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COVID research updates: A vaccine that mimics the coronavirus prompts potent antibodies

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timesdelhi wades through the literature on the new coronavirus — and summarizes key papers as they appear.

6 November — A vaccine that mimics the coronavirus prompts potent antibodies

A COVID-19 vaccine candidate made of tiny artificial particles could be more powerful than other leading varieties at triggering a protective immune response.

David Veesler and Neil King at the University of Washington in Seattle and their colleagues designed microscopic ball-shaped particles that mimic the structure of a virus (A. C. Walls et alCell https://doi.org/fg6r; 2020). The researchers fused 60 copies of SARS-CoV-2’s spike protein — the part of the virus that allows it to infect human cells — to the outside of each of these ‘nanoparticles’.

When the team injected mice with the nanoparticle vaccine, the animals produced virus-blocking antibodies at levels comparable to or greater than those produced by people who had recovered from COVID-19. Mice that received the vaccine produced about ten times more of these antibodies than did rodents vaccinated only with the spike protein, on which many COVID-19 vaccine candidates rely.

The vaccine also appears to produce a strong response from special immune cells that help to mount a fast defence after infection with SARS-CoV-2.

A customer shopping for groceries at a Pyaterochka supermarket in Moscow's Severnoye Tushino District.
Door handles at grocery stores were among the sites where researchers found the RNA of the new coronavirus.Credit: Sergei Bobylev/TASS/Getty

4 November — Many surfaces carry coronavirus RNA — but not much of it

Swabbing of bank machines, shop-door handles and other frequently touched surfaces in a US city revealed that 8% of samples were positive for SARS-CoV-2 genetic material, but that material was present in small amounts.

Amy Pickering at Tufts University in Medford, Massachusetts, and her colleagues repeatedly sampled 33 surfaces in public places in Somerville, Massachusetts (A. P. Harvey et al. Preprint at medRxiv https://doi.org/fgx9; 2020). The handles of a rubbish bin and a liquor store were the most frequently riddled with coronavirus RNA. All samples showed only “low-level” contamination, and the infection risk from touching one of the contaminated surfaces is low, the researchers say.

The team found that the percentage of positive samples in one postal district peaked roughly 7 days before a spike in COVID-19 cases in the same district. Sampling of heavily touched surfaces might provide a warning of a surge of infections, the authors write.

Doctors report to family members after taking a rapid test during a house-to-house coronavirus testing drive in Lima.
Medical workers conduct a door-to-door coronavirus testing campaign in Lima. An analysis suggests that nearly two-thirds of people in Peru have been infected.Credit: Raul Sifuentes/Getty

2 November — The coronavirus’s spread in households is fast and often silent

The new coronavirus spreads more efficiently in US homes than previous research suggested,sometimes without any symptoms to warn of its transmission, according to intensive monitoring of more than 100 US households.

Melissa Rolfes at the Centers for Disease Control and Prevention in Atlanta, Georgia, and her colleagues recruited 101 US residents who had tested positive for SARS-CoV-2 and had recently developed COVID-19 symptoms (C. G. Grijalva et alMorb. Mortal. Wkly Rephttps://doi.org/fgx3; 2020). For at least a week after enrolment, the researchers gathered daily coronavirus test results from 191 people who lived with the infected people.

For a conservative estimate of disease spread, the researchers excluded contacts who tested positive when their household signed up for the study. All the same, 35% of the remaining participants eventually tested positive — almost double one previous estimate. Fewer than one half of household contacts who became infected showed symptoms when they first tested positive, and 75% tested positive five days or less after the first infected person in their home began feeling ill.

2 November — How 45 countries rank on coronavirus infections

A country’s tally of COVID-19 deaths among those aged under 65 can be used to reveal the total number of people who have been infected.

Megan O’Driscoll at the University of Cambridge, UK, and her colleagues compared data on COVID-19 deaths across 45 countries (M. O’Driscoll et alNature https://doi.org/fgts; 2020). The researchers found that among people younger than 65, the risk of dying of COVID-19 increased with age in a pattern that was consistent across all countries.How many people has the coronavirus killed?

