its victims. Those figures continue to climb at an alarming rate. As of press time COVID-19 kills more Americans daily than the Sep 11, 2001 terrorist attacks.

Despite these figures, we are inundated by misinformation about the virus’s lethality, origin and how to prevent infection – let alone its very existence. Molecular biologists and an epidemiologist at UC Berkeley commented on the science of the plague to provide insight into what SARS-CoV-2, the virus that causes COVID-19, is, where it came from and what we can do to end this onslaught.

What is the SARS-CoV-2 virus?

Viruses are not living organisms,” said UC Berkeley professor of plant and microbial biology who focuses on virology and viral reproduction Britt Glausinger. “They lack some of the things we really associate with the core features of life. For example, they cannot generate energy, respire or grow.”

She added that viruses have some features that make them similar to living organisms, though. Viruses can reproduce, evolve and take over a cell once they get in.

Viruses, according to Glaunsinger, are made of a stretch of genetic instructions in nucleic acid, such as DNA or RNA, coated with proteins and fats stolen from a host cell. SARS-CoV-2 uses RNA as its genetic material, she added.

“It has to do a remarkably sophisticated number of things with a really small set of instructions,” Glaunsinger said. “With that really compact super streamlined set of instructions, it has to figure out how to get into the cell... It can only amplify if it can break through that barrier and get to the inside of a cell.”

Viruses are essentially inert without a host cell to infect, Glausinger said. So, they need to find a way to get through a cell’s protective membrane. The coronavirus uses spike proteins that cover its surface to infect our cells, according to Glausinger.

Once the coronavirus gets into one of our cells, it can drop its payload, the genetic set of instructions from the virus that hijack the cell, convincing it to replicate the virus many times over, Glausinger said.

The coronavirus is different from other viruses, such as the flu-inducing influenza virus or cold-inducing rhinovirus, because it has a unique set of genetic instructions, Glausinger said.

She added that SARS-CoV-2 belongs to a class of viruses called zoonotic viruses, or viruses that were introduced to humans by animals. SARS-CoV-2 most likely came from bats, according to Glausinger. It is still unclear, however, if this jump was from bats to humans directly, or if there was an intermediate host animal.

Some scientists posited earlier in the pandemic that SARS-CoV-2 came from pangolins because this virus has genetic similarities to pangolin coronaviruses, according to Glausinger. She added that it could be possible that pangolins were an intermediate host for SARS-CoV-2, but the virus’s genesis is still unclear.

Glausinger said any time people are interacting with animals, there is a chance a pathogen jumps from one species to another. Interspecies pathogen transmission is more likely when animals are in high stress situations as their immune responses are reduced and there is more viral shedding, according to Glausinger.

She added that there were examples of pathogen jumping events at live animal markets.

Medical doctor and chair of Epidemiology at UC Berkeley’s school of Public Health Arthur Reingold said people are in contact with bats, non-human primates and rodents frequently. These animals all have their own viruses which can spill-over into humans.

“In some cases, when those are transmissible from one person to another, then we have a problem because no one is immune to the virus,” Reingold said. “The risk of something like this happening again is very real.”

SARS-CoV-2 is capable of producing a pandemic because it is highly contagious, Glausinger said. However, she added that some viruses that are very contagious are easier to stop than COVID-19 because they cause a higher proportion of symptomatic infections.

Smallpox killed one tenth of everyone who ever lived until it was eradicated, but everyone who got infected developed symptoms, Glausinger said. She added that those who were infected with smallpox could be quarantined very effectively because it was obvious when they were infected.

Unfortunately, the coronavirus only produces symptoms in about half of all infections – the rest are either asymptomatic or mildly symptomatic, Glausinger said. She added that it would be impossible to have the same precision in individual quarantining for the coronavirus as with smallpox due to the coronavirus’s high asymptomatic infection rate.

Severe COVID-19, on the other hand, happens when the body doesn’t pick up on early infection signals, according to Glaunsinger. Our bodies then try to catch up by sending in a heavy immune response, leading to inflammation.

Normally, inflammation is useful to eradicate a pathogen, Glaunsinger said, but, in severe COVID-19, the body overreacts and can inadvertently destroy lung tissue.

“An army that is deployed inappropriately will cause a lot of damage that is unintended and unhelpful,” Glaunsinger said. “You need it to fight appropriately when a danger is encountered in the body – if you get too much, or it goes to the wrong place because it got misinformation somehow, then it can cause collateral damage.”

How and why our immune system responds this way to SARS-CoV-2 is still an active area of research for immunologists, Glaunsinger noted.

How to stop the coronavirus:

Glausinger said finding the coronavirus vaccine was challenging because there was not a pre-existing vaccine upon which researchers could build. There were also no data to indicate that a particular vaccine would prove effective against the coronavirus, she added.

Researchers had to deal with many unknowns that made developing the vaccine more difficult than other vaccines, such as the yearly flu vaccine, Glausinger said.

