Category: COVID

Is COVID Really Causing New-onset Type 1 Diabetes in Young People?

Diabetes - person measures blood glucose
Photo by Photomix Company from Pexels

New research on Scottish data has found SARS-CoV-2 infection is linked to an increased incidence of new-onset type 1 diabetes in under-35s – but only in the first month after infection, likely due to increased testing as well as COVID bringing forward the progression of diabetes.

The study, presented at this year’s European Association for the Study of Diabetes (EASD) Annual Meeting, linked data on COVID tests results to the Scottish diabetes register for the period between March 2020 and November 2021, and tested whether this period of COVID infection was associated with an increased risk of diabetes.

“Our findings call into question whether a direct association between COVID and new-onset type 1 diabetes in adults and children exists”, says co-lead author Professor Helen Colhoun from Public Health Scotland and the University of Edinburgh, Scotland. “One recent report by researchers at the US Centers for Disease Control and Prevention (CDC), analysing two large insurance-claim databases of those under age 18, found that children with COVID were 2.5 times as likely to be diagnosed with diabetes over a month after infection than those who were never infected. If replicated, this is going to create a large number of people with newly diagnosed diabetes and might also alter the risk–benefit balance for COVID vaccination in young children. Importantly, we did not confirm that finding.”

In type 1 diabetes, which usually appears during childhood or adolescence, the immune system attacks insulin-producing cells, but it is not known why. One theory is that the immune system may be triggered by a viral infection and then accidentally also attacks insulin-producing cells. It has also been suggested that viral infections may increase the rate of progression of type 1 diabetes in people who still have normal blood sugar levels.

In this study, Prof Colhoun and colleagues linked individual-level data on PCR-confirmed SARS-CoV-2 infections from the Electronic Communication of Surveillance Database, which captures all PCR tests for COVID-19 nationally, with precise dates of all new type 1 diabetes diagnoses from the national register in Scotland (that is updated daily).

During the study period a confirmatory PCR test was mandatory for all those with a positive lateral flow test.

The important aspect of this study is the exact dates of diabetes diagnosis were available, unlike in some earlier studies, ensuring that the time sequence of COVID and type 1 diabetes could be established.

Between March 2020 and November 2021, a total of 365 080 children and adults had at least one detected SARS-CoV-2 infection, and 1074 were diagnosed with type 1 diabetes.

The analysis found no association between SARS-CoV-2 infection and new-onset type 1 diabetes 30 days or more after infection, or in those aged younger than 16 years, contrary to several previously reported studies.

However, the researchers did find that children and adults with a first positive SARS-CoV-2 test were 2.5 times as likely to be diagnosed with diabetes within 30 days of infection compared to those who did not have a previous registered infection; this risk was more than three times higher in those younger than 16 years.

But the authors stress strong arguments against a causal effect of COVID underlying this association.

Further analyses investigating the pattern of COVID- testing in relation to type 1 diabetes diagnosis found an increased frequency of SARS-CoV-2 testing in the days before and after diabetes presentation, for both negative and positive results. This suggests, says the authors, that the association may partly be explained by higher detection of infection at this time.

The authors also note that the average time from the onset of type 1 diabetes symptoms to diagnosis under 16s in England is around 25 days. So, it is likely that many of those who tested positive for COVID-19 within 30 days of a diabetes diagnosis already had type 1 diabetes at the time of infection.

No link was found between between COVID vaccination status and new-onset type 1 diabetes in adults (few children were vaccinated during the study period), providing further evidence against a causal effect of SARS-CoV-2 infection on the development of diabetes.

The researchers also looked at trends in type 1 diabetes incidence in Scottish children aged 0–14 years before and during the pandemic, finding that the incidence in 2020–2021 was around 20% higher than the 7-year average for 2015–2021.

However, they point out that based on estimates from England, the time course of the increase in diabetes incidence in those aged 0–14 years predated most of the cumulative incidence of SARS-CoV-2 infection in this age group (June 2021 onwards), suggesting no causal link between COVID and rates of diabetes.