The team also compiled statistics from 22 studies in 16 countries on the percentage of people who had SARS-CoV-2 antibodies, which indicate that they have previously been exposed to the virus. This helped the authors to estimate the infection fatality rate, which is the proportion of people who die after being infected with SARS-CoV-2, for the 45 study countries.

The researchers combined the infection fatality rates and the under-65 death statistics to estimate that by the beginning of September, some 5% of the 3.4 billion people in the 45 countries studied had been infected with SARS-CoV-2. South Korea had the lowest infection rate, at just 0.06%, and Peru had the highest with 62%.

This method could be used to estimate how many people have been infected in areas that cannot carry out large antibody surveys, the researchers say.

Doctor and nun visit a patient with Covid-19 in Alme, in Lombardy region.
A medical team visits a woman with COVID-19. Even people who do not become seriously ill with the disease mount a vigorous antibody response.Credit: Miguel Medina/AFP/Getty

30 October — Coronavirus-fighting antibodies linger for months

The body’s antibody defence against the coronavirus remains strong for at least three months after infection, according to a study of more than 100 people who mostly had mild to moderate COVID-19.

Ania Wajnberg at the Icahn School of Medicine at Mount Sinai in New York City and her colleagues analysed blood samples from more than 30,000 people who had been infected with SARS-CoV-2 (A. Wajnberg et alScience https://doi.org/fgfs; 2020). More than 90% of the infected people had moderate or high levels of antibodies in their blood, and experiments showed that these antibodies could block the virus from infecting cells.

The team also re-tested a subset of 121 individuals at two later dates and found that their antibody levels were stable for at least three months. Five months after symptom onset, the individuals’ antibodies showed only a modest decline . The authors say that it is “very likely” that the antibodies shield people from re-infection.

Racoon-dogs in their cages at a farm which breeds animals for fur in Zhangjiakou, in China's Hebei province.
Raccoon dogs at a fur farm in Zhangjiakou, China. Experiments show the animals can pass SARS-CoV-2 to each other.Credit: Greg Baker/AFP/Getty

28 October — A fur-farm animal can spread the coronavirus

The small fox-like animals called raccoon dogs (Nyctereutes procyonoides) can be infected with SARS-CoV-2, and can spread it among themselves.

Conrad Freuling at the Friedrich Loeffler Institute in Greifswald–Isle of Riems, Germany, and his colleagues deliberately infected nine raccoon dogs with the new coronavirus (C. M. Freuling et al. Emerg. Infect. Dis. https://doi.org/ffzf; 2020). Six began shedding the virus from their noses and throats several days later. When three uninfected animals were put in cages next to the infected animals, two got infected. None of the animals became visibly sick, but some were slightly lethargic.

These findings suggest that SARS-CoV-2 could spread undetected in fur farms in China, where more than 14 million raccoon dogs live in captivity. The coronavirus that caused the pandemic of severe acute respiratory syndrome in 2002–2004 was also isolated in raccoon dogs, and could have first jumped to people from the canids.

A health worker collects a swab sample from a man to test for coronavirus infection, New Delhi, India.
A health care worker in New Delhi prepares to collect a sample for SARS-CoV-2 testing.Credit: Vipin Kumar/Hindustan Times/Getty

27 October — Basketball stars score with coronavirus insights

Professional basketball players in the United States have helped to provide details of a poorly understood phase of SARS-CoV-2’s life cycle: its behaviour in the bodies of newly infected people.

After a four-month hiatus, US basketball games resumed in July. Before and after play restarted, athletes and staff members were repeatedly checked for SARS-CoV-2 with a version of the highly sensitive polymerase chain reaction method, which can be used to assess a person’s viral levels. The intensive testing offered a rare chance to monitor viral levels in infected people who had not yet developed symptoms, and in those who never felt ill.

