Momentum is building around a few key theories.1. One is that...

Momentum is building around a few key theories.

1. One is that the infection or remnants of the virus persist past the initial illness, triggering inflammation that leads to long COVID.

2. Another is that latent viruses in the body, such as the Epstein-Barr virus that causes mononucleosis, are reactivated. A recent study in the journal Cell pointed to Epstein-Barr in the blood as one of four possible risk factors, which also include pre-existing Type 2 diabetes and the levels of coronavirus RNA and certain antibodies in the blood. Those findings must be confirmed with more research.

3. A third theory is that autoimmune responses develop after acute COVID-19.

In a normal immune response, viral infections activate antibodies that fight invading virus proteins. But sometimes in the aftermath, antibodies remain revved up and mistakenly attack normal cells. That phenomenon is thought to play a role in autoimmune diseases such as lupus and multiple sclerosis.

Justyna Fert-Bober and Dr. Susan Cheng were among researchers at Cedars-Sinai Medical Center in Los Angeles who found that some people who have had COVID-19, including cases without symptoms, have a variety of these elevated “autoantibodies" up to six months after recovering. Some are the same ones found in people with autoimmune diseases.

4. Another possibility is that tiny clots play a role in long COVID. Many COVID-19 patients develop elevated levels of inflammatory molecules that promote abnormal clotting. That can lead to blood clots throughout the body that can cause strokes, heart attacks and dangerous blockages in the legs and arms.

In her lab at Stellenbosch University in South Africa, scientist Resia Pretorius has found microclots in blood samples from patients with COVID-19 and in those who later developed long COVID. She also found elevated levels of proteins in blood plasma that prevented the normal breakdown of these clots.

She believes that these clotting abnormalities persist in many patients after an initial coronavirus infection and that they reduce oxygen distribution to cells and tissue throughout the body, leading to most if not all symptoms that have been linked to long COVID.


ATL1102 should be able to apply to some of the abovementioned theories (if not all...)

Refer to ASX announcement dated 24th February 2022:
"Long Neuro COVID-19 is hypothesized to follow SARS-CoV-2 virus specific pathophysiological changes, with aberrant inflammatory disease and immune responses post-acute infection, similar to that reported with other viral infections including Epstein-Barr Virus (EBV) and associated Chronic Fatigue Syndrome. Notably patients who had COVID-19 while also infected with EBV were at an increased risk of memory loss and EBV infection increases the risk of autoimmune diseases such as Multiple Sclerosis and associated adverse neurological manifestations. ANP’s immunomodulatory drug ATL1102 has previously demonstrated biologic activity in MS patients "

“Vaccination didn’t cure long COVID symptoms, but didn’t worsen them either, which is a reason given by some long-haulers for not getting vaccinated,” Koralnik said. “As new variants emerge and the number of patients impacted by long COVID rises, we’re now focusing our research on understanding the root cause of long COVID. We’re also devising interventions to improve the management of those patients and find the best treatment options for them.” -- as at 24th May 2022...