“Our findings show that causes other than COVID infection itself need to be considered in relation to the increased incidence of type 1 diabetes”, said co-lead author Professor Paul McKeigue from Public Health Scotland and the University of Edinburgh, Scotland. “We need to consider what has happened regarding the spread of viruses such as enteroviruses during the pandemic, and whether there are any other environmental factors, such as sunlight exposure and vitamin D levels, that might have altered during lockdown that might also be relevant.”

The authors note that although their study was large, further analyses with more recent data is needed, and that the delay in mass testing meant many COVID cases in the young went undetected.

Source: EurekAlert!

Food Allergies may Protect Some against COVID

Image from Pixabay

A recent study in the journal Frontiers in Immunology may explain why some cases of COVID are asymptomatic: common foods, vaccines, bacteria and viruses may all prime the immune system to attack SARS-CoV-2 due to bearing similar antigens to the virus. The study paves the way for new immunotherapies or vaccines that lead to stronger immunity against COVID.

Proteins present in bacteria, human cells, vaccines, and even foods may all share similarities with those in SARS-CoV-2. The researchers behind this latest study hypothesised that similarities between SARS-CoV-2 and other common proteins may affect our susceptibility to the virus.

After the initial infection by a pathogen has passed, T and B cells retain a memory of it, ready to rapidly produce more antibodies if needed. Food allergies are a result of the immune system targeting the proteins in what are otherwise harmless substances.

Testing antibody cross-reactions

Could such an ‘immune memory’ to proteins we have encountered in our past underlie immune resistance and reduced susceptibility to Covid-19? To begin to test this hypothesis, these researchers investigated whether antibodies that target proteins in the SARS-CoV-2 virus could also bind to proteins in other agents, such as foods or common bacteria.

The researchers tested the ability of these antibodies to bind to 180 different proteins from common foods, two different vaccines, and 15 bacterial and viral proteins. The antibodies reacted most strongly with a common gut bacterium called E. faecalis and a vaccine against diphtheria, tetanus, and pertussis. Interestingly, they also reacted very strongly against proteins found in common foods, including broccoli, roasted almonds, pork, cashews, milk, soy, and pineapple.    

Eat for immunity?

Unfortunately, you will likely not be able to eat your way to COVID immunity. ‘Immunity’ against a food type, for instance, is typically characterised by a food allergy. “Usually only people with leaky gut can make antibodies against food, so I wouldn’t actually recommend eating foods that give you leaky gut, because this would give you a whole new set of problems,” said Dr Aristo Vodjani of Cyrex Laboratories in Arizona, lead author on the study.

Indeed, the researchers caution that although these agents could potentially provide some protection from SARS-CoV-2, they are no replacement for current vaccines. Further studies are also needed to confirm that these proteins do indeed confer some protection, and if so, whether it is mediated through a short-lived antibody response or a longer-term memory cell response.

The findings may shed some light on our variable responses to COVID infection. With more research, these results could lead to more effective treatments or better vaccines against the virus. Another application may lie in assessing an individual’s susceptibility to the virus before they have even been infected. 

Source: EurekAlert!

COVID Damages Placenta’s Immune Response

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In a study published in the American Journal of Obstetrics & Gynecology, researchers found that, if a woman is infected by SARS-CoV-2 during her pregnancy, the infection damages the placenta’s immune response to further infections – even if the infection was mild.

“This is the largest study to date of placentas from women who had COVID during their pregnancies,” said Professor Kristina Adams Waldorf, at the University of Washington School of Medicine and senior author of the study. “We were surprised to find that women who had COVID during their pregnancies had placentas with an impaired immune response to new infection.”

This finding, Prof Adams Waldorf added, “was the tip of the iceberg” in how COVID might affect foetal or placental development.

During the early stages of the pandemic, many thought that COVID did not appear to harm the developing foetus because there were so few babies born with COVID infection, she noted.

“But what we’re seeing now is that the placenta is vulnerable to COVID-19, and the infection changes the way the placenta works, and that in turn is likely to impact the development of the foetus,” Prof Adams Waldorf said.

“To date, the studies about how COVID might affect foetal or child development are very limited as the children are still very young,” noted co-author Dr Helen Feltovich, professor at Intermountain Healthcare.