Stephen Kissler at the Harvard T.H. Chan School of Public Health in Boston, Massachusetts, and his colleagues analysed test results from 68 people involved in the season (S. M. Kissler et al. Preprint at medRxiv https://doi.org/ffxk; 2020). Study participants’ viral levels peaked about three days after they tested positive. The researchers found that two tests given within two days can indicate whether a person’s viral level is rising or falling — information that can influence treatment decisions. The findings have not yet been peer reviewed.

26 October — A maths-based strategy streamlines COVID testing

In ‘pooled’ testing for SARS-CoV-2, samples from multiple people are combined into one batch that is then analysed for the virus. Now, a large-scale trial has shown that pooled testing can be highly efficient — even more so than theory predicted.The mathematical strategy that could transform coronavirus testing

Moran Yassour at the Hebrew University of Jerusalem and her colleagues tested 133,816 nose and throat samples by pooling either five or eight individual samples into one group sample (N. Barak et al. Preprint at medRxiv https://doi.org/ffkx; 2020). If a group tested positive, every constituent sample was retested. Groups that tested negative were not retested.

Using this method, the researchers required only one-quarter of the tests they would have needed to check every sample individually. They needed fewer tests than expected, because people from the same household, university, care home or hospital tend to get tested together, increasing the likelihood that positive samples are in the same groups. The findings have not yet been peer reviewed.

A pharmacist displays boxes of tocilizumab.
The drug tocilizumab tamps down an immune-system protein that promotes inflammation but does not extend the lives of people with moderate COVID-19, according to a rigorous trial.Credit: Alamy

23 October — Promising drug for COVID-19 does not save lives

A study of a drug that mutes the body’s immune response found that it did not prevent the deaths of people with moderate COVID-19, dealing a blow to a once-popular hypothesis about treatments for the disease.

In some people with severe COVID-19, the immune system launches an excessive inflammatory response, suggesting a link between grave illness and an overly vigorous immune defence against SARS-CoV-2. The link is bolstered by the association between high levels of a protein called IL-6, which stimulates the immune system, and both death and the need for ventilation in people with COVID-19.

John Stone at the Massachusetts General Hospital in Boston and his colleagues tried to dampen inflammation in people with COVID-19 by treating them with the drug tocilizumab, which interferes with IL-6 activity (J. H. Stone et alN. Engl. J. Medhttps://doi.org/ffjp; 2020). But in a randomized, controlled trial of 243 people with moderate disease, the team found no statistically significant reduction in deaths or the need for ventilation among those who received tocilizumab compared with those who didn’t. The study does not rule out the possibility that a larger trial with more statistical power could uncover a benefit.

A University of Colorado Boulder student chugs a beer at a graduation party outside of a home, US.
Student parties have sparked university outbreaks of COVID-19, which can then seep into the surrounding communities.Credit: Jeremy Papasso/MediaNews Group/Boulder Daily Camera/Getty

20 October — Genomics ties university COVID cases to care-home deaths

An explosive outbreak of COVID-19 among young people in a US university town spilt into the surrounding community, leading to the deaths of two people in local care homes.

Public-health officials have long warned that SARS-CoV-2 infections in young adults could easily cascade into a community’s older population. That scenario has now been confirmed in La Crosse, Wisconsin, which has three universities.How anti-ageing drugs could boost COVID vaccines in older people

Paraic Kenny at the Gundersen Medical Foundation in La Crosse and his colleagues analysed 111 SARS-CoV-2 genomes from people in La Crosse County, where cases spiked to 2,002 in September — the month when students began in-person classes (C. S. Richmond et al. Preprint at medRxiv https://doi.org/fdt3; 2020). The team found that the “overwhelming majority” of those cases was caused by only two viral variants that spread swiftly during the first three weeks of September. Most of the cases were in people aged 17 to 29.

Clusters of young people were infected with the same variant, suggesting that the virus spread at gatherings, such as packed student parties, which took place both indoors and outdoors. One of the variants made its way into two care homes. Eight home residents were infected, and two died. The findings have not yet been peer reviewed.

