Follow our live coronavirus updates here Coronavirus: the symptoms

The PM's spokesman confirmed Boris Johnson has tested negative for Covid-19 Coronavirus: the symptoms Follow our live coronavirus updates here

Follow our live coronavirus updates HERE Coronavirus: The symptoms

Follow our live coronavirus updates here

Coronavirus: the symptoms Read our LIVE updates on the coronavirus here

Dominic Raab will today be grilled over the Government's handling of the coronavirus crisis amid calls for an inquiry into its "slow response".

The historic "hybrid" sitting of the House of Commons will be the springboard for further modernisation of Westminster, Speaker Sir Lindsay Hoyle told the Standard.

Follow our live Covid-19 updates HERE

Boris Johnson watched Dominic Raab take on Sir Keir Starmer at PMQs from Chequers today as he continues his recovery from coronavirus.

The EU's chief negotiator has branded progress in post-Brexit talks disappointing and warned the "clock was ticking".

A row has broken out over Boris Johnson's chief adviser Dominic Cummings attending meetings of the senior scientists advising the Government on the coronavirus outbreak.

Boris Johnson will not take part in Prime Minister's Questions today following the birth of his son.

The pair announced the exciting news this morning

He has now been absent from the front line of the Government response for a month, after his three-week recovery period at the Chequers official residence in Buckinghamshire.

It is "too early" to begin easing any lockdown measures "in any meaningful way", Nicola Sturgeon has said.

Nigel Farage has become the butt of mocking jokes online after sharing his Clap for Carers effort.

Too many workers are still falling through cracks in the Covid rescue package, a former cabinet minister warned today as he called for the lockdown to be eased "as quickly as possible".

Jennie Formby has resigned as Labour's general secretary as new leader Sir Keir Starmer reshapes the party.

One of Boris Johnson's closest allies quit as a minister today after being found to have breached the MPs' code of conduct by trying to "intimidate" a company chairman involved in a loan row with his father.

Admission that faster testing might have helped as UK hit by top death toll in Europe

He also said he "bitterly regrets" the crisis in care homes, where staff have hit out at a lack of testing and PPE. The latest figures show that nursing home fatalities are continuing to rise, standing at 2,794 in the week to April 24, despite deaths in all settings beginning to fall.

Cardi B invited Bernie Sanders to join her on Instagram Live last night to talk politics, coronavirus and manicures.

Adele posted a rare photo of herself to celebrate her birthday, unveiling a dramatically altered appearance.

It seems like people who get infected with SARS-CoV-2 retain immunity, but we can’t be sure how long that immunity will last. We still lack the testing capabilities to be certain.eamesBot / Shutterstock

This story was updated post-publication to include information from a study published on the preprint server medRxiv on April 17, 2020.

With more than half a million cases of COVID-19 in the United States1 and the number of deaths increasing daily, it remains unclear when and how we might return to some semblance of pre-pandemic life. This leaves many grappling with an important question: Do you become immune after SARS-CoV-2 infection? And, if so, how long might that immunity last?

In 2019, the virus SARS-CoV-2 jumped to a human host for the first time, causing the disease COVID-19. When you become infected with a new virus, your body does not possess the antibodies necessary to mount a targeted immune response. Antibodies, proteins belonging to the immunoglobulin family, consist of four chains of amino acids that form a characteristic Y-shaped structure. Antibodies are manufactured by the immune system to bind to antigens (viral proteins) to neutralize viral infectivity.

When you inhale an aerosolized droplet containing SARS-CoV-2, the virus encounters the cells of the mucous membrane lining the respiratory tract. If effective contact is made, the virus binds to a particular receptor on these cells called ACE-2. After binding ACE-2, a host enzyme is co-opted to cleave the virus’ surface protein, called the spike protein, allowing the virus to enter the cell.

It appears that individuals with COVID-19 do create neutralizing antibodies—the basis of immunity.

Within the first few hours of infection, the body’s first line of defense—the innate immune response—is activated. The innate immune response is non-specific. When a “foreign” molecule is detected, innate immune cells signal to other cells to alter their response or prepare to combat infection.

