Tag: covid transmission

Nose-picking Healthcare Workers Were More Likely to Get COVID

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A study of healthcare workers (HCW) found that those who picked their nose were more likely to get COVID than the people who refrained from such explorations. The Dutch researchers published their probing results in the journal PLOS One.

In the early stages of the COVID pandemic, researchers noted a wide range of efforts to prevent the spread of SARS-CoV-2, such as the wearing of personal protective equipment and maintaining social distancing, especially in the hospital setting. Much research went into the impacts of, eg, wearing glasses on the effectiveness of masking, but little if any attention was paid to a widespread but secretive habit.

Sikkens and colleagues retrospectively surveyed healthcare workers at Amsterdam University Medical Centers were in December 2021 about their behaviours during the first and second waves of the pandemic. They matched these responses were matched against prospectively collected COVID test results at the hospitals from March to October 2020. The nose pickers were nearly three times more likely to catch COVID (17.3% vs 5.9%) than those who refrained at all costs. Surprising results were found for those HCWs who owned up to the habit.

Secret nose pickers can take some comfort in that 85% of the cohort admitted that they picked their nose either daily, weekly, or monthly, and nose pickers tended to be younger. More men picked their nose (90%) than women (83%), and doctors were the most likely to be among the nose-picking offenders: 100% of residents admitted to it, along with 91% of specialists.

Sikkens et al. noted that one limitation of the study was that nose pickers were not asked about “the depth of penetration and eating of boogers”.

Other behaviours such nail biting, having a beard were not associated with COVID infection, nor was wearing glasses, though it showed a relevant trend. Interestingly, nose picking frequency was not linked to difference in COVID infection risk; 27% of those who reported monthly picking, 35% among weekly pickers, and 32% of daily pickers.

Frequency of nose picking did not appear to be linked with any difference in COVID infection risk, with positive cases in 27% of those who reported monthly picking, 35% among weekly pickers, and 32% of daily pickers. No participants reported picking their nose every hour, thankfully.

One-third of the cohort reported nail biting, two-thirds wore glasses, and 31% of the men had beards.

A study strength was that SARS-CoV-2 positivity was determined by prospective longitudinal serological sampling, though this may not be generalisable to the current era of vaccines and circulating Omicron variants. The retrospective nature of the survey may have introduced recall bias.

Sikken et al. noted that it is surprising that SARS-CoV-2 transmission routes had been so thoroughly researched, yet simple behaviours had been overlooked. “Possibly this sensitive subject is still taboo in the health care profession. It is commendable we assume HCWs to not portray bad habits, yet we too are only human after all, as illustrated by the pivotal proportion of nose pickers in our cohort (84.5%).”

Not Yet Time to Ditch Masks in Healthcare, Experts Argue

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A new commentary by infectious disease experts published inĀ Annals of Internal Medicine says that, for patient safety, masking should continue in health care settings. This message, from authors at George Washington University School of Medicine and the National Institutes of Health (NIH), conflicts with a recent commentary from authors from 8 US institutions suggesting that the time for universal masking is over.

Masking has been a controversial mitigation strategy during the COVID pandemic because high-quality evidence of efficacy is lacking and because the topic has become highly politicised. Regardless, real-world experience demonstrates the effectiveness of mask-wearing in clinical settings where data shows that transmission from patient-to-staff and staff-to-patent, when both are masked, is uncommon. Since health care personnel report being driven to show up for work even when they are ill themselves, the argument in support of mask-wearing becomes even more compelling.

Those without symptoms may also transmit respiratory viruses, particularly SARS-CoV-2. While the Omicron strain has been milder, infection could still cause severe or life-threatening disease or prolonged illness if transmitted to at-risk patients, such as the elderly or immunocompromised. With the still-looming risks, now does not seem the time to take off masks in the health care setting. Instead, the authors advocate strongly for continued mask use for infection prevention.

Source: EurekAlert!