“Our study suggests that babies born to mothers infected with COVID at any point during their pregnancy will need to be monitored as they grow up,” she said.

Studies led by Adams Waldorf have shown that pregnant women who contract COVID have a significantly higher mortality rate than those who do not contract COVID. Other studies have found that pregnant women are more likely to risk hospitalisations or preterm birth, according to the Center for Disease Control and Prevention.

It’s unknown how different COVID variants may affect the mother or foetus, Profs Adams Waldorf and Feltovich agree.

“Studying each of the variants in real time is really challenging because they just keep coming so fast, we can’t keep up,” Prof Adams Waldorf said. “We do know that the COVID Delta variant was worse for pregnant individuals, because there was a spike in stillbirths, maternal deaths and hospitalisations at that time.”

Regardless of the variant, Prof Adams Waldorf stressed taking precautions, such as vaccination and booster shots, limiting social contact a bubble of vaccinated individuals even if it means isolating for the duration of the pregnancy.

“The disease may be mild, or it may be severe, but we’re still seeing these abnormal effects on the placenta,” she said. “It seems that after contracting COVID in pregnancy, the placenta is exhausted by the infection, and can’t recover its immune function.”

In this study, a total of 164 pregnant individuals were studied, consisting of 24 uninfected healthy patients as a control group and 140 individuals who contracted COVID. Both groups delivered at about the same time, 37 to 38 weeks. Preterm birth occurred at nearly three times the rate with the patients with COVID when compared with those without. About 75% of the COVID patients had either asymptomatic COVID or mild symptoms.

Source: University of Washington School of Medicine/UW Medicine

Third of Unvaccinated People Lose SARS-CoV-2 Antibodies A Year after Infection

Image from Pixabay

Findings from a prospective seroprevalence study in Spain reveal falling SARS-CoV-2 antibody levels in unvaccinated but infected individuals a year after their infection. This reinforces the necessity of vaccination even after infection, and confirms that hybrid immunity – gained from both infection and vaccination – is the most robust. The study findings appears in BMC Medicine.

Both infection and vaccination against SARS-CoV-2 contribute to population immunity, an important factor for deciding when and to whom booster shots should be offered. Although immunity against a pathogen is more than antibodies, the easiest strategy for assessing population immunity is to perform seroepidemiological studies.

“Most of the serological studies performed after COVID vaccination focused on specific groups such as healthcare workers, did not distinguish between people with or without previous infection, or did not have clinical and immunological data of the infection,” explained senior co-author Manolis Kogevinas, ISGlobal researcher.

In this study, the research team performed a second measurement in a population-based cohort from Catalonia six months after the start of the vaccination campaign (the first one was just after the first confinement), to monitor the level and type of antibodies against five viral antigens (the whole Spike (S) protein, the RBD receptor binding domain, the S2 fragment, the full nucleocaspid (N) protein, or the N-terminal fragment). They also used information from a questionnaire and health records to identify potential factors that determine the magnitude and duration of the antibody response in unvaccinated, vaccinated, or vaccinated and infected persons. A total of 1076 people, aged 43 to 72 years, were included in the analysis.

The results yielded three main conclusions: First, that in 36% of infected but unvaccinated persons, antibodies were no longer detectable almost a year after the infection, particularly in those older than 60 years and smokers.

The second conclusion was that vaccination induced significantly higher antibody levels in people who had a prior infection, as compared to those without prior infection; and that these levels were strongly associated with the magnitude of the response during the infection. “Our data underscore the importance of vaccinating people even if they have been previously infected, and confirm that hybrid immunity is superior and more durable. This means that people who have been vaccinated but have not been infected would need a booster earlier than those who have,” pointed out Marianna Karachaliou, first author of the study together with Gemma Moncunill.

The third was that the factor most strongly associated with the level of antibodies is the type of vaccine, with Moderna’s Spikevax generating the highest levels of antibodies. Other factors also appear to play a role: people older than 60 or with mental illness had lower antibody levels post-vaccination. “The association between mental health and antibody responses requires further investigation, but it is known that people with disorders such as depression, chronic stress or schizophrenia have a lower response to vaccination in general,” explained co-author Carlota Dobaño.

