Mysterious driving factor behind Long-COVID may have been identified: ScienceAlert

About 5-10% of people with COVID infections go on to develop long COVID illness, with symptoms lasting three months or longer.

Researchers have proposed several biological mechanisms to explain long COVID. However, in a perspective article published in the latest issue Medical Journal of AustraliaWe argue that much, if not all, of Long-COVID appears to be caused by the virus itself remaining in the body.

It was recognized relatively early in the pandemic that SARS-CoV-2 – or at least remnants of the virus – can remain in various tissues and organs in some people for long periods of time. This theory is known as “viral persistence.”

While the long-term presence of remaining virus fragments in some people’s bodies is now well established, it is less certain whether the live virus itself and not just old virus parts remain – and if so, whether this is the cause of long COVID.

This distinction is crucial because live viruses can be attacked by specific antiviral approaches in ways that “dead” virus fragments cannot.

Virus persistence has two main effects:

1. When it occurs in some severely immunocompromised people, it is thought to be the source of new and significantly different-looking variants, such as. B.JN.1
2. It has the potential to cause symptoms in many people in the general population long after the acute illness. In other words: Long COVID could be caused by a long infection.

What does the research say?

While there is not yet a single study confirming that persistent viruses are the cause of long COVID, taken together, several recent key papers make a compelling argument.

In February a study was carried out in Nature found that a large number of people with mild COVID symptoms had the virus’s genetic material, called viral RNA, shed from their respiratory tract for extended periods of time.

Those who persistently shed this viral RNA — which almost certainly indicates the presence of a live virus — had a higher risk of developing long COVID.

Other important work has found replication of viral RNA and proteins in the blood fluid of patients years after their initial infection, a sign that the virus likely replicates over long periods of time in some hidden reservoirs in the body, possibly including blood cells.

In another study, viral RNA was detected in ten different tissue sites and blood samples 1–4 months after acute infection. This study found that the risk of long COVID disease (measured four months after infection) was higher in people with persistently positive viral RNA.

The same study also provided clues about where in the body the persistent virus is located. The gastrointestinal tract is a site of great interest as a long-term viral hiding place.

Earlier this week, further evidence that persistent viruses increase the likelihood of long COVID disease was published as part of the RECOVER initiative, a collaborative research project aimed at studying the impact of long COVID.

However, formal proof that viruses that can replicate can survive in the body for years is yet to be achieved. This is because isolating the live virus from reservoirs inside the body where the virus “hides” is technically challenging.

Since this is not the case, we and other scientists argue that the accumulated evidence is now compelling enough to prompt action.

What has to happen next?

The obvious response to this is accelerated trials of known antivirals to prevent and cure long COVID.

This should include more left-field-oriented therapies such as the diabetes drug metformin. This potentially has two benefits in the context of Long-COVID:

However, another important focus should be the development of new drugs and the establishment of clinical study platforms for rapid tests.

Science has discovered exciting therapeutic options. However, translating these findings into clinically viable forms represents a major hurdle that requires government support and investment.

Demystifying and Preventing Long COVID

The idea of ​​a “long infection” as a contributor or even driver of long COVID is a powerful message. This could help demystify the condition in the eyes of the general public and raise awareness among the general public and medical professionals.

This is intended to help raise public awareness of the importance of reducing reinfection rates. Not only is it your first infection, but any subsequent COVID infection carries the risk of long COVID illness.

Long COVID is common and is not limited to people at high risk of severe acute illness, but affects all age groups. In one study, the greatest effects were seen in people ages 30 to 49.

So for now, we all need to reduce our exposure to the virus using the tools available, a combination of:

• clean indoor air is approaching. In its simplest form, this means being aware of the importance of well-ventilated indoor spaces, opening windows and improving air circulation as COVID spreads through the air. More sophisticated methods of ensuring safe indoor air include monitoring the quality and filtering air in rooms that cannot easily be ventilated naturally
• Use high-quality masks (that fit well and do not let in air, such as N95 masks) in environments where you do not have confidence in the quality of indoor air and/or where it is crowded
• Test so you know when you are positive. Then, if you are eligible, you can seek treatment. And you can make sure to protect those around you with masks, stay at home if possible and ventilate rooms
• Stay informed about COVID booster doses. Vaccines reduce long-term COVID and other post-COVID complications.

Hopefully one day there will be better treatments and even a cure for long COVID.

But in the meantime, increased awareness of the biomedical underpinnings of long-COVID should prompt doctors to take patients more seriously as they try to access the treatments and services that already exist.

Brendan Crabb, Director and CEO, Burnet Institute; Gabriela Khoury, Topic Leader, Antiviral Immunity, Burnet Institute, and Michelle Scoullar, Senior Research Fellow, Burnet Institute

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