Face Masks for Kids Slow Aerosol Spread, Especially from Sneezing

Photo by Kelly Sikkema on Unsplash

In a new study published inĀ Pediatric Investigation,Ā researchers demonstrate that face masks reduce the release of exhaled particles when used by school-aged children, helping to slow the spread of various respiratory viruses. While there was little difference between no protection and masking in exhaled particles from breathing, sneezing saw a significant reduction in the number of particles produced.

Respiratory viruses, including SARS-CoV-2, are transmitted via respiratory droplets and aerosols generated by all activities that involve exhalation, including tidal breathing, speaking, singing, coughing, and sneezing. Droplets, large particles subject to gravitational forces, are rapidly deposited from air and form fomites on surfaces. Aerosols, fine solid or liquid particles which remain suspended in the air, can travel long distances (> 6m) and reach high concentrations in poorly-ventilated areas. The relative contribution of the various modes of infection (direct contact, indirect contact via fomite, large droplet, or aerosol) for various respiratory viruses is difficult to determine, but survival of infectious viruses has been demonstrated in aerosols.

For the study, 23 healthy children were asked to perform activities that ranged in intensity (breathe quietly, speak, sing, cough, and sneeze) while wearing no mask, a cloth mask, or a surgical mask.

The production of exhaled particles that were 5Ī¼m or smaller, which is the dominant mode of transmission of many respiratory viruses, increased with coughing and sneezing. Face masks, especially surgical face masks, effectively reduced the release of these and other sized particles.

ā€œUnderstanding the factors that affect respiratory particle emission can guide public health measures to prevent the spread of respiratory infections, which are a leading cause of death and hospitalisation among young children worldwide,ā€ said corresponding author Peter P. Moschovis, MD, MPH, of Massachusetts General Hospital and Harvard Medical School.

Source: Wiley

Ceiling Vents Above COVID Patient Beds Provide Optimal Protection for HCWs

Source: Martha Dominguez de Gouveia on Unsplash

Researchers have modelled the transmission of SARS-CoV-2-containing aerosol particles within an isolation room, and found the optimal layout to reduce the exposure risk for health care workers. InĀ Physics of Fluids, Wu et al. share their findings and guidance for isolation rooms. Their work focuses on the location of the room’s air extractor (air outlet) and filtration rates, the location of the patient’s bed, and the health and safety of the health care workers (HCWs) within the area.

The researchers modelled an isolation room at the Royal Brompton Hospital in London, with the aim of finding out the optimal room layout to reduce the risk of infection for health care staff.

“We modelled the virus transport and spreading processes and considered the effect of the temperature and humidity on the virus decay,” said Fangxin Fang, of Imperial College London. “We also modelled fluid and turbulence dynamics in our study, and explored the spatial distribution of virus, velocity field, and humidity under different air exchange rates and extractor locations.”

They discovered that the area of highest risk of infection is above a patient’s bed at a height of 0.7 to 2 metres, where the highest concentration of SARS-CoV-2 virus is found. After the virus is expelled from a patient’s mouth, it gets driven vertically by buoyancy and wind forces within the room.

Based on the group’s findings, the optimal layout for an isolation room to minimise infection risk is to use a ceiling extractor with an air exchange rate of 10 air changes per hour. The study focused on an isolation room within a hospital and its numerical results are limited due to the omission of droplet evaporation and particle matters, the researchers point out.

Now, the group plans to include evaporation and particle processes in models of a standard hospital patient room, intensive care unit, and waiting room.

“Further work will also focus on artificial intelligence-based surrogate modelling for rapid simulations, uncertainty analysis, and optimal control of ventilation systems as well as efficient energy use,” said Fang.

Source: American Institute of Physics

How SARS-CoV-2 Evolved Past its Own Weaknesses

Image from Pixabay

New research suggests that the first pandemic-accelerating mutation in the SARS-CoV-2 virus evolved as a way to correct vulnerabilities that were caused by the mutation that started the SARS-CoV-2 pandemic.

Published in Science Advances, this new evidence addresses important biological questions about two key mutations in the virus’ surface spike protein, say the researchers. It suggests that a spike protein mutation called D614G, which emerged a few months after the virus began spread among humans, was not an adaptation to humans. Instead, the mutation was an adaptation to the major changes that happened in the spike gene just before the pandemic, changes which allowed spread via respiratory transmission.

