Merck & Co. has revealed the discovery of novel oral SARS-CoV-2 3C-like proteinase (3CLpro; Mpro) inhibitors for the potential treatment and/or prophylaxis of COVID-19. 3CLpro plays a key role in viral life cycle by cleaving viral protein and helps in replication and infection, which make 3CLpro a target for designing drugs to treat COVID-19.
The research on novel vaccines against SARS-CoV-2 with improved characteristics continues. These ideal features include rapid development to target variants of concern, easy manufacturing, and an excellent safety profile while inducing humoral and cellular immune responses.
Macquarie University has identified 3C-like proteinase (3CLpro; Mpro; nsp5) (SARS-CoV-2; COVID-19 virus) inhibitors reported to be useful for the treatment of SARS-CoV-2 infection (COVID-19).
Imunon Inc. has released promising results from a live virus challenge study conducted by the Wistar Institute with IMNN-101 against the SARS-CoV-2 variant XBB.1.5. This study was conducted using the clinical vector that Imunon intends to bring into its phase I study during the second quarter, and showed IMNN-101 immunogenicity and protective activity in a live viral mouse challenge.
Avitar Biosciences Inc. has divulged 3C-like proteinase (3CLpro; Mpro; nsp5) (SARS-CoV-2; COVID-19 virus) inhibitors reported to be useful for the treatment of SARS-CoV-2 infection (COVID-19).
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.
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.