In the following days, the adaptive immune response is activated, which is more specific. The adaptive immune response will peak one to two weeks post-infection and consists of antibodies and specialized immune cells. It is called the “adaptive” immune response because of its ability to tailor the response to a specific pathogen. Antibodies can neutralize viral infectivity by preventing virus from binding to receptors, blocking cell entry, or causing virus particles to aggregate.2 Once an infection has resolved, some of these antibodies remain in the body as immunological memory to be recruited for protection in the case of reinfection. To be immune to a virus is to possess this immunological memory.

Many vaccines work by activating the adaptive immune response. Inactivated virus, viral protein, or some other construct specific to a particular virus are introduced into the body as vaccines to initiate an immune response. Ideally, the body creates antibodies against the viral construct so that it can mount a succinct response when infected by the virus. However, in order to work effectively, a vaccine must provoke an immune response that is sufficiently robust. If the body only produces low concentrations of neutralizing antibodies, adequate immunological memory may not be sustained.

While there is still much that we have to learn about SARS-CoV-2, it appears that individuals with COVID-19 do create neutralizing antibodies—the basis of immunity. However, we don’t know for certain how long that immunity might offer protection. On the question of COVID-19 re-infection, Matt Frieman, a coronavirus researcher at the University of Maryland School of Medicine, commented in a recent interview with NPR: “We don’t know very much … I think there’s a very likely scenario where the virus comes through this year, and everyone gets some level of immunity to it, and if it comes back again, we will be protected from it—either completely or if you do get reinfected later, a year from now, then you have much less disease. That’s the hope, but there is no way to know that.”3

Immunity to a virus is measured by serological testing—patient blood is collected and analyzed for the presence of antibodies against a particular virus. Serological data is most informative when collected long-term, so the data we have been able to obtain on SARS-CoV-2 is limited. However, data on other coronaviruses that we’ve had the opportunity to study in more depth can inform our estimations on how this outbreak may evolve.

First, we can look to the coronaviruses that are known to cause the common cold. Following infection with one of these coronaviruses, disease is often mild; therefore, the concentration of antibodies detected in the blood is low. This is because mild disease often indicates a less robust immune response. Interestingly, it is not the virus itself that causes us to feel sick, but, rather, our body’s response to it. Typically, the sicker we feel, the stronger the immune response; therefore, after a cold, we are often only protected for a year or two against the same virus.4 While SARS-CoV-2 wouldn’t necessarily act like these common coronaviruses, the body’s response to these coronaviruses serves as a point of reference upon which to make predictions in the absence of virus-specific data.

We can also look to coronaviruses that are known to cause severe disease, such as SARS-CoV, which caused the 2002-2003 outbreak of SARS in China. One study discovered that antibodies against SARS-CoV remained in the blood of healthcare workers for 12 years after infection.5 While it is not certain that SARS-CoV-2 will provoke a response similar to that of SARS-CoV, this study provides us with information that can inform our estimates on immunity following COVID-19 and provide hope that immunity will provide long-term protection.

If immunity to SARS-CoV-2 diminishes as it does for common cold coronaviruses, it is likely that wintertime outbreaks will recur.

Scientists have also been working to analyze antibodies in samples from individuals infected with SARS-CoV-2. A research group in Finland recently published a study detailing the serological data collected from a COVID-19 patient over the course of their illness.6 Antibodies specific to SARS-CoV-2 were present within two weeks from the onset of symptoms. Similarly, another recent report analyzing patients with confirmed COVID-19 indicated that it took approximately 11-14 days for neutralizing antibodies to be detected in blood.7 Both of these studies, while preliminary, suggest that the basis for immunity is present in patients infected with SARS-CoV-2.

Another report looked at the possibility for recurrence of COVID-19 following re-infection with SARS-CoV-2.8 In this study, rhesus macaques were infected with SARS-CoV and allowed to recover after developing mild illness. Once blood samples were collected and confirmed to test positive for neutralizing antibodies, half of the infected macaques were re-challenged with the same dose of SARS-CoV-2. The re-infected macaques showed no significant viral replication or recurrence of COVID-19. While macaques “model” human immunity, not predict it, these data further support the possibility that antibodies manufactured in response to SARS-CoV-2 are protective against short-term re-infection.