Detail of test tubes analyzed with new equipment in the Policlinico di Bari on August 19, 2020 in Bari, Italy.
Bar-coded tubes used in coronavirus testing in Bari, Italy.Credit: Donato Fasano/Getty

19 October — The coronavirus test results that predict an outbreak’s course

Viral levels in people infected with SARS-CoV-2 in a specific town or city could be used to assess whether the epidemic there has passed its peak.

A common test for SARS-CoV-2 allows doctors to measure an infected person’s ‘viral load’, an indicator of the amount of virus in their body. James Hay at the Harvard T.H. Chan School of Public Health in Boston, Massachusetts, and his colleagues, used modelling to show that the viral loads of a population correlate with the rate of viral spread in that population (J. A. Hay et al. Preprint at medRxiv https://doi.org/ghfm73; 2020).

Early in an epidemic, the average infected person has been recently exposed to the virus and therefore has a high viral load. Later in the epidemic, the average infected person has had the virus for longer and has a low viral load.

As a result, a snapshot of the viral-load distribution in a random sample of a population can reveal whether cases in that population are on the rise or are declining, the researchers say. They add that their method is less susceptible to biases from changing COVID-testing practices than simply counting daily cases. The findings have not yet been peer reviewed.

A health worker collects a nasal swab sample from people during weekly market for Covid-19 Rapid Antigen Testing.
A health worker at a market in New Delhi collects a sample for rapid antigen testing.Credit: Mayank Makhija/NurPhoto/Getty

16 October — Are rapid coronavirus tests effective? It depends

Rapid antigen tests for the coronavirus provide results within 30 minutes. But not all of the tests on the market are equally effective at detecting the virus.

Antigen-based assays detect specific surface proteins, or antigens, on SARS-CoV-2 particles, and are easy to use and inexpensive to produce. Marion Koopmans at the Erasmus University Medical Center in Rotterdam, the Netherlands, and her colleagues used 5 commercially available rapid antigen assays on samples from 1,754 people who had already tested positive for the coronavirus with the standard polymerase chain reaction test, which is highly sensitive but slow (J. van Beek et al. Preprint at medRxiv https://doi.org/fdmg; 2020).

The 2 most sensitive tests detected the virus more than 97% of the time, whereas the least sensitive test did it in about 75% of cases.

All samples came from people with COVID-19 symptoms, who tend to have high levels of coronavirus. The researchers caution that rapid antigen tests might be less effective at picking up the presence of the virus in people with low levels of virus. The finding has not yet been peer reviewed.

Woman with a masks reading on the beach under a parasol.
The arrival of swimsuit weather will not necessarily lead to a drop in transmission of SARS-CoV-2.Credit: Carlos Castro/Europa Press/Getty

15 October — The coronavirus shrugs at seasonal temperature changes

The arrival of spring and summer do not slow transmission of SARS-CoV-2, say researchers who studied the early stages of the pandemic.

Influenza viruses survive for longer outside the body in cold, dry air than in warmer, more humid environments, giving them the chance to infect more people in winter than in spring and summer. Research has given a mixed picture of whether the new coronavirus shows similar behaviour.

To see how the changing seasons affected the virus’s spread in China, Canelle Poirier and Mauricio Santillana at Harvard Medical School in Boston, Massachusetts, and their colleagues created a model incorporating data from China collected between mid-January and mid-February (C. Poirier et alSci. Rep10, 17002; 2020). These data included COVID-19 case counts, weather conditions and information about domestic travel. The model also took into account lockdowns instigated by the government.

The team found that the weather alone could not explain variability in the virus’s spread, which continued in areas of China with tropical climates as well those that are cold and dry.

Antibodies responding to coronavirus particle, illustration.
Antibodies (white) converge on a coronavirus particle (artist’s impression).Credit: Juan Gaertner/SPL

14 October — Theres more than one way to build a coronavirus-fighting antibody

Researchers have worked out how a range of potent immune proteins stop the new coronavirus infecting cells.