“This study has revealed that the first two genetic alterations in the evolution of the spike protein in SARS-CoV-2 are connected by their function, and this knowledge can improve our understanding of how the spike protein works and how the virus evolves, with important implications for vaccine design and effectiveness of COVID antibodies,” saysĀ Stephen Gould, professor of biological chemistry at the Johns Hopkins University School of Medicine, whose lab was studying the basic biology of the virus’s spike protein when the study began.

The initial mutation in the virus, Gould says, is known by scientists as the “furin cleavage site insertion mutation.”

Research by other scientists across the world has shown that this mutation enabled the virus’s spike protein to be cut and primed it for rapid infection of cells lining the airway.

While this initial mutation was essential in helping SARS-CoV-2 efficiently slip into human cells, the mutation’s effects weren’t all good, says Gould, as it cut the spike protein structure into two separate pieces.

According to Gould, this change disrupted other functions of the spike protein, creating evolutionary pressure for a second mutation to correct the disrupted functions of the spike protein while keeping the initial mutations’ rapid infection benefits .

In early 2020, researchers from the University of Toronto discovered a subsequent SARS-CoV-2 mutation, called D614G; however, its precise function was not known.

Gould, first author and graduate student Chenxu Guo, and the research team set out to understand the D614G mutation and its effect.

Working with dozens of blood samples from patients with COVID-19 hospitalized in April 2020 at the Johns Hopkins Hospital, Gould’s team isolated antibodies for the spike protein from the patients’ blood samples. Then, they used these antibodies to track the location of spike proteins in human cells genetically engineered to produce the spiky surface molecules.

They found that the D614G mutation redirects the spike protein and pulls the virus from the surface of human cells into a tiny compartment within the cell called a lysosome, which the spike protein reprograms into storage containers that are used to release infectious virus particles from the cell.

In addition, the D614G mutation caused a three-fold drop in the abundance of spike proteins at the cell surface.

“With less spike protein on the surface of virus-infected cells, it may be more difficult for the immune system to identify and kill those virus-containing cells,” says Gould.

The researchers caution that the study does not provide information about the still-debated origins of the virus. However, their work suggests that the two mutations likely arose in rapid succession.

The researchers are new examining whether spike protein mutations in more recent virus strains affect spike protein trafficking, studying the identity of the human proteins that deliver spike proteins to lysosomes, and researching how spike proteins convert lysosomes into compartments that release more virus.

Source: John Hopkins Medicine

What is the XBB.1.5 ‘Kraken’ Variant? An FAQ

SARS-CoV-2 infecting a human cell
Infected cell covered with SARS-CoV-2 viruses. Source: NIAID

By Sameer Elsayed for The Conversation

Despite intensive public health efforts to grind the COVID-19 pandemic to a halt, the recent emergence of the highly transmissible, extensively drug-resistant and profoundly immune system-evading XBB.1.5 SARS-CoV-2 subvariant is putting the global community on edge.

What is XBB.1.5?

In the naming convention for SARS-CoV-2 lineages, theĀ prefix ā€œXā€ denotes a pedigree that arose through genetic recombinationĀ between two or more subvariants.

The XBB lineage emerged following naturalĀ co-infection of a human host with two Omicron subvariants, namely BA.2.10.1 and BA.2.75. It wasĀ first identified by public health authorities in India during summer 2022. XBB.1.5 is a direct descendent, or more accurately, the ā€œfifth grandchildā€ of the original XBB subvariant.

Diagram of the genetic lineage of a COVID-19 subvariant
Genetic lineage of COVID-19 subvariant XBB.1.5. (Sameer Elsayed), Author provided

How does XBB.1.5 differ from Omicron?

XBB.1.5 is one of many Omicron subvariants of concern that have appeared on the global pandemic scene since the onset of theĀ first Omicron wave in November 2021. In contrast to other descendants of the original Omicron variant (known as B.1.1.529), XBB.1.5 is a mosaic subvariant thatĀ traces its roots to two Omicron subvariant lineages.