We can also analyze a virus’ structure, and the information gained from sequencing the viral genome, when trying to predict its behavior. All viruses continually undergo mutation in the process of rapid replication. They lack the necessary machinery to repair changes incurred to the genetic sequence (we as humans also incur mutations to our genetic sequence daily, but we have more sophisticated genetic repair mechanisms in place). The occurrence of significant genetic changes to the viral genome that result in viable genetic changes to a virus is termed antigenic variation. We see a lot of antigenic variation in influenza viruses (thus the need to create new vaccines each year); but the coronaviruses seem to be relatively stable antigenically.4 This is because most coronaviruses have an enzyme that allows them to correct genetic errors sustained during replication. The more stable a virus remains over time, the more likely that antibodies manufactured in response to infection or vaccination will remain effective at neutralizing viral infectivity.

All this considered, it appears that immunity is retained following SARS-CoV-2 infection. So too, that immunity might persist long enough to warrant the implementation of vaccination. However, we still have much to learn about this virus, and whether there may be some cross-immunity between SARS-CoV-2 and other coronaviruses. The widespread variation in patient immune responses adds an additional layer of complexity. We still don’t have a good understanding of why people have different responses to viral infection—some of this variation is owed to genetic variation, but how and why some people have more robust immune responses and more severe disease is still unknown.4 In some cases, individuals show a high immune response because the concentration of virus is high. In other cases, individuals show a high immune response because they differ in some aspect of immune regulation or efficiency. However, as levels of immunity increase generally across a population, the population approaches what is called “herd immunity”—when the percentage of a population immune to a particular virus is sufficiently high that viral load drops below the threshold required to sustain the infection in that population.9

How the pandemic will evolve in the coming months is uncertain. Outcomes depend on a myriad of factors—the duration of immunity, the dynamics of transmission and how we mitigate those dynamics through social distancing, the development of therapeutics and or vaccines, and the ability of healthcare systems to handle COVID-19 caseloads. If immunity to SARS-CoV-2 diminishes as it does for common cold coronaviruses, it is likely that wintertime outbreaks will recur in coming years.10 Whether immunity to other coronaviruses might offer some cross protective immunity to SARS-CoV-2 will also play a role, albeit to a lesser extent. Widespread serological testing to assess the duration of immunity to SARS-CoV-2 is imperative, but many countries still lack this capability.

A recent study looking at serological data from 3,300 symptomatic and asymptomatic individuals in California estimates that there may be as many as 48,000-81,000 people who have been infected with SARS-Cov-2 in Santa Clara County, which is 50- to 85-fold more cases than we previously thought.11 This small-scale survey emphasizes the importance of serological testing in determining the true extent of infection.

The continuation of rigid social distance also hangs in a balance—one-time social distancing measures may drive the SARS-CoV-2 epidemic peak into the fall and winter months, especially if there is increased wintertime transmissibility.10 New therapeutics, vaccines, or measures such as contact tracing and quarantine—once caseloads have been reduced and testing capacity increased—might reduce the need for rigid social distancing. However, if such measures are not put in place, mathematical models predict that surveillance and recurrent social distancing may be required through 2022.10 Only time will tell.

Helen Stillwell is a research associate in immunobiology at Yale University.

References

1. The COVID Tracking Project https://covidtracking.com/data/us-daily (2020).

2. Virology Blog: About Viruses and Viral Disease. Virus neutralization by antibodies. virology.ws (2009).

3. GreenfieldBoyce, N. Do you get immunity after recovering from a case of coronavirus? NPR (2020).

4. Racaniello, V., Langel, S., Leifer, C., & Barker, B. Immune 29: Immunology of COVID-19. Immune Podcast. microbe.tv (2020).