Neutralizing antibodies recognize viral particles and keep them out of cells. They are an important component of the immune system’s attack on SARS-CoV-2, and a promising experimental treatment.

A team led by Pamela Bjorkman at the California Institute of Technology in Pasadena determined the 3D shapes of eight neutralizing antibodies attached to SARS-CoV-2’s spike protein, which helps the virus to gain a foothold in host cells (C. O. Barnes et alNature https://doi.org/fc8d; 2020). The structures revealed that these neutralizing antibodies can be divided into several classes, according to which part of the spike protein’s cell-attachment region they recognize.

Further experiments showed that mutations that allow viruses to evade one class of neutralizing antibody are unlikely to foil others.

13 October — Common-cold antibodies offer little defence against the coronavirus

Research on archived blood does not bear out hopes that antibodies against ‘seasonal’ coronaviruses can protect against severe COVID-19.

Paul Bieniasz and Theodora Hatziioannou at the Rockefeller University in New York City and their colleagues analysed 37 blood-serum samples collected before 2020 from people in the United Kingdom (D. Poston et al. Preprint at medRxiv https://doi.org/fc4g; 2020). All of the study participants had tested positive for one of the seasonal human coronaviruses, which can cause the common cold.The coronavirus is most deadly if you are older and male — new data reveal the risks

The team found that each serum sample contained antibodies that could disable at least one common-cold coronavirus, blocking the virus’s ability to infect human cells in a lab dish. But the serum could not disable a hybrid virus that had been engineered to carry SARS-CoV-2’s spike protein, a crucial player in the virus’s invasion of host cells.

The results suggest that antibodies to common-cold coronaviruses do not have a major role in determining why some people with COVID-19 fare worse than others, the authors say. The findings have not yet been peer reviewed.

Preciados Street in downtown Madrid crowded with people wearing protective face masks.
Dense cities such as Madrid (pictured) could endure longer but less intense COVID-19 epidemics than cities where people are less tightly packed.Credit: Marcos del Mazo/LightRocket/Getty

8 October — Dense cities should brace for long coronavirus outbreaks

The new coronavirus tears through areas where residents generally keep to their own small, close-knit communities. But the virus takes its time spreading in crowded cities where residents of different neighbourhoods tend to intermingle, ultimately infecting more people than in the relatively isolated areas.

Moritz Kraemer at the University of Oxford, UK, and his colleagues modelled the spread of SARS-CoV-2 through communities of various sizes and population densities(B. Rader et alNature Medhttps://doi.org/fcjk; 2020). The researchers validated their model by comparing its output with known data on individual movements and infection rates in crowded Chinese cities such as Wuhan and less densely packed provinces in Italy.

The team’s model predicts relatively short, intense spikes in COVID-19 cases in relatively uncrowded cities where residents stick to their own neighbourhoods rather than mingling freely. In crowded cities, however, people are more likely to have to cope with outbreaks that last longer than do those in the countryside.

The researchers applied their model to 310 cities worldwide, and predict that those with relatively even population distributions, such as Ulaanbaatar in Mongolia, could expect a short-term explosion in cases. But more densely settled urban centres, such as Madrid, can expect more protracted outbreaks.

Extended family enjoying a BBQ in the park in Melbourne, Australia.
Unwelcome guest: an analysis of infections at a family reunion illustrates how the coronavirus can spread among people living in close quarters.Credit: Getty

6 October — Teenager spreads coronavirus on family holiday

A 13-year-old girl gave the new coronavirus to her grandparents and 9 other relatives who occupied the same holiday house for up to 3½ weeks, confirming that adolescents can seed clusters of COVID-19 cases.

