Could this gene double your risk of dying from COVID-19?

Soon after the pandemic began, we knew that certain groups of people are more at risk of dying from COVID-19 than others. It was immediately clear that those with specific underlying health conditions such as diabetes and cardiovascular disease were at increased risk, but slowly it became evident that certain ethnic groups were also being disproportionately affected.

Social factors have played an important role in why these groups have been more affected than others, but genetics may also play a part.

Scientists at Oxford University have now identified a version of a gene that may be associated with doubling the risk of respiratory failure from COVID, and it could go some way to explaining why people from particular backgrounds are more likely to die from the virus. The study’s authors said that their work identifying the gene was extremely difficult because it wasn’t merely the presence of the gene they were looking for, but whether it was switched “on”, making it more high risk.

The researchers found the increased risk comes from a gene that regulates the activity of other genes, including one called LZTFL1 involved in the response of lung cells to viruses. They found the higher-risk version of the gene prevented the cells in the airways and lungs from responding to the virus properly. If the lung cells are unable to protect themselves adequately, then the SARS-Cov-2 virus that causes COVID-19 is more likely to get inside and infect them, causing widespread damage and eventual breathing difficulties more quickly.

This is important as, so far, most medical treatment for people sick with COVID has been aimed at the immune system, but this study may open the door for treatments aimed at improving or enhancing the way the airways protect themselves against invading viruses. The researchers were quick to point out that the gene does not affect the immune system, and there is no evidence to suggest it will change the way the vaccines work in individuals who had the higher-risk version of the gene.

Interestingly, the study also found the gene was more prevalent in people with South Asian ancestry – 60 percent of them carried the high-risk version compared with 15 percent of those with European ancestry. But only 2 percent of those from Afro-Caribbean backgrounds carried the gene. This means that the genetic factor does not completely explain the higher death rates reported for Black and minority ethnic groups.

In reality, the reasons why minority groups are disproportionately affected are complex and multifactorial. Almost every serious analysis of COVID deaths has found that Black and minority people are over-represented compared with what we would expect if the illness affected everyone the same way.

Social factors play a big part in this; when governments were encouraging people to work from home at the peak of the pandemic, key workers still had to go in to keep the country moving. In the United Kingdom, Bangladeshi and Pakistani ethnic groups are more likely than others to work in transport jobs, increasing their risk of exposure. Minority groups are also over-represented in health and social care jobs, again meaning occupational exposure to the virus, and we have seen people from these ethnic backgrounds who work in health and social care die in higher numbers.

The researchers from Oxford pointed out that the gene they identified is only a small part of a bigger picture as to why certain ethnic groups are at higher risk.

People from Black and South Asian groups are also at higher risk of having underlying health conditions such as type 2 diabetes that can increase the risk of complications should they get COVID.

But it goes further than this; because of health inequalities that were exposed by the pandemic, people from minority groups suffered greatly. Minority groups tend to have poorer socioeconomic circumstances which can put them at increased risk of catching and dying from COVID. As well as working in jobs that cannot be done from home, they are more likely to live in overcrowded homes with multiple generations residing in them. Combined with their increased propensity to having high-risk underlying health conditions, these social inequalities mean they are at high risk of not only getting COVID but also becoming sick and dying from it.

The researchers from Oxford pointed out that the gene they identified is only a small part of a bigger picture as to why certain ethnic groups are at higher risk.

Any information that helps safeguard the most vulnerable in our society is welcome, and if this leads to better medicine in the future that reduces the risk of death, then that can only be a good thing. But until we take action against the ongoing inequalities that exist in our societies, which were highlighted by the pandemic, the most disadvantaged among us will continue to suffer.

The evidence to support this is overwhelming; multiple studies have shown how minority groups suffered the worst as a result of COVID. The time for talking about it is over; we now need action.

Progress report: Pfizer’s pill could reduce hospitalisation from COVID by 89%

A pill to treat COVID-19, developed by the US pharmaceutical giant Pfizer, cuts the risk of hospitalisation or death by 89 percent in vulnerable adults, the company claims. But the results of the trials are yet to be peer-reviewed.

The drug, known as paxlovid, appears to have surpassed those seen with Merck & Co Inc’s pill, molnupiravir, which reduced the likelihood of dying or needing hospital treatment by half, and was approved for use in the UK.

The regimen Pfizer is proposing involves taking three pills twice a day for five days. One of the pills, a protease inhibitor, works by blocking an enzyme the SARS-Cov-2 virus needs to multiply; it is to be taken alongside an antiviral medication called ritonavir. It is the combination of both drugs that is thought to yield such promising results. If the medication is approved by healthcare regulatory bodies, Pfizer recommends them for those who are at high risk with underlying health conditions and that they should be taken as soon as symptoms develop to prevent hospitalisation and death.

The data that Pfizer has released shows that the trial included adult patients only. Participants were unvaccinated, had mild-to-moderate COVID-19, and were considered high risk due to health problems – including obesity, diabetes or heart disease. The scheduled interim analysis showed an 89 percent reduction in risk of COVID-related hospitalisation or death from any cause, compared with the placebo in patients treated within three days of symptom onset. Seven patients given the placebo died, while there were no deaths among those in the group given the pill. Pfizer has said the reports of side effects were similar in both groups.

The benefits of the drugs led to the trial being stopped early on recommendation of an independent group of medical specialists. Although both the US and UK have ordered large quantities of the drugs, they have yet to be approved by medicines’ regulatory bodies in either country.

If the results of the trials are confirmed through peer review and the regulatory bodies approve their use, we could see the dawn of a new era in managing COVID. The arrival of oral pills to manage the disease at home will mean those who are vulnerable, such as the elderly or immunocompromised who may not mount as strong an immune response to the vaccines, are offered an extra layer of protection.

