Why SARS-CoV-2 bounces back after #Paxlovid treatment
A NEW study found that the antiviral treatment, especially when given early in the course of the infection, can leave behind target cells that can still be infected with the virus. 1/
In addition, the treatment may not completely clear the virus, leaving behind infectious particles that invade the target cells. 2/
If at the end of 5 days of treatment, there's still virus and target cells around, then the infection can basically restart. Though the antiviral stops existing viruses from replicating, it doesn't remove the viral particles or the infected cells. 3/
Paxlovid, an antiviral combination of nirmatrelvir and ritonavir, is beneficial for mild COVID-19 symptoms with a high hospitalization risk. The virus returns in some patients, who may develop more symptoms and spread the illness. 4/
To better understand the underlying mechanism, researchers used a mathematical model to analyze changes in the viral load of 51 patients, all treated with nirmatrelvir-ritonavir and 20 of whom experienced a rebound case. 5/
The model incorporated what researchers knew about how the viral load changed over the course of an infection. The amount of virus grows rapidly at first and peaks after 3 or 4 days, which is when symptoms become apparent. 6/
Cells respond by secreting interferons that interferes with infection. Over first week, the adaptive immune system responds by producing antibodies that coat the virus & prevent spreading & infection. The real cleaning up of the virus is done by the adaptive immune response 7/
When they added patient data about the antiviral treatment to the model, they observed that the dynamics changed. While the remaining virus could no longer replicate, it could still infect cells that hadn't been killed by the virus or were not protected by interferon. 8/
Notably, starting antiviral treatment earlier preserved more target cells, which increased the likelihood of a rebound after treatment was stopped. 9/
Patients take antiviral treatment for 5 days as the standard of care. The new study suggests that a 10-day course may more effectively reduce a person's risk of a rebound. That duration may give the body enough time to develop a robust immune response. 10/
#LongCOVID: Not only a living nightmare, but a most neglected entity!
LongCOVID is costing countries billions of dollars a year in lost productivity & increased health and social welfare spending. 1/
One analysis of 8 countries by Economist media group suggested longCOVID could have cut their GDP by between 0.5% & 2.3% last year.
They have described it as "a mass disabling event", but a dearth of data makes it hard to gauge the economic impact & estimates vary wildly. 2/
The absence of a universal longCOVID definition worsens the issue. Patients have reported >200 symptoms involving the whole body. They include cognitive impairment, extreme fatigue, dyspnea, cardiac difficulties & joint discomfort.The cause is unknown and there's no cure. 3/
Is it possible to halt childhood brain tumor before it forms?
Researchers have found a strategy to prevent medulloblastoma, the most prevalent juvenile malignant brain cancer, from growing. They find a protein that wakes up'sleeping' stem cells and drives tumor growth. 1/
Brain cancer presents a unique set of challenges for researchers—by the time a person experiences symptoms, the tumors are often so complex that the fundamental mechanisms driving the tumor growth are no longer easy to identify. 2/
A research team working to combat this challenge for sonic hedgehog (SHH) medulloblastoma.
The researchers identify that a protein #OLIG2 is responsible for the waking up of 'sleeping' stem cells and driving SHH medulloblastoma tumor formation and regrowth. 3/
Oxygen is essential for human life, yet a growing body of preclinical research is demonstrating that chronic continuous hypoxia (low levels of oxygen in your body tissues) can be beneficial in models of mitochondrial disease, autoimmunity, ischemia, and aging. 1/
This research is revealing exciting new and unexpected facets of oxygen biology, but translating these findings to patients poses major challenges, because hypoxia can be dangerous. 2/
Overcoming these barriers will require integrating insights from basic science, high-altitude physiology, clinical medicine, and sports technology. 3/
SARS-CoV-2 can be found in the pancreas following infection. In a NEW study, researchers investigated whether the pancreas is damaged by the infection & whether there are changes of the pancreatic enzymes that the pancreas produces & circulates around the rest of the body. 1/
A particular protein called the placenta-associated protein 8 (PLAC8) expression was found in people who died following SARS-CoV-2 infection. Researchers show this protein is required for SARS-CoV-2 pancreatic infection and viral replication. 2/
Their findings indicate that the human pancreas as a SARS-CoV-2 target with plausible signs of injury and demonstrate that the host factor PLAC8 is required for SARS-CoV-2 pancreatic infection 3/
👇SARS-CoV-2 infects pancreatic cell lines in a PLAC8-dependent manner.
Many treatments for autoimmune disorders cause systemic immunosuppression, leading to severe & chronic toxicities.
If immunity could be suppressed locally, only in targeted tissues, this could provide overcome these systemic toxicities to treat such diverse diseases 1/
🔥 Now, researchers have found a way to circumvent toxicities of systemic immunosuppression. They have engineered synthetic suppressor T cells that execute locally targeted immunoprotective programs. 2/
In theory, cell-based treatments could be set up to protect specific tissues from immune attack without immunosuppression. To make tailored suppressor cells, one could direct endogenous cells, like regulatory T cells or myeloid suppressor cells, to find disease sites.
White blood cell count could predict severity of future #LongCovid (PASC) in women
➡️ A higher level of pre-pandemic leukocyte count was prospectively and independently associated with a higher #LongCovid a.k.a PASC symptom count. 1/
Although dysregulated inflammation has been postulated as a biological mechanism associated with PASC and shown to be a correlate and an outcome of PASC, it is unclear whether inflammatory markers can prospectively predict PASC risk. 2/
Researchers examined the association of leukocyte count and high-sensitivity C-reactive protein (hsCRP) concentrations, measured ~25 years prior to the COVID-19 pandemic, with PASC, PASC severity, and PASC-associated cognitive outcomes at follow-up among postmenopausal women. 3/