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This study demonstrated differences in immune profiles and hormone levels in individuals with long COVID, more than one year after acute infection.
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.
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.
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.
These findings revealed different patterns of anti-chemokine autoantibodies in recovered convalescents after COVID-19 and patients with long COVID
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.
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.
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.
The SARS-CoV-2 spike protein suppresses immune synapse assembly in cytotoxic T lymphocytes, resulting in impaired cytotoxicity and cytokine production.
Other Entries
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 vaccination promoted the development of a prominent adaptive immune tolerance and profoundly impaired the immune response established by conventional course.