Among those vaccinated, only 2.1% had no antibodies at the time of testing and approximately 1% had a breakthrough infection. “However, it should be noted that this study was done before the Omicron variant became dominant,” warned Kogevinas.

Source: Barcelona Institute for Global Health (ISGlobal)

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 journal Science 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.

The publication highlights that sustained investment for diagnostics and genomic surveillance in Africa was needed to not only combat SARS-CoV-2 on the continent, but establish a platform to address the emerging, re-emerging, endemic infectious disease threats, such as Ebola, HIV/AIDS, TB and Malaria. These investments are crucial for pandemic preparedness and response and will serve the health of the continent well into the 21st century,” 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 – the Centre for Epidemic Response and Innovation (CERI) at Stellenbosch University and the KwaZulu Natal Research and Innovation Sequencing Platform (KRISP) at the University of KwaZulu-Natal, in close coordination with the Africa CDC, WHO AFRO and 300 other institutions across the continent.
 
“The enormous leap Africa made in genomic surveillance during the past two years is the silver lining in the COVID pandemic,” said Dr Matshidiso Moeti, WHO Regional Director for Africa. “The 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.”
 
“It 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,” says Houriiyah Tegally, Bioinformatician at KRISP and CERI and first author on this report.
 
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  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. “The 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,” explains Dr Eduan Wilkinson, head of bioinformatics at CERI at Stellenbosch University and senior author on this report.
 
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.
 
“The 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,” says Prof Tulio de Oliveira, director of CERI and KRISP, which lead the consortium analysis with the Africa CDC and WHO AFRO.
 
“This study is a testament of the Africa CDC – 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,” said Dr. Ahmed Ogwell, Acting Director of the Africa CDC.

Provided by Stellenbosch University

More Evidence Linking Blood Clotting and COVID Severity

Source: CC0

New research shows that the Omicron variants cause significantly lower levels of blood clotting, thereby providing further evidence for the link between the severity of the disease and the prevalence of persistent micro blood clots in individuals with acute and Long COVID.

Prof Resia Pretorius, a researcher in the Department of Physiological Sciences at Stellenbosch University (SU), South Africa, first made this connection late in 2020 when she detected small amyloid-like blood clots in the plasma of individuals suffering from COVID. Amyloids are a type of protein associated with various inflammatory diseases. As part of a long-term collaboration with Prof Douglas Kell from the University of Liverpool, they showed that these micro clots contained pro-inflammatory molecules. The results of both studies were published in the journal Cardiovascular Diabetology, in 2020 and 2021.  

These insoluble micro clots inhibit or may temporarily block blood flow to capillaries and hence impair oxygen transfer to tissues. At present, they believe that this oxygen impairment in various parts of the body can account for most of the symptoms of Long COVID, such as constant fatigue, shortness of breath, brain fog, joint and muscle pain.

Prof Resia Pretorius

Prof Pretorius said the persistent prevalence of micro clots may have significant clinical value: “Our findings suggest that hypercoagulation and vascular damage are key role players causing the wide range of symptoms we see in patients with Long COVID. There is a golden thread running through pathologies noted in post-viral syndromes such as Long COVID.”

More recently, Prof Pretorius and Prof Kell worked with a team of clinicians in South Africa and the United States, to ascertain whether the difference in the degree of clotting between different viral strains of the SARS-CoV-2 virus provides a plausible explanation for the relatively low severity of the Omicron variants during acute COVID infection.

While the earlier variants caused severe disease and critically ill patients, the heavily mutated Omicron variants have been shown to have milder symptoms, most commonly a runny nose, rhinitis headaches, fatigue (from mild to severe), sneezing and a sore throat.

For the purposes of the study, they revisited data and blood samples from stored blood samples from ten patients with COVID due to the Beta and Delta variants between October 2020 and September 2021 before the patients received treatment.

The team also collected blood from patients infected with the Omicron variants. In all ten samples it was found that the Omicron samples presented with a significantly lower total amount of microclots compared to earlier Beta and Delta variants.  