XBB.1.5 is arguably the most genetically rich andĀ most transmissibleĀ SARS-CoV-2 Omicron subvariant yet.

Where is XBB.1.5 prevalent?

According to the World Health Organization, XBB.1.5 is circulating in at least 38 countries, with the highest prevalence in the United States, where itĀ accounts for approximately 43 per cent of COVID-19 cases nationwide. Within the U.S., there is wide geographic variation in the proportion of cases caused by XBB.1.5, ranging fromĀ seven per cent in the Midwest to over 70 per cent in New England.

XBB.1.5 has also been officially reported by governmental agencies inĀ Australia,Ā Canada, theĀ European Union,Ā Japan,Ā Kuwait,Ā Russia,Ā Singapore,Ā South AfricaĀ and theĀ United Kingdom.Ā Real-time surveillance dataĀ reveals that XBB.1.5 is rapidly spreading across the globe and will likely become the next dominant subvariant.

XBB.1.5 has also been detected in municipal wastewater systems in theĀ United States,Ā EuropeĀ and other places.

How likely is XBB.1.5 to cause serious illness?

Illustration of five coronaviruses of different colours in a line
The XBB lineage emerged following natural co-infection of a human host with two Omicron subvariants, namely BA.2.10.1 and BA.2.75. (Shutterstock)

There is limited data about the ability of XBB.1.5 to cause serious illness. According to theĀ World Health Organization, XBB.1.5 does not have any specific mutations that make it any more dangerous than its ancestral subvariants.

Nonetheless, XBB.1.5 is perceived as being equally capable of causing serious illness in elderly and immunocompromised persons compared to previous Omicron subvariants of concern.

Are current mRNA vaccines effective against XBB.1.5?

XBB.1.5 and XBB.1 are the Omicron subvariants with theĀ greatest immune-evasive properties. Therefore, one of the most contentious issues surrounding XBB.1.5 relates to the degree of protection afforded by currently available mRNA vaccines, including the latest bivalent booster formulations.

Researchers from the University of TexasĀ determined that first-generation and bivalent mRNA booster vaccines containing BA.5 result in lacklustre neutralizing antibody responses against XBB.1.5. A report (yet to be peer reviewed) from investigators at theĀ Cleveland ClinicĀ found that bivalent vaccines demonstrate only modest (30 per cent) effectiveness in otherwise healthy non-elderly people when the variants in the vaccine match those circulating in the community.

Furthermore, some experts believe the administration of bivalent boosters for the prevention of COVID-19 illness in otherwise healthy young individuals isĀ not medically justifiedĀ norĀ cost-effective.

In contrast,Ā public health experts from Atlanta, Ga. and Stanford, Calif.Ā reported that although the neutralizing antibody activity of bivalent booster vaccines against XBB.1.5 is 12 to 26 times less than antibody activity against the wild-type (original) SARS-CoV-2 virus, bivalent vaccines still perform better than monovalent vaccines against XBB.1.5.

However,Ā investigators from Columbia UniversityĀ in New York found that neutralizing antibody levels following bivalent boosting were up to 155ā€“fold lower against XBB.1.5 compared to levels against the wild-type virus following monovalent boosting.

This suggests that neither monovalent nor bivalent booster vaccines can be relied upon to provide adequate protection against XBB.1.5.

How can you protect yourself against XBB.1.5?

A blue sign reading 'wearing a mask is recommended,' in French and English
Standard infection control precautions including indoor masking, social distancing and frequent handwashing are effective measures against XBB.1.5 and other subvariants of concern. THE CANADIAN PRESS/Graham Hughes

The rapid evolution of SARS-CoV-2 continues to pose a challenge for the management of COVID-19 illness using available preventive and therapeutic agents. Of note, all currently available monoclonal antibodies targeting the spike protein of SARS-CoV-2 areĀ deemed to be ineffective against XBB.1.5.

Antiviral medicines such as remdesivir and Paxlovid may be considered for the treatment of eligible infected patients at high risk of progressing to severe disease.

Standard infection control precautions including indoor masking, social distancing and frequent handwashing are effective measures that can be employed for personal and population protection against XBB.1.5 and other subvariants of concern.

