This study demonstrated differences in immune profiles and hormone levels in individuals with long COVID, more than one year after acute infection.
COVID-19/ Long COVID, Immunity & Inflammation
The diversity of intracellular microbes in immune cells of SARS-CoV-2 positive and COVID-19 recovered individuals
This study demonstrates diversity of intracellular microbes in immune cells of healthy individuals, SARS-CoV-2 positive patients, and COVID-19 recovered individuals.
This study showed that SARS-CoV-2 infects CD4+ T cells, and that the S glycoprotein binds directly to the CD4 molecule.
Spike protein binds directly to bacterial lipopolysaccharide, boosting the inflammatory response and forming spike protein aggregates
The S protein binds to LPS through multiple sites on the S1 and S2 subunits, and that this interaction enhances the inflammatory response in vitro and in vivo.
The presence of concurrent intracellular pathogens can lead to T-cell exhaustion and potentially severe consequences
This theoretical paper discusses the possible interactions between intracellular pathogens, such as viruses, bacteria, fungi and protozoan parasites when they concurrently infect the same host cells. Concurrent intracellular pathogens can lead to T-cell exhaustion and subvert innate and adaptive immune defenses, with severe consequences.
Autoantibodies against certain chemokines have favorable outcome in recovered COVID-19 convalescents
These findings revealed different patterns of anti-chemokine autoantibodies in recovered convalescents after COVID-19 and patients with long COVID
An immunohistologic analysis of cerebral venous thrombi caused by vaccine-induced immune thrombotic thrombocytopenia
The immunohistological analysis of clots from three people who died from cerebral venous thrombosis related to vaccine-induced immune thrombotic thrombocytopenia after receiving a single dose of ChAdOX1-nCoV-19 vaccines.
Unique monocyte signatures in subgroups of long COVID patients indicate that long COVID phenotypes could be driven by distinct mechanisms
This study shows unique monocyte signatures that define subgroups of long COVID patients. Given the heterogeneity of clinical presentations, it seems likely that different long COVID phenotypes are caused by distinct pathophysiological pathways.
The authors proposed a pathophysiological model of long COVID based on the persistence of SARS-CoV-2 virus. It apears that long COVID is an infection-associated chronic disease that affects every single organ system, and results in multisystem injury in both adults and children.
Graves’ disease after mRNA vaccination against COVID-19, with the presence of autoantibodies one year after the vaccination
A case report of new-onset Graves’ disease after mRNA vaccination against COVID-19, with the presence of autoantibodies one year after the vaccination.
A recent detailed review article discusses the known underlying mechanisms, possible trigger factors and consequences of persistent thromboinflammation in post-acute COVID-19 syndrome.
Spike protein suppresses immune synapse assembly in cytotoxic T lymphocytes, leading to impaired cytotoxicity and cytokine production
The SARS-CoV-2 spike protein suppresses immune synapse assembly in cytotoxic T lymphocytes, resulting in impaired cytotoxicity and cytokine production.
Repeated SARS-CoV-2 mRNA vaccination results in a class switch to noninflammatory spike-specific IgG4 antibodies
Repeated immunization with SARS-CoV-2 mRNA vaccines can cause an increase in anti-spike IgG4 antibodies and IgG4-switched memory B cells 5 to 7 months after the second mRNA immunization. This class switch has been linked to a reduced capacity of the spike-specific antibodies to mediate antibody-dependent cellular phagocytosis and complement deposition.
Prolonged SARS-CoV-2 receptor binding domain booster vaccination promotes humoral and cellular immune tolerance in the Balb/c mice
Prolonged vaccination promoted the development of a prominent adaptive immune tolerance and profoundly impaired the immune response established by conventional course.