In a recent webinar on the topic, Dr Mark Walsh, an emergency medicine physician at the Saint Joseph Regional Medical Center in the United States of America, said the foundational work of Profs Pretorius and Kell has helped them to explain the clotting complications of COVID-induced coagulopathies (CAC) of patients with acute COVID. He is also one of the co-authors on the article.

“We could not understand why patients with CAC would clot and bleed at the same time. We now have the pathophysiological foundation for a point-of-care bedside medicine approach, based on the foundations of excellent research,” he said.

Early in the pandemic, Dr Walsh and his team of emergency physicians in the USA, developed a protocol to provide safe anticoagulation treatment to severely ill COVID patients. The team was guided by thromboelastography, a point-of-care protocol to monitor bleeding and clotting.

According to Prof Kell, more importantly, the findings are consistent with the view that these insoluble micro clots are not a side-effect of COVID-19, but a part of how the disease develops. However, he warned, we do not yet know how this will impact or relate to other post-viral syndromes such as Long-COVID, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), post-Zika or post-Dengue diseases.

The paper, titled “Relative hypercoagulopathy of the SARS-CoV-2, Beta and Delta variants when compared with the less severe Omicron variants is related to TEG parameters, the extent of fibrin amyloid microclots, and the severity of clinical illness” is in press in the journal Seminars in Thrombosis and Hemostasis, and a preprint is available at https://www.researchsquare.com/article/rs-1970823/v1

The webinar, “COVID-induced Coagulopathy (CAC): The clot thickens…or not?” is presented by Dr Mark Walsh, Prof Resia Pretorius and Prof Douglas Kell, and moderated by Dr Asad Khan. It is available at https://youtu.be/yyf7xunWydM

Increased Alzheimer’s Disease Risk Seen after COVID Infection

Plaques and neurons. Source: NIAH

In a study published in the Journal of Alzheimer’s Disease, researchers report that people 65 and older who were infected with COVID show a substantially higher risk, up to 80% higher than without infection, of developing Alzheimer’s disease within a year, according to a study of more than 6 million patients 65 and older. The researchers found that the highest risk was observed in women at least 85 years old.

The findings showed that the risk for developing Alzheimer’s disease in older people nearly doubled (0.35% to 0.68%) over a one-year period following infection with COVID. The researchers say it is unclear whether COVID triggers new development of Alzheimer’s disease or accelerates its emergence.

“The factors that play into the development of Alzheimer’s disease have been poorly understood, but two pieces considered important are prior infections, especially viral infections, and inflammation,” said study co-author Professor Pamela Davis at the Case Western Reserve School of Medicine.

“Since infection with SARS-CoV2 has been associated with central nervous system abnormalities including inflammation, we wanted to test whether, even in the short term, COVID could lead to increased diagnoses,” she said.

The research team analysed health records of 6.2 million adults 65 and older in the US who received medical treatment between February 2020 and May 2021 and had no prior diagnosis of Alzheimer’s disease.

They then divided this population two groups: one composed of people who contracted COVID during that period, and another with people who had no documented cases of COVID. More than 400 000 people were enrolled in the COVID study group, while 5.8 million were in the non-infected group.

“If this increase in new diagnoses of Alzheimer’s disease is sustained, the wave of patients with a disease currently without a cure will be substantial, and could further strain our long-term care resources,” Prof Davis said. “Alzheimer’s disease is a serious and challenging disease, and we thought we had turned some of the tide on it by reducing general risk factors such as hypertension, heart disease, obesity and a sedentary lifestyle. Now, so many people in the U.S. have had COVID and the long-term consequences of COVID are still emerging. It is important to continue to monitor the impact of this disease on future disability.”

Professor Rong Xu, the study’s corresponding author, said the team plans to continue studying the effects of COVID-19 on Alzheimer’s disease and other neurodegenerative disorders — especially which subpopulations may be more vulnerable — and the potential to repurpose FDA-approved drugs to treat COVID’s long-term effects.