Although bivalent boosters may be considered for elderly, immunocompromised and other risk-averse individuals, their effectiveness in preventing COVID-19 illness due to XBB.1.5 remains uncertain.

Why is XBB.1.5 nicknamed ā€˜Krakenā€™?

Some scientists have coined unofficially-recognized nicknames for XBB.1.5Ā and other SARS-CoV-2 subvariants of concern, arguing that they are easier to remember than generic alphanumeric designations.

The ā€˜Krakenā€™ label for XBB.1.5 is currently in vogueĀ on social media sites and news outlets, and the nicknames ā€˜Gryphonā€™ and ā€˜Hippogryphā€™ have been used to denote the ancestral subvariants XBB and XBB.1, respectively.Ā KrakenĀ refers to a mythological Scandinavian sea monster or giant squid, Gryphon (orĀ Griffin) refers to a legendary creature that is a hybrid of an eagle and a lion, while Hippogryph (orĀ Hippogriff) is a fictitious animal hybrid of a Gryphon and a horse.

Notwithstanding their potential utility as memory aids, the use of nicknames or acronyms in formal scientific discussions should be avoided.

Sameer Elsayed is Professor of Medicine, Pathology & Laboratory Medicine, and Epidemiology & Biostatistics at Western University.

Source: The Conversation

African Scientists Show How COVID Variants Spread across Africa

Source: Fusion Medical Animation on Unsplash

A major scientific report from Africa is featured in the journalĀ ScienceĀ today. This scientific report shows how the rapid expansion of genomics surveillance in Africa allowed the continent to describe the introduction and spread of the SARS-CoV-2 variants in African countries in real time during the COVID pandemic.

The scientific report includes over 300 authors from Africa and abroad who worked together to describe and analyse over 100 000 genomes and characterise SARS-CoV-2 variants in real time. This was the largest consortium of African scientists and public health institutions ever to work together to support data-driven COVID response in Africa.

This report shows how the large investment, collaboration and capacity building in genomic surveillance on the African continent enabled real-time public health response. Particularly it describes the setting up of the Africa Centres for Disease Control (CDC) – Africa Pathogen Genomics Initiative (Africa PGI) and the continental network by the Africa CDC and World Health Organisation (WHO) Regional Office for Africa (WHO AFRO) to expand access to sequencing and cover surveillance blind spots, in parallel with the growth of the number of countries that are able to sequence SARS-CoV-2 within their own country.

ā€œThe publication highlights that sustained investment for diagnostics and genomic surveillance inĀ Africa was needed to not only combatĀ SARS-CoV-2 on the continent, but establish a platform to address the emerging, re-emerging, endemic infectious disease threats, such asĀ Ebola, HIV/AIDS, TB and Malaria.Ā These investments are crucialĀ for pandemic preparedness and response and will serve the health of the continent well intoĀ the 21st century,ā€ said Dr. Yenew Kebede, Head Division of Laboratory Systems and Acting Head: Surveillance and Disease Intelligence at the Africa CDC.

African Scientists receiving training in genomics surveillance at the KwaZulu-Natal Research Innovation and Sequencing Platform (KRISP), South Africa.

This study was led by two labs that setup the network for genomics surveillance in South Africa ā€“ theĀ Centre for Epidemic Response and InnovationĀ (CERI) atĀ Stellenbosch UniversityĀ and theĀ KwaZulu Natal Research and Innovation Sequencing PlatformĀ (KRISP) at the University of KwaZulu-Natal, in close coordination with the Africa CDC, WHO AFRO and 300 other institutions across the continent.
Ā 
ā€œThe enormous leap Africa made in genomic surveillance during the past two years is the silver lining in the COVID pandemic,ā€ said Dr Matshidiso Moeti, WHO Regional Director for Africa. ā€œThe continent is now better prepared to face down both old and emerging pathogens. This is a model of how when Africans are in the driving seat we can come up with lasting change and stay a step ahead of dangerous diseases.ā€
Ā 
ā€œIt has been an inspiring experience to continuously share knowledge, support and learn from colleagues all over the continent during the pandemic. We witnessed small countries with no previous genomics experience become empowered in sequencing and bioinformatics methods, and how they started to actively participate in regular pathogen genomic surveillance for SARS-CoV-2. I think it will be a real model of how scientists and public health officials across countries can form a unified front against infectious diseases in the future,ā€ says Houriiyah Tegally, Bioinformatician at KRISP and CERI and first author on this report.
Ā 
The results also highlight the early warning capacity that genomic surveillance in Africa has had for the rest of the world with the detection of new lineages and variants, the most relevant being the detection of the Beta and various Omicron subvariants. The report highlights that most SARS-CoV-2 variants, which caused Ā an epidemic in Africa, were introduced from abroad.