5. Guo, X., et al. Long-Term persistence of IgG antibodies in SARS-CoV infected healthcare workers. bioRxiv (2020). Retrieved from doi: 10.1101/20202/02/12/20021386

6. Haveri, A., et al. Serological and molecular findings during SARS-CoV-2 infection: the first case study in Finland, January to February 2020. Euro Surveillance 25, (2020).

7. Zhao, J., et al. Antibody responses to SARS-CoV-2 in patients of novel coronavirus disease 2019. Clinical Infectious Diseases (2020). Retrieved from doi: 10.1093/cid/ciaa344

8. Bao, L., et al. Reinfection could not occur in SARS-CoV-2 infected rhesus macaques. bioRxiv (2020). Retrieved from doi: 10.1101/20202.03.13.990226

9. Virology Blog: About Viruses and Viral Disease. Herd immunity. virology.ws (2008).

10. Kissler, S.M. Tedijanto, C., Goldstein, E., Grad, Y.H., & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the post-pandemic period. Science eabb5793 (2020).

11. Bendavid, E., et al. COVID-19 antibody seroprevalence in Santa Clara County, California. medRxiv (2020). Retrieved from doi: 10.1101/2020.04.14.20062463

There’s an old belief that truth will always overcome error. Alas, history tells us something different. Without someone to fight for it, to put error on the defensive, truth may languish. It may even be lost, at least for some time. No one understood this better than the renowned Italian scientist Galileo Galilei.

It is easy to imagine the man who for a while almost single-handedly founded the methods and practices of modern science as some sort of Renaissance ivory-tower intellectual, uninterested and unwilling to sully himself by getting down into the trenches in defense of science. But Galileo was not only a relentless advocate for what science could teach the rest of us. He was a master in outreach and a brilliant pioneer in the art of getting his message across.

Today it may be hard to believe that science needs to be defended. But a political storm that denies the facts of science has swept across the land. This denialism ranges from the initial response to the COVID-19 pandemic to the reality of climate change. It’s heard in the preposterous arguments against vaccinating children and Darwin’s theory of evolution by means of natural selection. The scientists putting their careers, reputations, and even their health on the line to educate the public can take heart from Galileo, whose courageous resistance led the way.

A crucial first step, one that took Galileo a bit of time to take, was to switch from publishing his findings in Latin, as was the custom for scientific writings at the time, to the Italian vernacular, the speech of the common people. This enabled not just the highly educated elite but anyone who was intellectually curious to hear and learn about the new scientific work. Even when risking offense (which Galileo never shied away from)—for instance, in responding to a German Jesuit astronomer who disagreed with him on the nature of sunspots (mysterious dark areas observed on the surface of the sun)—Galileo replied in the vernacular, because, as he explained, “I must have everyone able to read it.” An additional motive may have been that Galileo wanted to ensure that no one would somehow distort the meaning of what he had written.

Galileo also understood that while the Church had the pomp and magic of decades of art and music, science had the enchantment of a new invention—the telescope. Even he wasn’t immune to its seductive powers, writing in his famous booklet The Sidereal Messenger: “In this short treatise I propose great things for inspection and contemplation by every explorer of Nature. Great, I say, because of the excellence of the things themselves, because of their newness, unheard of through the ages, and also because of the instrument with the benefit of which they make themselves manifest to our sight. “ And that gave him his second plan for an ambitious outreach campaign.

With alternative facts acting like real facts, there are Galileo’s heirs, throwing up their hands and attempts to make lies sound like truth.

What if he could distribute telescopes (together with detailed instructions for their use and his booklet about the discoveries) all across Europe, so that all the influential people, that is, the patrons of scientists—dukes and cardinals, could observe with their own eyes far out into the heavens. They would see the stunning craters and mountains that cover the surface of the moon, four previously unseen satellites of Jupiter, dark spots on the surface of the sun, and the vast number of stars that make up the Milky Way.

But telescopes were both expensive and technically difficult to produce. Their lenses had to be of the highest quality, to provide both the ability to see faint objects and high resolution. “Very fine lenses that can show all observations are quite rare and, of the more than sixty I have made, with great effort and expense, I have only been able to retain a very small number,” Galileo wrote on March 19, 1610. Who would front the cost of such a monumental and risky project?