Previous COVID-related studies led by CWRU have found that people with dementia are twice as likely to contract COVID; those with substance abuse disorder orders are more likely to contract COVID; and that 5% of people who took Paxlovid for treatment of COVID symptoms experienced rebound infections within a month.

Source: Case Western Reserve University

Debunking the Myth that Africa Responded Well to COVID

COVID heat map. Photo by Giacomo Carra on Unsplash

By Nathan Geffen and Francois Venter

There is a view being promoted that COVID didn’t hit Africa as badly as the rest of the world. The reason for this, as recently expressed in an article by Boniface Oyugi in The Conversation, was the effective and well-coordinated response of African governments.

We understand the desire to find good news on the continent. But, on balance, the very little evidence available shows that COVID has hit Africa hard. The continent is highly diverse with over 50 states, so broad generalisations should be treated cautiously but, with an exception or two, there is little evidence of an effective response to the COVID pandemic. For one thing, Africa has the lowest vaccination rate of any continent.

Oyugi uses the WHO’s official COVID infection and death statistics to claim that the continent fared better than elsewhere. These state that as of late July, less than 2% of global cases and less than 3% of global deaths occurred in Africa, which has about 17% of the world’s population. (Oyugi also cites a study which pretty much says the same thing.)

COVID test statistics and confirmed COVID deaths don’t paint an accurate picture of how seriously the pandemic has hit a country (see here). If you don’t measure something properly, you can’t conclude that it’s a small problem. COVID tests are typically only administered with any regularity to a small, predominantly better off, part of a country’s population, and countries that test more tend to find more cases. Official COVID death tolls typically count people who have died in hospital with a confirmed positive test result. But it often doesn’t happen this way, especially on a continent with large rural populations and under-resourced hospitals.

Excess deaths: a vital measure

This is why the most important measure of how hard COVID has hit a country is the excess death toll. By excess deaths, we mean the number of deaths that occurred above what you’d expect given recent historical mortality. In sub-Saharan Africa, the only country that has a system capable of reliably estimating this is South Africa. Every week since the beginning of the epidemic, the Medical Research Council (MRC), using death certificate data provided by Home Affairs, has diligently analysed excess deaths. (Many countries wealthier than South Africa do not have as good a system, so it’s something to be proud of.)

The MRC researchers calculate that there have been over 320 000 excess deaths in South Africa since May 2020 (as of July 2022). As they’ve explained, conservatively 85% of these are COVID deaths. It may be as high as 95%. We can conclude that close to 300 000 people have died of COVID in South Africa. Over the past two years about 1 in 200 people in the country have died of this new infection.

The Economist has been reporting excess deaths by country. It states: “Among developing countries that do produce regular mortality statistics, South Africa shows the grimmest picture, after recording three large spikes of fatalities.”

Official deaths are much lower than excess deaths

But if you look at South Africa’s official, and much less accurate, COVID death toll you get a very different picture: Then we’re only 65th worst in the world (source: Worldometer deaths per million people). Lesotho is in 167th place, suggesting it has had a very small epidemic. Is it plausible that an area with a porous border entirely surrounded by South Africa has a completely different epidemic? (See this set of tweets – by one of the authors of South Africa’s weekly mortality report – that explains how the little mortality data we have from Lesotho suggests it had a serious pandemic.)

What about Namibia at position 74 in the Worldometer list, Botswana at 89, Zimbabwe at position 143 and Mozambique at position 190? Is it plausible that this ordering, almost in reverse order of industrial development, accurately reflects how these countries were affected by COVID?

Depending on your bias, you can approach these statistics in two ways. You can be very optimistic and see this as evidence of a smaller epidemic in sub-Saharan Africa. Or you can be realistic and acknowledge that the official numbers are likely very badly undercounted.

We can’t know for sure though because nearly all African governments did not have the systems in place to count excess deaths.

Most African countries need much better death registration systems

Attempts to estimate excess mortality in most African countries are based on almost no data. To the extent that there is data, it supports the view that the numbers have been badly undercounted. For example, a study published in the British Medical Journal, albeit with many caveats, found death rates in developing countries were twice those of rich countries.

