SARS-CoV-2 infects human CD4+ T helper cells by binding its spike glycoprotein to the CD4 molecule, impairing cell function and potentially causing cell death.
This mechanism involves the interaction of the virus with both CD4 and ACE2 receptors.
“Imagine, in the 1980s...
‘I finally got HIV - just in time for Christmas. And I couldn't be happier. Here's why.’
Think that's a stretch? Covid is sparking what were once AIDS-defining conditions. It's disastrous for the immune system. And every other organ/system of the body.”
“Notably, we also found that activation of RAAS caused substantial damage to the lymph nodes, which hasn't been shown in COVID-19 before," said Beheshti, who is also director of McGowan's Center for Space Biomedicine . "This could explain the long-lasting immune dysregulation seen in survivors of COVID-19 and may contribute to long COVID."
It's also possible that damage to lymph nodes could impair the immune system's ability to detect and destroy cancerous cells, which could potentially help explain the post-pandemic increase in cancer cases.”
Study in the US followed 1,154 hospitalized COVID-19 patients for 12 months.
It found reactivation of latent viruses like EBV and CMV during acute COVID-19.
Persistent reactivation of certain viruses correlated with Long COVID symptoms.
“Looks like Yale school of public health has finally started to say what I have been repeatedly saying since 2020
1) covid creates longlasting autoimmunity by harming t regs 2) harms adaptive immunity 3) causes immune dysregulation 4) persists etc”
Severe COVID-19 can cause persistent alterations in the innate immune system, leading to high levels of inflammation even after recovery.
Changes in gene expression in blood-forming stem cells were found, which were passed down to immune cells.
“Immune Parallels: HIV/AIDS & Long COVID’s Lasting Impact
HIV/AIDS & COVID-19, particularly long COVID, share several significant similarities, especially in terms of viral persistence, T cell damage, immune system dysfunction, & activation of other pathogens. These parallels are important for understanding the long-term effects of both infections and their impact on the immune system…” A thread:
“In the blood of the long COVID patients, the team [at the University of Alberta] found higher levels of various proteins related to systemic inflammation—especially galectin-9 and artemin.. higher levels of galectin-9 in patients are associated with increased inflammation and brain fog.. higher levels of artemin are associated with widespread pain, more severe pain and cognitive impairment.. galectin-9 is shed by stressed neutrophils—the most abundant white blood cells—in long COVID patients. This released galectin-9 can promote chronic inflammation by affecting various immune cells.. long COVID dysregulates the production of red blood cells, which results in an abundance of immature red blood cells in the blood of these patients. Normally, immature red blood cells are present in the bone marrow but not in the blood of healthy people. It is these immature red blood cells in the blood that suppress the immune system and contribute to the elevation of artemin in the plasma of long-COVID patients."
“Long COVID’ affects nearly one in five adults who have had coronavirus disease 2019 (COVID-19), yet the mechanisms underlying this disorder remain poorly understood. In a new study, Cheong et al. show that the epigenetic and transcriptional state of myeloid immune cells and their progenitors are durably altered in patients following severe COVID-19.”
“Long COVID, or post-acute COVID syndrome (PACS), is now estimated to occur in 19% of adults having presented with COVID-19.. PACS is believed to be caused by immunological changes that persist after acute infection. Furthermore, it is now increasingly recognized that these changes include not only those in the adaptive immune system, such as production of autoantibodies or autoreactive T cells due to molecular mimicry, but also those in the innate immune system.. A new study by Cheong et al. in Cell reveals crucial differences in the transcriptional and epigenetic state of innate immune cells and their progenitors [among PASC patients].. the study team demonstrated that myeloid cells and hematopoietic progenitor cells harbored transcriptional and chromatin accessibility changes that did not return to baseline even 1 year after acute SARS-CoV-2 infection. These data provide powerful evidence that persistent changes (i.e., trained immunity) may underlie PACS..”
T cell exhaustion in #MECFS & #LongCovid from predominant sympathetic state & the T cells engage the sympathetic fibers & adrenergic signaling decreases their effector function. Sympathetic nerves suppress T-cell responses in infection and in cancer
Anecdote: "My absolute lymphocytes count is below 1 again. My lymphocytes subsets are as bad or worse as they were in 2020. Numbers had normalized in 2022 with Evusheld. So far as I know, I haven't been reinfected. It's not #HIV, but it's acquired immune deficiency. #LongCOVID #AIDS"
Detailed analysis on Twitter: "As of now, people choose whether or not they have Long Covid based upon their symptoms
However, if most people, after mild infection have changes to their immune systems like reductions in plasmacytoid dendritic cells, without reporting symptoms, what should this be called?"
Oct 1 2021, Title: Uncertainty around the Long-Term Implications of COVID-19 ”perspective on some long-term risks of mutational escape, viral persistence, reinfection, immune dysregulation and neurological and multi-system complications (Long COVID).”