COVID-19 infection and pulmonary sarcoidosis: a systematic review and meta-analysis of morbidity, severity and mortality
Peer-Reviewed Publication
Updates every hour. Last Updated: 2-May-2025 23:09 ET (3-May-2025 03:09 GMT/UTC)
Key findings
• Sarcoidosis patients are prone to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, increased severity, morbidity and greater mortality of coronavirus disease 2019 (COVID-19).
What is known and what is new?
• Subjects with sarcoidosis are more vulnerable to SARS-CoV-2 infection.
• Severity of COVID-19 was also more serious in subjects stricken with sarcoidosis.
What is the implication, and what should change now?
• Vaccination against SARS-CoV-2 for sarcoidosis may be a compulsory measure.
Kyoto, Japan -- Six years before the start of the COVID-19 pandemic, an Ebola outbreak in West Africa had people fearing the possibility of a global outbreak. This was the first time many had ever heard of the virus, but since it was first identified in 1976, there have actually been more than 20 serious Ebola incidents. Thankfully, none of them had the global reach of the coronavirus.
Ebola has not been eradicated, however. This deadly virus, which causes severe hemorrhagic fever in humans and has a fatality rate of about 50%, is still at large and could thus still cause a major outbreak, unless further research finds an effective solution.
A major challenge lies in the virus' structure and regulatory mechanisms, which have remained largely unclear. In particular, scientists have long struggled to fully understand its nucleocapsid, the protein shell that plays an important role in genome replication and transcription.
Researchers at the University of Cologne have discovered that mRNA-based COVID-19 vaccines have a persistent effect on the innate immune system. These mechanisms may help the human body to better protect itself against potential future infections / publication in ‘Molecular Systems Biology’
An immune system defect makes affected individuals vulnerable to severe viral diseases such as influenza or COVID-19. It is caused by the body's own antibodies, which inhibit important defense proteins known as type I interferons. UZH researchers have now generated “decoy molecules” that intercept these autoantibodies and restore the immune defense – the foundation for a possible new therapy.
A study by A*STAR Infectious Diseases Labs (A*STAR IDL) and A*STAR Institute of High Performance Computing (A*STAR IHPC) has assessed the airborne transmission risk of mpox compared to SARS-CoV-2 and smallpox. Using computational modelling and virological data, researchers found that mpox is significantly less likely to spread via respiratory aerosols in its current form. However, potential viral evolution underscores the need for continued surveillance. The study, published in The Lancet Microbe, highlights the value of interdisciplinary research in understanding infectious disease transmission.
Ashraf Ibrahim, PhD, an investigator at The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center for more than 33 years, and Assistant Research Scientist, Yiyou Gu, PhD, at TLI for more than eight years, have been conducting research using monoclonal antibodies to address mucormycosis, a fungal infection caused by Mucorales, has high mortality rates in people with weakened immune systems and those suffering from severe trauma like burns, blast injuries or victims of natural disasters. The disease caused serious infection among COVID-19 patients treated with high doses of corticosteroids with mortality rates close to 60 percent. In the United States, there are approximately 4,000 cases per year with a rate of 200,000 in Southeast Asia where the disease is endemic to India. While vaccines and immunotherapies are available for viruses and bacteria, effective antifungal immunotherapies for mucormycosis, specifically, are lacking.