World COVID-19 hotspots are anchored in the Americas and western Europe, with more than 1000 cases per million population recorded in several countries, including Argentina, Colombia, France, Spain, the UK and Iceland. During 12–18 October, 927,433 new cases were reported in Europe, an increase of 25% on the previous seven days. In the same period, Europe accounted for 38% of total new global cases.
According to the WHO (at 21 October), national death tolls are highest in the US (218,641), Brazil (154,176), India (115,914), Mexico (86,338) and the UK (43,967).
In Australia, daily new case numbers have returned to the low double-digit levels experienced from late April to mid-June, after the initial spike of the virus.
As at 17:47 CEST on Wednesday 21 October, cases confirmed worldwide by national authorities stood at 40,665,438 (350,424 of them reported in the preceding 24 hours). 1,121,843 deaths have been recorded (5192). (Source: WHO Coronavirus Disease Dashboard)
Johns Hopkins University’s Centre of Systems Science and Engineering (CSSE) reported (at 14:15 AEST on Thursday 22 October) 41,148,042 confirmed cases and 1,130,405 deaths.
The Department of Health reported on 21 October that national confirmed cases stood at 27,444, a rise of 16 in 24 hours. 905 deaths have been recorded.
State by state: ACT 113 total cases (first case reported 12 March); NSW 4356 (25 January); NT 33 (20 March); Qld 1165 (29 January); SA 485 (2 February); Tas 230 (2 March); Vic 20,323 (25 January); WA 739 (21 February).
A new case in Australia is being treated as a reinfection. If confirmed, it would be the first in the country and only the seventh globally.
Among Australian experts asked for initial comment was Dr Larisa Labzin from the Institute for Molecular Bioscience at the University of Queensland, who says there are two possible scenarios for why someone could test positive twice.
“The first is that they have genuinely been re-exposed to COVID-19 and that they have caught it again. This can be determined by genetically sequencing the virus during the first and the second test and comparing the viral sequences.
“The virus accumulates enough small changes with time that we can distinguish a virus that was caught in July from a virus that was caught now – in October.
“The alternative is that the person who caught COVID in July never truly cleared that original infection, in which case this wouldn’t be a ‘new’ case of COVID-19. Actual reinfection that has been confirmed with genetic sequencing has now been reported in a few rare cases worldwide, indicating that it is indeed possible.”
Professor Sarah Palmer from Westmead Institute for Medical Research commented that revelations of reinfections pose a big challenge for vaccine efforts “as many vaccines were developed to be active against strains identified early in the progression of the pandemic”.
“As more infections occur, we will be in a race for vaccines to stay apace with the evolutionary curve of this virus,” she says.
On that note, an article in the medical journal The BMJ is concerning. Associate editor Peter Doshi writes that none of the current COVID-19 vaccine trials is designed to tell us if they will save lives.
While several are in the most advanced Phase 3 stage, he says, it is not clear what it will exactly mean when a vaccine is declared “effective”.
“None [is] designed to detect a reduction in any serious outcome such as hospitalisations, intensive care use, or deaths,” he writes. “Nor are the vaccines being studied to determine whether they can interrupt transmission of the virus.”
All ongoing Phase 3 trials for which details have been released are evaluating mild not severe disease, Doshi says, yet vaccine manufacturers have done little to dispel the notion that severe COVID-19 was being assessed.
Why is this virus so infectious?
Two international studies just published in the journal Science shed light on why the virus that causes COVID-19 is so infectious compared to other SARS viruses – and hopefully on a way to potentially prevent it infecting cells.
The SARS-CoV-2 virus is known to use a protein called Spike to enter host cells by binding to ACE2, a receptor on human cells, and using it as a doorway. Now a European-led team has shown it also can enter using a receptor called neuropilin.
The researchers discovered that the neuropilin receptor, NRP1, is found on a variety of human cells, including those in the upper airways, which could explain why SARS-CoV-2 is more infectious and more extensively invasive than similar viruses.
The fact that antibodies blocking NRP1 are able to block infection by 40% strongly suggests, they say, that this pathway is key for the virus’ infectivity.
“The discovery that NRP1 binds to Spike opens the door to in-depth research into the virus’ neurotropism – its ability to infect nerve tissue — as well as new therapeutic avenues,” says co-author Frederic Meunier, from Australia’s University of Queensland.
In the second study, researchers led by the UK’s University of Bristol were able to show exactly how the virus binds to a host cell by modelling the site where they interact.
They used X-ray crystallography to see the structure of proteins at the atomic level and visualise the binding sites at a spectacular level of detail.
“We discovered that by blocking the virus protein from attaching to cells, it was possible to reduce the infection rate of the virus,” says Bristol’s Yohei Yamauchi said. “If we can make a drug that blocks the virus from binding to cells, this has potential as a new therapy for treating COVID-19.”
Just Google it
A new study from the Mayo Clinic in the US suggests there is value in analysing Google web searches for keywords related to COVID-19.
Neurosurgeon Mohamad Bydon and colleagues report finding strong correlations between keyword searches on Google Trends and outbreaks in parts of the US. These were observed up to 16 days prior to the first reported cases in some states.
“If you wait for the hot spots to emerge in the news media coverage, it will be too late to respond effectively,” Bydon says. “In terms of national preparedness, this is a great way of helping to understand where future hot spots will emerge.”
The study – described in Mayo Clinic Proceedings – searched for 10 keywords chosen based on how commonly they were used and emerging patterns on the internet and in Google News. They included “COVID symptoms”, “loss of smell”, “antibody” and “face mask”.
Most had moderate to strong correlations days before the first COVID-19 cases were reported in specific areas, with diminishing correlations following the first case.
There’s a lot to absorb, but we’re coping
The ever-increasing body of research around COVID-19 and our response to it may create the impression that understanding of its spread is frequently overturned or not well understood. But that’s certainly not the case, five experts from John Hopkins University, US, argue in a Perspective article in Science.
“Although our knowledge of SARS-CoV-2 transmission is constantly deepening in important ways, the fundamental engines that drive the pandemic are well established and provide a framework for interpreting this new information,” Elizabeth Lee and colleagues write.
The authors offer an overview on the established knowns of SARS-CoV-2 across various contexts and spatial scales, including household, residential and community settings and during superspreading events.
They highlight when these transmission-spreading events can be considered part of a more general phenomenon: overdispersion in transmission, or more of a variation in cases than expected. This phenomenon has driven much of the debate around the relative importance of different modes of transmission, they note.
They also highlight distinct unknowns. “The relative risk of transmission in different community settings, such as restaurants and retail stores, is still unclear, as is the impact of mitigation measures in these contexts,” they write.
Safety in the classroom
Physicists have been prominent in the battle to understand COVID-19, undertaking a number of studies into flow velocity distribution and particle size, which are key in aerosol transport – one of the main ways the virus spreads
In new work, published in the journal Physics of Fluids, a team from the University of New Mexico, US, looked specifically at air-conditioned school classrooms, using computational fluid-particle dynamics to explore aerosol transport.
They found that just opening windows can increase the number of particles that exit the system by nearly 40%, while also reducing aerosol transmission between students.
Khaled Talaat and colleagues were also surprised to discover how effective glass droplet screens placed in front of desks could be.
“Screens don’t stop one-micron particles directly, but they affect the local air flow field near the source, which changes the particle trajectories,” he says. “Their effectiveness depends on the position of the source with respect to the air conditioning diffusers.”
Nick Carne is the editor of Cosmos Online and editorial manager for The Royal Institution of Australia.
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