During the height of the AIDS pandemic in the 2000s there was much optimism that the massive influx of foreign aid in response could be used to build better health systems. Bits and pieces of evidence do suggest health on the continent has improved. But it’s very disappointing that most countries on the continent still do not have the vital registration systems in place to measure mortality with decent accuracy. This is one of the most important measures of how a population is doing.

By claiming that African governments have responded well to COVID, when there’s no proper evidence to support this, we fail to hold politicians accountable. We also create the impression that institutions like the World Health Organisation and the African Union’s African Centre for Disease Control are more successful than they’ve actually been. This is a disservice to the vast majority of people living in Africa.

Geffen is GroundUp’s editor. Professor Venter is an infectious diseases clinician and head of Ezintsha at Wits University.

This article is republished from GroundUp under a Creative Commons Attribution-NoDerivatives 4.0 International License.

Source: GroundUp

Low Testosterone may be a Risk Factor for Severe COVID

Testosterone molecule
Model of a testosterone molecule. Source: Wikimedia CC0

Among men with COVID, those with low testosterone levels are more likely to become seriously ill and be hospitalised than men with normal levels of the hormone, according to a study which appears in JAMA Network Open.

Analysis of data for 723 men who tested positive for COVID, mostly in 2020 before vaccines were available, indicated that low testosterone is an independent risk factor for COVID hospitalisation, similar to diabetes, heart disease and chronic lung disease.

They found that men with low testosterone who developed COVID were 2.4 times more likely to require hospitalisation than men with hormone levels in the normal range. Further, men who were once diagnosed with low testosterone but successfully treated with hormone replacement therapy were no more likely to be hospitalised for COVID than men whose testosterone levels had always tested in the normal range.

The findings, by researchers from the Washington University School of Medicine in St. Louis and Saint Louis University School of Medicine, suggest that treating men with low testosterone may help protect them against severe disease and reduce the burden on hospitals during COVID waves.

“It is very likely that COVID is here to stay,” said co-senior author Abhinav Diwan, MD, a professor of medicine at Washington University. “Hospitalizations with COVID are still a problem and will continue to be a problem because the virus keeps evolving new variants that escape immunization-based immunity. Low testosterone is very common; up to a third of men over 30 have it. Our study draws attention to this important risk factor and the need to address it as a strategy to lower hospitalisations.”

Prof Diwan and co-senior author Sandeep Dhindsa, MD, an endocrinologist at Saint Louis University, had previously shown that men hospitalised with COVID have abnormally low testosterone levels. However, severe illness or traumatic injury can cause a temporary drop in hormone levels, so causation cannot be proved in data from men already hospitalised with COVID. Data were needed for men with chronically low testosterone before COVID infection.

Profs Diwan, Dhindsa and colleagues identified 723 men whose testosterone levels had been measured between Jan. 1, 2017, and Dec. 31, 2021, and who had documented cases of COVID in 2020 or 2021. In some cases, testosterone levels were measured after the patient recovered from COVID. Since low testosterone is a chronic condition, men who tested low a few months after recovering from COVID probably had low levels before as well, Prof Dhindsa said.

The researchers identified 427 men with normal testosterone levels, 116 with low levels, and 180 who previously had low levels but were being successfully treated, meaning that they were on hormone replacement therapy and their testosterone levels were in the normal range at the time they developed COVID.

“Low testosterone turned out to be a risk factor for hospitalisation from COVID, and treatment of low testosterone helped to negate that risk,” Prof Dhindsa said. “The risk really takes off below a level of 200 nanograms per decilitre, with the normal range being 300 to 1000 nanograms per decilitre. This is independent of all other risk factors that we looked at: age, obesity or other health conditions. But those people who were on therapy, their risk was normal.”

Men with low testosterone levels can experience sexual dysfunction, depressed mood, irritability, difficulty with concentration and memory, fatigue, loss of muscular strength and a reduced sense of well-being overall. When a man’s quality of life is clearly diminished, he is typically treated with testosterone replacement therapy. When the symptoms are mild, though, doctors and patients may hesitate to treat.