The scientists proceeded carefully in analysing genomic and epidemiological data collected in over 50 countries that experienced quite heterogenous epidemics in order to reconstruct transmission dynamics of the virus in the most accurate way. ā€œThe phylogeographic methods that we employ to investigate the movement of the SARS-CoV-2 virus and its variants into, out of, and within the African continent account for uneven testing and sampling proportions across countries, arising from the realities of doing genomic sequencing in the middle of a pandemic, often in low resourced settings,ā€ explains Dr Eduan Wilkinson, head of bioinformatics at CERI at Stellenbosch University and senior author on this report.
Ā 
The initial waves of infections in Africa were primarily seeded by multiple introductions of viral lineages from abroad (mainly Europe). The Alpha variant that emerged in Europe at the end of 2020, was responsible for infections in 43 countries with evidence of community transmission in Ghana, Nigeria, Kenya, Gabon and Angola. For the Delta variant, the bulk of introductions were attributed to India (~72%), mainland Europe (~8%), the UK (~5%), and the US (~2.5%). Viral introductions of Delta also occurred between African countries in 7% of inferred introduction. For Omicron, the scientific results indicate more reintroductions of the variant back into Africa, with at least 69 (95% CI: 60 – 78) from Europe and 102 (95% CI: 92 – 112) from North America than from other African countries. This was amplified for Omicron BA.2; the results suggest at least 99 separate introduction or reintroduction events of BA.2 into African countries, ~65% of which are from Europe and ~30% from Asia.
Ā 
ā€œThe ironical part of these results is that most of the introductions of variants in Africa were from abroad, but Africa was the most discriminated and penalized continent in the world with travel bans imposed. Instead of unscientific and inappropriate reactions, we should be building on the infrastructure established in Africa so that the continent can rapidly pivot to other epidemics without the fear of being punished,ā€ says Prof Tulio de Oliveira, director of CERI and KRISP, which lead the consortium analysis with the Africa CDC and WHO AFRO.
Ā 
ā€œThis study is a testament of the Africa CDC ā€“ Africa PGI efforts to expand access to sequencing to member states and create a platform of coordination and collaboration among institutions within and outside of the continent,ā€ said Dr. Ahmed Ogwell, Acting Director of the Africa CDC.

Provided by Stellenbosch University

Modelling Suggests COVID Will Reach Endemic Stage by 2024

COVID heat map. Photo by Giacomo Carra on Unsplash

A new study on coronavirus transmission in rats suggests that COVID will enter the endemic stage in about two years. The study also suggested that infections from high-risk conditions such as close contact with infected individuals produced more robust immunity than by exposure in low-risk settings.

The study, published in PNAS Nexus, made use of rats to determine when and how SARS-CoV-2 would eventually become endemic. Rats, like humans, are susceptible to coronaviruses. By collecting data on coronaviral reinfection rates among rats, the researchers were able to model the potential trajectory of COVID.

SARS-CoV-2 is just one of many coronaviruses, and there are several that cause the common cold. Many livestock animals live with endemic coronaviruses, too, and a key factor identified in the spread of animal and human coronaviruses alike is their tendency to evoke non-sterilising immunity.