If more people with COVID are managed at home and kept out of hospitals, it means healthcare workers can get on with the job of clearing the backlog of non-COVID-related work that has built up during the pandemic.

Good news: Common cold may protect against COVID-19

A new study has suggested that previous common cold infections may help protect against COVID-19. The study, carried out by University College London and published in the journal Nature, tracked more than 750 healthcare staff who were working closely with COVID patients and likely exposed to the virus on a regular basis. A group of 58 of the participants never tested positive for COVID despite repeated exposure to patients who had the virus.

Blood samples were taken from all participants, but the 58 who tested negative throughout were found to have higher levels of immune cells, called T-cells, in their blood than healthcare workers who got COVID. These T-cells are the part of the immune system that act as memory cells, able to recognise specific invaders when they appear in the body. The researchers think these specific T-cells halt SARS-CoV-2 by disabling a cluster of viral proteins called the replication transcription complex, which helps the virus to reproduce. They found that these T-cells were present in blood samples collected before the pandemic.

The SARS-CoV-2 virus belongs to the family of viruses known as coronaviruses, of which there are many. The hypothesis is that these T-cells were most likely generated by previous coronavirus infections that were not the SARS-CoV-2 virus – the most likely being the coronaviruses that cause the common cold.

Most common colds are caused by a group of viruses known as rhinoviruses, but about one in 10 is caused by a coronavirus that may have a shape or part that is not dissimilar to the SARS-CoV-2 coronavirus. The T-cells recognise this part as being similar to a previous invading virus and mount an attack, killing it before it has a chance to infect a person.

Nineteen of the participants also had increased levels of an immune-system protein called IFI27, which the study’s authors say might be an early marker of SARS-CoV-2 infection. This would suggest the SAR-CoV-2 virus attempted to get inside of the cells of these people and infect them but was thwarted by their immune system before it could.

The study has many limitations, one being that all the participating healthcare workers were healthy and there is no definitive evidence that those who tested negative had a SARS-CoV-2 infection to begin with; it may be that they were just lucky enough to avoid it altogether.

Either way, the best way to protect oneself from COVID is not through getting a cold, but by being fully vaccinated.

Personal account: Is it right to mandate vaccines?

As of November 11, 2021, all staff who work in care homes in the UK must be fully vaccinated or have a solid medical reason for not being so – or face losing their job. The UK government made a similar announcement for National Health Service (NHS) staff that will come into force in April 2022.

The UK is not alone in mandating vaccines. Italy was the first country in Europe to make the COVID vaccine mandatory for healthcare workers and, in France, 3,000 health workers were suspended without pay for refusing the vaccine. Globally, Indonesia, Canada and New Zealand are also mandating COVID vaccines for parts of their populations.

So, is it right to mandate vaccines for health and social care workers?

Well, the first thing I will say is that I am now “triple-jabbed” – having recently had my booster shot (I also got my flu vaccine at the same time). I am an advocate of the vaccine and have spent time at many a clinic talking to patients about why the vaccine is their best protection against COVID.

I have been having an internal debate about whether it is ethical to make people who do not want the vaccine choose between their job or the jab. It is difficult. As a doctor you are always taught it is your job to give patients all their options and arm them with information, but the ultimate decision as to whether they take any treatment is up to them. There are, of course, exceptions to this if mental health or safeguarding issues are involved, but these are few and far between.

But this time, it is more complex than a simple choice about what treatment is best for the patient in front of you. This is about population health and whatever decision a person makes about taking up the vaccine will have ramifications for those around them – none more so than those who work in health and social care.

Freedom of Information data collected from NHS trusts across England revealed more than 11,000 patients who died in hospital probably caught the virus while on a ward. They may have caught it from healthcare staff who exhibited no symptoms or from other nearby patients – we can’t be sure; either way, they caught it because of being in hospital. That figure is truly shocking.

We know that vaccines reduce the risk of becoming seriously sick from the virus, but they do not completely stop someone from getting it. There are cohorts of the population, such as the immunocompromised, who do not have as strong an immune response to the vaccines and remain at risk of serious illness despite being vaccinated; they are at higher risk of needing medical attention for other things, and they need protecting.

There is increasing evidence the vaccines do help reduce transmission of the virus, particularly in the first few months after having them. So by getting the vaccines, health and social care workers are protecting the people they care for.

I am also mindful that many who are refusing the vaccine have fallen victim to misinformation online and the ideal solution to that is to put those refusing the vaccine in touch with an expert who can allay their fears; but this is impractical and onerous. The information is out there for them to find should they want to; in a way, they are choosing to ignore the science.

On the other hand, the vaccines are not risk-free. Although it is extremely rare, serious adverse effects have been reported and by making healthcare workers choose between their job or the jab, who will be responsible if one of them is unlucky enough to suffer an adverse event?

These are all the things I have been debating with myself. After much back and forth, I am of the opinion that the elderly and vulnerable have suffered enough and that we all want this pandemic to end one way or another. Vaccines are the best way of protecting ourselves and those around us, and as a healthcare worker you have a duty of care to those you look after. With this in mind, I would say, on balance, it is right to mandate vaccines for those who work in health and social care.

Reader’s question: Can having COVID-19 make my hair fall out?

Although not an official symptom of COVID, hair loss can occur after any serious illness, particularly one associated with fever. Although it is not technically hair “loss”; it is referred to as hair “shedding”.

Fever from any illness, including COVID, can force more hairs than usual into the shedding phase of the hair growth cycle. Most people see noticeable hair shedding two to three months after having a fever or illness, and it can last anywhere between six and nine months.

There is no specific treatment for hair shedding, it will stop on its own. Time is all that is needed, although I understand that losing hair can be stressful.