The two main concerns related to testosterone therapy are an increased risk of prostate cancer and heart disease. Testosterone is well known to boost prostate cancer, but for heart disease, the evidence for risk is more ambiguous. A large clinical trial on the relationship between heart health and testosterone supplementation is expected to be completed soon.

“In the meantime, our study would suggest that it would be prudent to look at testosterone levels, especially in people who have symptoms of low testosterone, and then individualise care,” said Prof Diwan, whose specialty is cardiology. “If they are at really high risk of cardiovascular events, then the doctor could engage the patient in a discussion of the pros and cons of hormone replacement therapy, and perhaps lowering the risk of COVID hospitalisation could be on the list of potential benefits.”

Since this study is observational, it only suggests that boosting testosterone levels may help men avoid severe COVID, Diwan cautioned. A clinical trial would be needed to demonstrate conclusively whether such a strategy works.

Source: Washington University School of Medicine

Returning to Sport after COVID Infection

Rugby players
Photo by Olga Guryanova

A first-of-its-kind study published in Scientific Reports has investigated how the immune system of elite student-athletes responded to the COVID virus. Unlike older adults with comorbidities, American Football players who were diagnosed with COVID were able to have their immune system back to its baseline after their CDC-recommended isolation period.

“When COVID really started moving out of control, we met with Neil Johannsen, an exercise physiologist at LSU, and the athletic trainers Derek Calvert and Jack Marucci, and we discussed what we could do to make sure our athletes remained healthy. We especially wanted to make sure that athletes were not at risk for secondary infections when they came back from isolation,” said Guillaume Spielmann, associate professor in LSU’s School of Kinesiology.

Isolation effective after COVID infection

“When the idea started for the research, we discussed why not turn something negative into a positive, and assist with the research to find some answers. If we can do things to understand the virus better, let’s do it,” said Jack Marucci, LSU’s Director of Athletic Training. “The student-athletes were willing to be a part of it.”

During that time at the start of the COVID pandemic, the CDC had recommended 14 days of isolation.

“There was a lot unknown during this time. We are looking at a population that are extremely close to each other during plays and during games. We wanted to make sure that since they are literally face-to-face with other players, that their salivary defences, their oral defences were pretty much intact and that that part of their immune system was not affected by the disease; that there were no long-lasting effects of the disease,” Assoc Proff Spielmann said.

Saliva samples were collected from 29 student-athletes in 2020, before a COVID vaccine. Fourteen were COVID positive and 15 had no history of infection. Of the 14, only six reported mild symptoms from the virus, the other eight were asymptomatic throughout the isolation period.

“Salivary immunity is extremely important to ensure that people don’t contract secondary infections, so when athletes are coming back we need to make sure they are as healthy as can be. We found that the isolation period was sufficient to restore the athletes’ salivary immunity to the level seen in non-infected players,” Assoc Prof Spielmann said.

Safely return to play after COVID

These findings suggested the student-athletes could safely return to practice and play football without a risk of secondary infection; that their immune system wasn’t at risk when playing the close contact sport.

“I was worried a bit about long-haulers and other more significant outcomes like the concerns for the development of myocarditis. Engaging in athletic activities at an elite level can be stressful on the body and you would want to arm yourselves with the best scientific information to help understand potential outcomes. This data helped to validate some of these decisions that were made. Providing a safe environment for your student-athletes is paramount and this helped that process along,” said Shelly Mullenix, LSU’s Senior Associate Athletics Director for Health & Wellness.

For this study, three graduate students also participated in the research.

“This kind of access is unique in Division I sports. You typically don’t have access to football players, so the fact that we have access is hugely instrumental as well,” Assoc Prof Spielmann said. “LSU is a great place for this field.”

“I think this COVID research is something that we are really proud to be a part of and contribute to finding answers to such a devastating virus,” Marucci said.

Assoc Prof Spielmann, an immunologist, researches the impact of stress on the immune system of elite and tactical athletes, including astronauts and fire fighters. But this study isn’t the first for Spielmann and LSU Athletics. They have worked together to study psychological and physiological health, along with performance measures in other student-athletes and sports teams. A new study will take a closer look at female athletes’ mental, physiological and immune resilience to stress.

Source: Louisiana State University