ā€œIt means that initially there is fairly good immunity, but relatively quickly that wanes,ā€ explained the study’s senior author, Caroline Zeiss, a professor of comparative medicine at Yale School of Medicine. ā€œAnd so even if an animal or a person has been vaccinated or infected, they will likely become susceptible again.ā€

Over the past two years, scientists have come to see that SARS-CoV-2 yields non-sterilising immunity as people become re-infected.

The strong similarities between animal and human coronaviruses, animal data helps improve the understanding of SARS-CoV-2, said Prof Zeiss.

ā€œThere are many lessons to be learned from animal coronaviruses,ā€ she said.

In this study, Prof Zeiss and her colleagues observed how a coronavirus similar to one that causes the common cold in humans was transmitted through rat populations. The team modelled the exposure scenario to resemble human exposures in the US, where a portion of the population is vaccinated against COVID and where people continue to face natural exposure to SARS-CoV-2. They also reproduced the differentĀ typesĀ of exposure experienced by people in the US, with some animals exposed through close contact with an infected rat (high risk of infection) and others exposed by being placed in a cage once inhabited by an infected rat (low risk of infection).

Infected animals contracted an upper respiratory tract infection and then recovered. Three to four months later, the rats were then reorganised and re-exposed to the virus. The rates of reinfection showed that natural exposure yielded a mix of immunity levels, with those exposed to more virus through close contact having stronger immunity, while those exposed to lower virus levels by (being placed in a contaminated cage) having higher rates of reinfection.

The takeaway, said Prof Zeiss, is that with natural infection, some individuals will develop better immunity than others. People also need vaccination, which is offered through a set dose and generates predictable immunity. But with both vaccination and natural exposure, the population accumulates broad immunity that pushes the virus toward endemic stability, the study showed.

Mathematical models using the data predicted that the median time for SARS-CoV-2 to become endemic in the United States is 1437 days, or just under four years from the start of the pandemic in March 2020.

In this model’s scenario, 15.4% of the population would be susceptible to infection at any given time after it reaches endemic phrase.

ā€œThe virus is constantly going to be circulating,ā€ said Prof Zeiss. So it will be important to keep more vulnerable groups in mind. ā€œWe canā€™t assume that once we reach the endemic state that everybody is safe.ā€

Four years is the median time predicted by the model, she said, so it could take even longer to reach the endemic stage. And this doesnā€™t take into account mutations that could make SARS-CoV-2 more harmful.

ā€œCoronaviruses are very unpredictable, so there could be a mutation that makes it more pathogenic,ā€ said Prof Zeiss. ā€œThe more likely scenario, though, is that we see an increase in transmissibility and probable decrease in pathogenicity.ā€ That means the virus would be easily transmitted between people but less likely to cause severe illness, much like the common cold.

There is precedent for this trajectory. In the late 1800s, the ‘Russian flu’ killed approximately one million people around the world. Researchers now think that virus was a coronavirus that originated in cattle, which eventually evolved into one of the common cold viruses still in circulation. Reduced pathogenicity associated with the transition from epidemic to endemic status has also been observed in pig coronaviruses. And almost all commercial chicken flocks across the globe are vaccinated for an endemic respiratory coronavirus that has been present since the 1930s.

Longstanding experience with coronaviral infections in other animals can help navigate a pathway to living with SARS-CoV-2.

However, endemic stability in the United States also depends on what happens to the virus elsewhere.

ā€œWe are one global community,ā€ Zeiss said. ā€œWe donā€™t know where else these mutations are going to arise. Until we reach endemic stability around the entire globe, we are vulnerable here to having our US endemic stability disrupted by introduction of a new variant.

ā€œBut I think overall the pictureā€™s hopeful. I think we will be in endemic stability within the next year or two.ā€

Source: Yale University

Omicron Viral Load Shedding May Be Unaffected by Vaccination

SARS-CoV-2 virus
SARS-CoV-2 virus. Source: Fusion Medical Animation on Unsplash

A small study published in the New England Journal of Medicine has found that viral load shedding of the omicron variant is similar to other strains, and is not significantly affected by vaccination status.

The SARS-CoV-2 omicron variant has a shorter incubation period and a higher transmission rate than previous variants. Recently, the Centers for Disease Control and Prevention recommended shortening the strict isolation period for infected persons from 10 days to 5 days after symptom onset or initial positive test, followed by 5 days of masking. However, the viral delay kinetics and load shedding of omicron is still unclear.