According to an investigation by Noah Schwartz at the Centers for Disease Control and Prevention in Atlanta, Georgia, and his colleagues, the girl was exposed to SARS-CoV-2 in June. After a rapid test suggested that she was not infected, she joined 13 family members for an extended stay in a 5-bedroom house (N. G. Schwartz et alMorb. Mortal. Wkly Rep. https://doi.org/10.15585/mmwr.mm6940e2; 2020). Family members neither wore masks nor maintained distance from each other.

Twelve people in the house, including the teenage girl, developed COVID-19 symptoms and either tested positive for the coronavirus or were classified as probable cases. Six other relatives visited those staying in the house but remained outdoors and kept their distance. Of those six, all four who took a coronavirus test tested negative, and none fell ill.

A health worker collected samples for coronavirus antigen testing, in New Delhi, India.
A medical worker in New Delhi collects a sample for SARS-CoV-2 testing.Credit: Sonu Mehta/Hindustan Times/Getty

5 October — Massive contact-tracing effort in India reveals striking trends

The patterns of infections and deaths caused by the new coronavirus differ starkly between resource-poor settings and wealthier places, according to the largest contact-tracing study conducted so far, carried out using data from India.

Joseph Lewnard at the University of California, Berkeley, and his colleagues analysed data from almost 85,000 people with COVID-19, as well as their close contacts — who numbered nearly 600,000 — in the states of Tamil Nadu and Andhra Pradesh (R. Laxminarayan et al. Science https://doi.org/10.1126/science.abd7672; 2020).

The incidence of COVID-19 in the two states declines steadily with age for people aged 40 and older — in contrast to the United States, where incidence climbs with age from age 65. Mortality rates for those aged 75 and above were markedly lower in India than in the United States — perhaps, the researchers say, because people in India who live to old age tend to be relatively wealthy compared with those who die younger.

The study also found that people were most likely to infect others within their own age group. This is especially true of children, suggesting that socialising among kids could contribute to viral spread.

TEM of SARS-CoV-2 virus particles.
Particles of SARS-CoV-2Credit: NIAID (CC BY 2.0)

2 October — The immune trait that could allow viral reinfection

Waning antibody levels or a poorly developed immune response to SARS-CoV-2 could put people at risk of reinfection, one case suggests.

In March, a care-home resident in their sixties developed severe pneumonia and tested positive for the new coronavirus. The individual spent more than one month in hospital before testing negative. In July, the individual tested positive again, with milder symptoms of coughing and shortness of breath.What the immune response to the coronavirus says about the prospects for a vaccine

Genomic analysis by Jason Goldman at the University of Washington, Seattle, and his colleagues (J. D. Goldman et al. Preprint at medRxiv https://doi.org/fbvj; 2020) showed that these were two separate infection events. The team also found that after the second infection, the individual produced only low levels of antibodies, and that these decreased over time. The person might have had a similar response to the first infection, which could explain why the individual was not protected against the second infection, the authors say.

The team also measured the individual’s neutralizing antibodies, which protect cells against infection. The person had lower levels of these potent antibodies against the version of SARS-CoV-2 that caused the first infection than against the version that caused the second infection.

The researchers say that these measurements provide a useful benchmark for antibody levels that do not protect against reinfection. The research has not yet been peer reviewed.

Moderna COVID-19 Vaccine Trial Underway in DeLand, Florida.
Clinical-trial volunteer Tony Potts, 69 and a resident of Ormond Beach, Florida, receives a dose of the experimental Moderna vaccine against COVID-19.Credit: Paul Hennessy/NurPhoto/Getty

1 October — A fast-spreading viral variety shows higher infectiousness

Variants of SARS-CoV-2 with a widespread mutation are more infectious in human cells and hamsters, compared with viral variants lacking the change.

In February 2020, researchers examining samples from people with COVID-19 detected a SARS-CoV-2 mutation that alters the amino acid sequence of the virus’s spike protein, which the virus uses to infect cells. The amino-acid alteration, known as D614G, became common in Europe, North America and elsewhere in spring 2020, and now nearly all viruses isolated worldwide carry the alteration.COVID has killed more than one million people. How many more will die?

