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20
January
2023
|
08:09
Europe/London

Does COVID really damage your immune system and make you more vulnerable to infections? The evidence is lacking

Over the past month or two, many including the US and the UK have seen a large wave of respiratory viral infections. These include RSV (), flu and COVID in all ages, as well as bacterial infections such as in children.

Sometimes these infections can be very serious. The UK has seen a huge surge in hospital admissions during winter, putting the health service .

This had led some to question whether COVID damages our immune systems, leaving those who have been infected more vulnerable to other infectious diseases like the flu.

Another idea put forward to explain the surge in respiratory viruses is that children 鈥渕issed out鈥 on common childhood infections during the height of the pandemic, and that this has left them more vulnerable to these infections now owing to an 鈥渋mmunity debt鈥. But how credible are these explanations?

COVID and our immune systems

The human immune system has evolved to deal with a host of different infections. It has a variety of weapons it can deploy which work together not only to eradicate infectious agents, but also to remember them for a more rapid and tailored response upon any subsequent encounter.

Likewise, many infectious agents have developed tricks to try to evade our immune system. For example, a parasite called disguises itself to avoid the immune system detecting it.

SARS-CoV-2, the virus that causes COVID-19, similarly has tricks up its sleeve. Like many other viruses, it鈥檚 been shown to , particularly . Recent studies showed it can interfere with immune cells鈥 ability to detect it . This is concerning, but it鈥檚 not clear that such changes impact immunity to other infections.

Short-lived changes in a person鈥檚 immune defences are normal when they鈥檝e been exposed to an infection. Several studies have now shown that, in response to SARS-CoV-2, specialised white blood cells called lymphocytes grow in number. These lymphocytes also display changes in their features typical of cell , such as changes in .

Such changes may sound dramatic to the non-expert if taken out of context (called 鈥渁scertainment bias鈥). But they鈥檙e normal and merely indicate that the immune system is working as it should. Research has confirmed that, for most people, the immune system following recovery.

Some exceptions

SARS-CoV-2, like many viruses, doesn鈥檛 affect everyone equally. We鈥檝e known for some time that certain groups, including older people and those with underlying health complications such as , can be more susceptible to severe disease when they contract COVID.

This vulnerability is associated with an irregular immune response to SARS-CoV-2 that results in inflammation. Here we see, for instance, reduced numbers of lymphocytes and changes to known as .

Still, for most of these vulnerable people, the immune system over the next two to four months. However, a small subset of patients, particularly those who had severe COVID or have underlying medical issues, retain beyond six months after infection.

The significance of these findings isn鈥檛 clear, and longer-term studies considering the impact of underlying health conditions on immune function will be needed. But for most people, there鈥檚 no evidence to suggest immune damage following a COVID infection.

For some people with underlying health conditions, immune changes appear to last longer.

What about long COVID?

Emerging the most differences in immune cells after a COVID infection occur in people who have developed .

So far, no data points to immune deficiency in long COVID patients. But an overactive immune response can actually cause harm, and the immune cell changes seen in long COVID patients seem consistent with a vigorous immune response. This may explain the variety of post-infection consequences and symptoms that people with face.

Immunity debt

The 鈥渋mmunity debt鈥 hypothesis suggests the immune system is like a muscle requiring near-constant exposure to infectious agents to keep it functioning. So, the argument goes, a lack of exposure due to lockdowns damaged immune development, especially in children, by making our immune systems 鈥渇orget鈥 earlier knowledge. This supposedly left them more vulnerable to infections when social mixing returned to normal.

Though this idea has gained traction, there鈥檚 no immunological evidence to support it. It鈥檚 not true to say we require a constant background of infection for our immune system to work. Our immune systems are immensely robust and powerful. For example, immune memory to the 1918 influenza pandemic was still evident .

It鈥檚 also not strictly true to say children weren鈥檛 exposed to viruses during the early pandemic. Lockdowns didn鈥檛 commence until after waves of the usual winter respiratory infections in 2019/2020, and schools in the UK reopened in autumn 2020 with variable preventive measures, so children were still exposed to infections, including COVID-19.

The cold-causing viruses didn鈥檛 completely vanish by any means. For example, there was a significant in the UK in 2021.

Nonetheless, lockdowns and other protective measures probably did reduce exposure to viruses, and for some children this shifted when and at what age they were first exposed to viruses such as RSV. This, taken alongside a high background of COVID, and relatively poor COVID and flu vaccine uptake, could all be making particularly bad. However, a change in the timing of when people are exposed leading to a surge of infections doesn鈥檛 necessarily mean that individual immunity has been damaged.

Our knowledge of the immune response to COVID is rapidly expanding. The most consistent findings show are protecting us from the very worst effects of SARS-CoV-2 and that, post-vaccination, our immune system is working exactly as it should.

However, findings of altered immune signatures in some recovered patients and those with long COVID require further investigation.The Conversation

, Professor in Biomedical Sciences,

This article is republished from under a Creative Commons license. Read the .