Today the papacy is arguably the single most influential and powerful religious institution in the world. But its power is mostly in the moral and religious realms. In Galileo’s time, the papacy was a political power of significance, gobbling up failed dukedoms elsewhere, merging them into what became known as the “papal states.” The persons with the greatest interest in appearing strong in front of the papacy were the heads of neighboring states at the time.

So it is not surprising that Galileo presented his grandiose scheme to the Tuscan court and the Grand Duke Cosimo II de’ Medici. Nor is it surprising that Cosimo agreed to finance the manufacturing of all the telescopes. On his own, he also instructed the Tuscan ambassadors to all the major European capitals to help publicize Galileo’s discoveries. In doing so he tied the House of Medici, ruler of the foundational city of the Renaissance, Florence, to modern science. A win-win for both the Grand Duke and Galileo.

Last, Galileo instinctively understood what modern PR specialists refer to as the “quick response.” He did not let even one unkind word be said about his discoveries without an immediate reply. And his pen could be sharp.

For example, the Jesuit mathematician Orazio Grassi (hiding behind the pseudonym of Sarsi) published a book entitled The Astronomical and Philosophical Balance, in which he criticized Galileo’s ideas on comets and on the nature of heat. In it, Grassi mistakenly thought that he would strengthen his argument by citing a legendary tale about the ancient Babylonians cooking eggs by whirling them on slings.

Really?

Galileo responded with a stupendous piece of polemic literature entitled The Assayer, in which he pounced on this fabled story like a cat on a mouse.

“If Sarsi wishes me to believe, on the word of Suidas [a Greek historian], that the Babylonians cooked eggs by whirling them rapidly in slings, I shall believe it; but I shall say that the cause of this effect is very far from the one he attributes to it,” he wrote. “ To discover the true cause, I reason as follows: ‘If we do not achieve an effect which others formerly achieved, it must be that we lack something in our operation which was the cause of this effect succeeding, and if we lack one thing only, then this alone can be the true cause. Now we do not lack eggs, or slings, or sturdy fellows to whirl them, and still they do not cook, but rather cool down faster if hot. And since we lack nothing except being Babylonians, then being Babylonian is the cause of the egg hardening.’”

Galileo understood what modern PR specialists refer to as the “quick response.” He did not let one unkind word go without an immediate reply.

Did Galileo’s efforts save science from being cast aside perhaps for decades, even centuries? Unfortunately, not quite. The trial in which he was convicted by the Inquisition for “vehement suspicion of heresy” exerted a chilling effect on progress in deciphering the laws governing the cosmos. The famous French philosopher and scientist René Descartes wrote in a letter: “I inquired in Leiden and Amsterdam whether Galileo’s World System was available, for I thought I had heard that it was published in Italy last year. I was told that it had indeed been published, but that all the copies had immediately been burnt in Rome, and that Galileo had been convicted and fined. I was so astonished at this that I almost decided to burn all my papers, or at least to let no one see them.”

I suspect that there are still too few of us who can tell exactly what Galileo discovered and why he is such an important figure to the birth of modern science. But around the world, in conversations as brittle as today’s politics, with alternative facts acting like real facts, there are Galileo’s heirs, throwing up their hands at such attempts to make lies seem like the truth and worse, the truth like a lie, responding with just four words: “And yet it moves.”

Galileo may have never really uttered these words. He surely didn’t say that phrase in front of the Inquisitors—that would have been insanely dangerous. But whether the motto came first from his own mouth, that of a supporter whom he met during the years the Church put him under house arrest after his trial, or a later historian, we know one thing for sure. That motto represents everything Galileo stood for. It conveys the clear message of: In spite of what you may believe, these are the facts! That science won at the end is not solely because of the methods and rules that Galileo set out for what we accept to be true. Science prevailed because Galileo put his life and his personal freedom on the line to defend it.

Mario Livio is an astrophysicist and author. His new book is Galileo: And the Science Deniers.

Lead image: Mario Breda / Shutterstock

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