To determine the effects of the D614G change, two independent teams engineered SARS-CoV-2 particles with the mutation. Pei-Yong Shi at the University of Texas Medical Branch in Galveston, Texas and his colleagues conducted one set of experiments (J. A. Plante et al. Preprint at bioRxiv https://doi.org/fbxz; 2020); Ralph Baric at the University of North Carolina-Chapel Hill and his colleagues conducted the other (Y. J. Hou et al. Preprint at bioRxiv https://doi.org/fbxx; 2020).

Both teams found that, compared with forms of the virus that lack the mutation, D614G variants replicated more efficiently in cells from human airway tissues. Baric’s team also found that D614G variants spread faster between hamsters, which are used to study SARS-CoV-2 transmission. Neither finding has been peer reviewed yet.

30 September — A front-runner vaccine shows promise in older people

Older people injected with one of the most prominent candidate vaccines for COVID-19 developed high levels of antibodies against the new coronavirus.

Evan Anderson at the Emory University School of Medicine in Atlanta, Georgia, and his colleagues studied the response of 40 people aged 56 and above to the vaccine developed by biotechnology firm Moderna, based in Cambridge, Massachusetts, and the US National Institute of Allergy and Infectious Diseases (E. J. Anderson et alN. Engl. J. Medhttps://doi.org/fbxj; 2020). The vaccine consists of a piece of RNA that encodes a modified version of a SARS-CoV-2 protein.

Participants developed several types of antibodies — immune molecules that fight infection — including neutralizing antibodies, which can disarm an invading microbe. After receiving a second dose of the vaccine, participants had antibody levels similar to those of control-group participants who had recovered from COVID-19. Any side effects were generally mild to moderate.

Health workers work with collected samples for coronavirus testing, New Delhi, India.
Health workers at a hospital in New Delhi process samples to test for COVID-19.Credit: Sonu Mehta/Hindustan Times via Getty

28 September — Tests reveal silent reinfections in hospital workers

Two staff members at a hospital in India who tested positive for the new coronavirus became reinfected several months later — and had no symptoms in either instance.

The hospital employees, a 25-year-old-man and a 28-year-old woman, worked in the COVID-19 ward. Both tested positive for SARS-CoV-2 in May, although neither had symptoms (V. Gupta et alClin. Inf. Dishttps://doi.org/d97d; 2020). After testing negative, they returned to work. Both tested positive again roughly three-and-a-half months after the first positive test. Neither had symptoms, but both had higher levels of virus than in May.

Genomic analysis by Vinod Scaria at the Institute of Genomics and Integrative Biology in New Delhi and his colleagues showed that the SARS-CoV-2 that infected the workers the second time was genetically different from the first virus that infected them — evidence that the workers were infected anew rather than harbouring leftover virus.

The results suggest that asymptomatic reinfections are often underreported, the authors say.

Nurses work in the intensive care unit of the Centre Hospitalier Universitaire (CHU) of Pointe-a-Pitre, Guadeloupe.
Nurses care for a person in the intensive-care unit of a hospital in the French region of Guadeloupe.Credit: Lara Balais/AFP/Getty

25 September — The immune breakdown linked to dire illness

Some severe cases of COVID-19, including those in young, healthy people, could be linked to dysfunction of immune-signalling chemicals called type-1 interferons, according to a survey of nearly 1,000 people with life-threatening SARS-CoV-2 infection.

Type-I interferons are crucial for mounting a defence against influenza and other viruses. Jean-Laurent Casanova at the Rockefeller University in New York City and his colleagues analysed DNA from people with severe COVID-19, looking for specific mutations in genes that trigger production of type-I interferons (Q. Zhang et alScience https://doi.org/d95p; 2020). The team found that 3.5% of study participants had such mutations, which rendered them unable to manufacture the signalling chemicals.

