Thumbnail Photo by Alvaro Reyes on Unsplash
Hi everyone!
Welcome to this week’s Long Covid Weekly! A couple of announcements before I jump into the news + research.
Announcements:
I created a Twitter for the newsletter here. I think Twitter definitely has among the liveliest LC communities(along with Reddit, of course). Also, I think Twitter is the most effective platform for announcements related to the newsletter.
I created a simple logo for the newsletter, and would love to hear what people have to think about it.
I have thought a little bit about where the newsletter should go in the future, I think I would like to incorporate interviews with other people/researchers in the field. More on this to come.
Media
Experts testify on the effects of long COVID at House hearing | full video
TL;DR: Long Covid experts testify to Congress. Hard to summarize this in a TLDR since its chalk full of content but would recommend this to be the thing you view from this week’s newsletter.
‘There’s no one long Covid’: Experts struggle to make sense of the continuing mystery
TL;DR: Pretty good overview of challenges faced by researchers in Long Covid. It is still a new field in need of better studies and better funding. This article highlights several different research routes currently being taken by different researchers including: covid impact on the lungs, & autoimmunity.
Science Lags Behind for Kids with Long COVID
TL;DR: This article highlighs lack of whats known about Long Covid for kids( a common theme in LC articles). Without a specialized treatment there is a focus on a ‘ rehabilitation-based approach focused on improving symptoms and functioning so that kids can go back to their usual activities as much as possible‘
Who’s most at risk of developing long COVID? Experts think these 6 groups of people might be
[submitted by reader, thank you!]
TL;DR: People at risk of LC include those who get covid multiple times, those with dormant EBV, those with autoimmune antibodies, those who haven’t been vaccinated, those with neurological symptoms during initial covid infection & those with high viral load during infection.
Polls
Which theory for the cause of Long Covid do you believe the most in?
Research
Orthostatic Challenge Causes Distinctive Symptomatic, Hemodynamic and Cognitive Responses in Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
TL;DR: This article really peaked my interest because the authors are well known in the ME/CFS world. Basically, they found that Long Covid & ME/CFS patients shared similar outcomes after a Lean Test (NLT). They found it aggravated symptoms and produced objective hemodynamic and cognitive abnormalities. I believe a major outcome of this is showing similarities between a subset of LC patients and ME/CFS patients.
Postural Orthostatic Tachycardia Syndrome as a Sequela of COVID-19
Tl:DR: [Side Note: This is a really informative read, if you have the time definitely read this] The paper mentions 2-14% of people with Covid develop POTS (much larger than I thought). Hypotheses for the development of post-covid POTS include ‘ autoimmunity related to SARS-CoV-2 infection, autonomic dysfunction, direct toxic injury by SARS-CoV-2 to the autonomic nervous system, and invasion of the central nervous system by SARS-CoV-2.’
Single-cell immune profiling reveals long-term changes in myeloid cells and identifies a novel subset of CD9+ monocytes associated with COVID-19 hospitalization
TL;DR: This was an extremely interesting, and somewhat distressing piece. The ‘results suggest that SARS-CoV-2 infection results in long-term changes in the immune cell compartment, and it is important to determine whether or not these changes impact symptoms experienced by patients with long-COVID.’ At 3-4 months post-infection a specific type of monocyte ( a type of WBC) was elevated in hospitalized patients compared to healthy patients.
SARS-CoV-2 infection in hamsters and humans results in lasting and unique systemic perturbations post recovery
TL;DR: Tested the effects of IAV (I believe this is swine flu) vs Covid-19 on Hamsters. The results indicated that ‘that SARS-CoV-2 (Covid-19) induces a more prolonged inflammatory profile alongside changes in appetite, these data suggest that SARS-CoV-2 induces a more severe systemic acute infection than IAV, which our data here indicates is likely mediated by inflammatory processes shared between the two viruses.’ The most unique response to Covid-19 took place in the olfactory tissue.
As always, if you have feedback or articles you would like to submit please fill out this form.