Almost all vaccines stop viruses from getting into human cells in the first place. So, researchers have to identify what specific viruses need to invade our cells and find ways to “jam that key,” Glaunsinger said.

mRNA COVID-19 vaccines, such as the Moderna and Pfizer vaccines, cause our cells to make spike proteins, display the protein along their cell membrane and induce our immune system to create antibodies, according to the Centers for Disease Control and Prevention.

Since the mRNA induces our cells to make spike protein, just as COVID-19 would, the antibodies created are effective against COVID-19 infection, according to the CDC.

Currently approved coronavirus vaccines also avoid inducing a COVID-19 infection because they only contain mRNA, unlike some other vaccines that use weakened or dead viruses, according to the CDC.

Vaccines since the seventeenth century have been injections of external proteins, according to UC Berkeley professor of Nutritional Science who studies vaccination longevity in humans Marc Hellerstein.

More traditional vaccines such as the polio or smallpox vaccines, according to Hellerstein, used weakened viruses to induce immunity against stronger versions of the virus one would encounter naturally.

“Most vaccines they have been testing have not been testing an attenuated coronavirus because we don’t want to give a whole virus,” Hellerstein said. “The (Food and Drug Administration) would have been reluctant to immediately approve a coronavirus vaccine that was still a virus.”

The Moderna and Pfizer vaccines are both about 95% effective. For comparison, the annual flu vaccine is 50% effective on average – some years it’s as low as 20%, Glaunsinger said.

Moderna calculated 95% efficacy during its phase three clinical trial, said Chief Scientists for the FDA, Denise Hinton in the Emergency Use Authorization Letter, or EUA. Hinton explained in the EUA that half of the 28,207 participants received the Moderna vaccine while the other group only received a placebo.

Researchers then waited for participants to contract COVID-19 naturally. Of the nearly 30,000 participants, 185 placebo participants while only 11 vaccinated participants caught COVID-19, according to Hinton.

The Pfizer vaccine had a similar phase three trial, but obtained 162 COVID-19 cases in the placebo group and 8 in the vaccine group out of 36,523 total participants, according to Hinton. That put Pfizer’s vaccine at roughly 95% effective, too.

"It’s pretty great,” Glaunsinger said. “People were not expecting it to be that high – they were cautiously hopeful for a vaccine that was 70% effective.”

What is the public response to the vaccine:

The best case scenario for the Moderna and Pfizer vaccine roll out in the US, according to Reingold, would be if we are flooded with enough vaccine doses to vaccinate a substantial proportion of the population. This would largely lead to the pandemic’s disappearance, he added.

Realistically, however, vast vaccination would not happen for another three to six months, Reingold said. We are not going to see a scenario in which everyone who wants a vaccine can get one until late spring or early summer.

Reingold said he hopes that in six months people who are not “high priority” will have access to a vaccine. He said he also thinks we will probably still wear face coverings in public, though.

“I don’t think we are ever going to go back to how things used to be, but life should be a lot more close to what life was by the summer,” Reingold said. “Our university hopes to be back fully in person classes in the fall.”

The pandemic will end with vast vaccination-based immunity, or herd immunity, Reingold said. Herd immunity refers to a situation in which a pathogen cannot effectively infect new hosts due to an overwhelming preponderance of immune individuals in a population, Reingold explained.

Immune herds prevent a pathogen from spreading to those most susceptible by preventing potential spreaders from getting infected in the first place, according to Reingold.

The key proportion of immune individuals to reach an effective herd immunity threshold changes depending on many factors, Reingold said. Factors, such as how transmissible the pathogen is, play a large role in determining that figure, he added.

The measles virus, which is extremely contagious, requires a herd immunity rate higher than 90%, according to Reingold, while other pathogens that are less contagious can be thwarted by herd immunity rates much lower than that.

Scientists are still unsure of the exact herd immunity rate we would need to prevent SARS-CoV-2 from spreading, Reingold said. Some scientists, according to Reingold, say the herd immunity rate could be as high as 70% while others posit it could be as low as 30-40%.

Regardless of what the true herd immunity proportion is, Reingold said, if we vaccinate 70% to 85% of the population with vaccines that are 90-95% effective, such as the Moderna and Pfizer vaccines, then the pandemic should largely disappear.

Reingold cautioned, however, that even though the pandemic would be over in such a scenario, there is still a high likelihood that SARS-CoV-2 would stick around.

“There’s a lot of mistrust surrounding the vaccine and vaccines in general,” Glaunsinger said. “That’s because it is a polarized topic, and polarization makes people distrustful. This vaccine has some side effects, most vaccines do, but they are pretty minor.”

She added that despite the data indicating the vaccine elicits good immunity, scientists still do not understand what that immunity will look like longterm.

Glaunsinger said it could be possible that we have to get vaccinated every year or so with a booster, depending on future data. If we do need to get booster shots to stave off the coronavirus, maintaining high compliance would add extra operational challenges, Glaunsinger said.

“If the vaccine is only effective for six months, then I don’t think it’s going to be easy to get people to get booster shots,” Hellerstein said. “Could you imagine if in a year and half from now vaccinated people get sick again? That would really destroy people’s trust in science.”

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I am a freelance science journalist who reports on novel science published around the San Francisco Bay Area.

Berkeley, CA

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