Using nasal swabs to measure viral load, sequencing, and viral culture, they enrolled 66 participants, including 32 with delta variant and 34 with omicron. Participants who received COVIDā€“specific therapies were excluded; only one participant was asymptomatic.

The characteristics of the participants were similar in the two variant groups except that more participants with omicron infection had received a booster vaccine than had those with delta infection (35% vs 3%). After adjustments for age, sex, and vaccination status, the number of days from an initial positive polymerase-chain-reaction (PCR) assay to a negative PCR assay and the number of days from an initial positive PCR assay to culture conversion were similar in the two variant groups.

The median time from the initial positive PCR assay to culture conversion was 4 days in the delta group and 5 days in the omicron group; the median time from symptom onset or the initial positive PCR assay, whichever was earlier, to culture conversion was 6 days and 8 days, respectively. There were no appreciable between-group differences in the time to PCR conversion or culture conversion according to vaccination status, although the sample size was quite small, which led to imprecision in the estimates.

In these participants with nonsevere COVID, the viral decay kinetics were similar with omicron infection and delta infection. No large differences in the median duration of viral shedding was seen among participants who were unvaccinated, vaccinated but not boosted, and those who were vaccinated and boosted.

Discussing limitations, the authors cautioned that the small sample size limits precision, and there are possible residual confounding variables. Further studies are need to properly correlate culture positivity with infectivity.

They conclude by saying: “Our data suggest that some persons who are infected with the omicron and delta SARS-CoV-2 variants shed culturable virus more than 5 days after symptom onset or an initial positive test.”

How Effective was Masking for SA in Preventing COVID?

Image by Quicknews

COVID restrictions have finally come to an end altogether in South Africa, as Health Minister Joe Phaahla gazetted a number of changes to the rules, as reported by BusinessTech. This means the end of mask use requirements, social gatherings restrictions and COVID border testing. Prof Shabir Madhi was welcoming of the move in a recent tweet, having criticised SA’s lockdowns as overly harsh and economically damaging. Around the world, many had questioned the widespread use of masks, or their use by some subset of the population, such as children ā€“ and even questioned locally by a scientist who argued that it didn’t and wouldn’t work in a South African setting, where people are less adherent to regulations.

Professor Salim Abdool Karim likened such a viewpoint to saying Africans with HIV can’t use ARVs because they didn’t have watches to take them at the right time, reminiscent of “a colonial mentality”.

The case for public mask use is well established. Experiments had shown that even simple cloth masks were moderately effective at hindering the transmission of SARS-CoV-2ā€“containing aerosol particle from infected individuals, though they were less effective at protecting a wearer against infection. Predictably, N95 masks and others are better at doing the job than simple cloth face coverings.

There are no real-world studies for South Africa comparing mask use vs non-mask use as mask wearing was compulsory from the early stages of the outbreak. It would have been downright unethical to ask people to not wear masks, although some people may have had exemptions due to medical conditions or other important reasons. There is a country with good COVID surveillance and a distinct division in mask wearing ā€“ the United States. Implementation of mask mandates in the US was down to local authorities, which provides a basis for comparison.

One US study, published in Health Affairs, found that, compared to nonmasking counties, masking counties saw a daily case incidence decline by 25% at four weeks, 35% at six weeks after introduction of masking mandates. The reductions were strongest in Republican-leaning counties, which is notable since Republican voters were less in favour of lockdowns and mask mandates.

Another study found a 16.9% drop in cases four weeks after counties introduced masking mandates. Real-world data also show mask use was effective in preventing infection. A case-and-control study done in California by the CDC showed a 29% drop for surgical mask/respirator use “some of the time” and a 56% drop for “all of the time”.

While a direct comparison between a wealthy country like the US and South Africa as a middle-income country is impossible, it is easy to believe that masking mandates reduced cases by a significant percentage, perhaps saving tens of thousands of lives especially against the country’s possible true COVID death toll of 300 000.