In a second study, of severely ill people, Casanova, Paul Bastard at the University of Paris and their colleagues looked for autoantibodies — antibodies that, for unknown reasons, attack the body’s own tissues and organs (P. Bastard et alScience https://doi.org/d95q; 2020). The researchers found that more than 10% of people with severe COVID-19 had autoantibodies that targeted type-I interferon activity, compared with 0.3% in the general population. Laboratory experiments confirmed that the auto-antibodies knocked out type-I interferon activity.

The researchers suggest that interferons could be used as therapies for the disease.

Aerial view showing a new area (R) cleared to accomodate new graves in the cemetery in Manaus.
A cemetery in Manaus, Brazil, has cleared ground (right) for the graves of people killed by COVID-19, which has devastated the city.Credit: Michael Dantas/AFP via Getty

24 September — Extreme infection level might have helped to quell a city’s epidemic

As much as two-thirds of the population of Manaus, a city of two million people in Brazil’s state of Amazonas, could have been infected with the new coronavirus. That’s a proportion high enough to have contributed to controlling the spread of the virus.

Ester Sabino at the University of São Paulo, Brazil, and her colleagues searched for antibodies against SARS-CoV-2 in more than 6,000 blood samples collected by a Manaus blood bank between February and August (L. F. Buss et al. Preprint at medRxiv https://doi.org/ghcm6h; 2020). From the proportion of donors who tested positive for antibodies, the authors estimate that about 66% of the population had been infected by early August — months after the epidemic in Manaus peaked in May .

The authors say that the high proportion of donors with antibodies to the virus suggests that Manaus might have reached ‘herd immunity’, the term for a scenario in which enough people are immune to an infection to control its spread.

The team says its estimate accounts for several potential sources of bias, including false positives and false negatives in antibody testing. The findings have not yet been peer reviewed.

Coloured TEM of SARS-CoV-2 coronavirus particles (red) isolated from a patient with the disease Covid-19.
Coronavirus particles (red; artificially coloured) isolated from a person with COVID-19.Credit: NIAID/NIH/SPL

22 September — Good timing might help the immune system to control COVID-19

People aged 65 and older who are infected with the new coronavirus tend to mount a disorganized immune response — a response that is also associated with severe COVID-19. This could help to explain why the disease strikes older people particularly hard.

The immune system’s ‘adaptive’ branch, which targets specific invaders, has three principle components: antibodies, CD4+ T cells and CD8+ T cells. Alessandro Sette and Shane Crotty at the La Jolla Institute for Immunology in California studied the adaptive immune response in 24 people whose COVID-19 symptoms ranged from mild to fatal (C. R. Moderbacher et alCell https://doi.org/ghbwh7; 2020).How many people has the coronavirus killed?

The team found that people whose immune systems failed to rapidly launch the entire adaptive immune system tended to have more severe disease than did people in whom all three arms ramped up production simultaneously. An uncoordinated response was particularly common among older people, and could indicate that both antibodies and T cells are important weapons against the coronavirus.

21 September — Business-class passenger spreads coronavirus on flight

Genetic evidence strongly suggests that at least one member of a married couple flying from the United States to Hong Kong infected two flight attendants during the trip.

Researchers led by Leo Poon at the University of Hong Kong and Deborah Watson-Jones at the London School of Hygiene & Tropical Medicine studied four people on the early-March flight (E. M. Choi et alEmerg. Infect. Dishttps://doi.org/d9jn; 2020). Two were a husband and wife travelling in business class. The others were crew members: one in business class and one whose cabin assignment is unknown. The passengers had travelled in Canada and the United States before the flight and tested positive for the new coronavirus soon after arriving in Hong Kong. The flight attendants tested positive shortly thereafter.

The team found that the viral genomes of all four were identical and that their virus was a close genetic relative of some North American SARS-CoV-2 samples — but not of the SARS-CoV-2 prevalent in Hong Kong. This suggests that one or both of the passengers transmitted the virus to the crew members during the flight, the authors say. The authors add that no previous reports of in-flight spread have been supported by genetic evidence.

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Business

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