Dr. Iwasaki: 'Broadly speaking, there are 4 different hypotheses we've been pursuing. Number one is persistent viral replication, or remnants of virus antigen or RNA hidden way in tissues that are causing chronic inflammation. Second is autoimmunity. When that autoimmune...
response happens, it's hard to stop. Third is reactivation of dormant viruses, such as herpes virus family members. Lastly, is the changing tissue inflammation status resulting from the acute phase of COVID."
“Targeting these viruses with antibodies or antivirals, whether that would have an impact or not, those are the things I think we need to be looking at next.”
“I am delighted to tell you that we have completed enrollment for the Yale Paxlovid study. The goal for this RCT, is to understand whether this 15-day course is beneficial for people with Long COVId, and if so, what are the biomarkers associated with such benefit."
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Host asks Akiko Iwasaki: '(26 minutes) Recently I want to hear a thought that, NIH Director Monica Bertagnolli recently stated that active COVID virus can be found in bodies months post-infection, and some research hypothesizes viral persistence as a driver for Long COVID...
.., as well as other post-viral illnesses like Myalgic encephalomyelitis or chronic fatigue syndrome. Can you talk about the significance of what Monica mentioned, from your perspective?"
Iwasaki: “There are roughly 4 possible hypotheses that can describe Long COVID…it is a heterogenous disease….viral reservoir or replicating virus that persists is one of the 4 hypotheses. There is numerous evidence for this…Dr. Amy Proal has published a very nice review
“CU Doctor Helps Long COVID Patients by Expanding Care, Research”
“There are so many patients who are suffering without clear answers and without clear therapies,” says Jolley, who is the medical director of the UCHealth Post-COVID Clinic
State models estimate there are between 300,000 and 500,000 Coloradans who have long COVID, she says.
“That's what keeps us wanting to do the research and the clinical work, because otherwise, potentially 500,000 Coloradans will be struggling with no one,” Jolley says.
“Some patients have also experienced extreme fatigue to the point that they cannot work or even get out of bed.”
“Seeing patients in the clinic motivates us to want to do the research so that we can offer them therapeutics, because their whole life has changed. Nobody fully
"From Seltzer’s perspective, an effective collaboration between patients and scientists can help both sides equally, because it leads to more effective and targeted research. “We have the resources to help you do what you do even better,” Seltzer says. The lived experiences of
patients can shape research priorities in several key ways, she says. These include finding the most efficient way to allocate limited funds on the basis of symptom burden; offering context on the prevalence and severity of symptoms; and identifying how the trial design can
“We also have a poor understanding of the causes of long COVID,” said Zeichner, a pediatric infectious disease expert at UVA Children’s. “If this turns out to be true, then developing treatments to deplete or block the rogue abzymes could be the most effective way to treat..”
“If patients with long COVID make abzymes that activate proteins that control processes such as coagulation and inflammation, that could explain the source of some of the long COVID symptoms and why long COVID symptoms persist even after the body has cleared the initial
"The researchers saw signs that the immune system had become “worn out” in ME/CFS participants. In the blood of this group, they found that killer T cells, which normally target infected cells for destruction, had reduced levels of a protein called CD226 that would otherwise
boost their proliferation and activity. In the cerebrospinal fluid, killer T cells had elevated levels of programmed cell death protein 1 (PD1). This protein is considered an “exhaustion” marker, and its presence can indicate that an overstimulated T cell has shut down.