The biological processes giving rise to the central nervous system symptoms of long COVID remain a mystery. But multiple studies suggest they do not appear to be a result of a direct viral infection of brain tissue. The latest such research, which appeared online in Nature Neuroscience on Feb. 16, 2024, demonstrated that local immune response in brain tissues persisted long after SARS-CoV-2 virus had disappeared.

COVID-19 severity remains open to several questions. Researchers at the University of California Los Angeles (UCLA) have revealed how SARS-CoV-2 causes acute inflammation instead of the symptoms of a common cold. This effect could be initiated by the peptide fragments of the coronavirus released when the host eliminates the virus, which can form pro-inflammatory complexes that trigger an amplified immune response.

A common molecular pathway associated with lung fibrosis may also hold the key to pulmonary vascular repair. A group of scientists at the University of Pennsylvania (Penn) found that when a viral infection damaged these vessels, the injury could be restored by activating the transforming growth factor-β receptor 2 (TGF-βR2) in endothelial cells, which led to cell proliferation.

COVID-19 severity remains open to several questions. Researchers at the University of California Los Angeles (UCLA) have revealed how SARS-CoV-2 causes acute inflammation instead of the symptoms of a common cold. This effect could be initiated by the peptide fragments of the coronavirus released when the host eliminates the virus, which can form pro-inflammatory complexes that trigger an amplified immune response.

Capricor Therapeutics Inc.'s Stealthx exosome-based multivalent vaccine for the prevention of SARS-CoV-2 has been selected to be part of the U.S. Department of Health and Human Services' Project Nextgen initiative aimed at developing COVID-19 vaccines offering broader and more durable protection.

Researchers at ETH Zurich have identified a proteomic signature that could recognize long COVID six months after acute infection. Biologically, the signature indicated that the complement system remained active in patients with long COVID six months after infection. Translationally, it could lead to a diagnostic test for long COVID, and suggests that targeting the complement system could be a therapeutic approach to prevent or treat the disorder.

Several highly pathogenic viruses, including SARS-CoV-2, share a conserved mechanism of infection via the fusion of the viral and host membranes employing a six-helix bundle (6-HB) heptad repeat.