There were a lot of mysteries surrounding COVID-19, some of which have been answered, but many more have not. Since the start of the pandemic, it has been a mystery as to why children appear to be considerably less vulnerable to the virus than grownups.
Why Children Might Be Better Protected Against COVID-19
Children are often less susceptible to COVID-19 infection than adults; they are not immune, but they are less likely to contract the virus and experience severe illness. Why?
According to Australian researchers from the University of Queensland, children’s nasal epithelium prevents infection and replication, especially of the original Wuhan wild-type strain of SARS-CoV-2 and the Delta variant. The Omicron version and its subvariants, on the other hand, do not appear to have the same trouble. Their research was printed in PLOS Biology.
The juvenile nasal epithelium may be crucial in lowering children’s vulnerability to SARS-CoV-2, according to the first experimental data the authors gave. The observations strongly imply that children’s nasal epithelium is different and that it may provide children with some degree of protection from the SARS-CoV-2.
In children’s nasal epithelial cells, they discovered that the wild-type virus multiplied less effectively and was associated with an enhanced antiviral response. The Omicron variant did not exhibit the effect, whereas the Delta variant did. Although they note that this was a tiny study and might be indicative of how the virus is changing. They also discovered that Omicron replicated more effectively in paediatric nasal epithelial cells than the wildtype or Delta.
Age-Related Diseases Are Treatable With New Molecules
The Hebrew University of Jerusalem’s researchers have discovered a collection of chemicals that aid in the mending of damaged cell parts. Several aging-related illnesses, including sarcopenia, Parkinson’s, and Alzheimer’s, are linked to impaired mitophagy.
A developing approach to treating the elderly is to increase mitophagy, the process by which damaged mitochondria are eliminated and replaced by healthy ones. The researchers created and examined a family of substances linked to spermidine, a known mitophagy-promoting substance. 1,8-diaminooctane (VL-004), a prototype, proved more effective than spermidine at inducing mitophagy and fending off oxidative damage.
The study was published in the Autophagy journal. The scientists formed Vitalunga, a biotech firm, to develop the medication.
A Special Subset of Immune Cells Prevents Strokes
A new subset of white blood cells called CD8+ regulatory-like T cells (CD8+TRLs), according to research from the University of Pittsburgh, appears to offer mice quick-acting and long-lasting protection against ischemic stroke.
These cells were drawn to the area of ischemia injury by a distinctive “homing” signal given off by the brain cells that had been injured. 24 hours after the stroke, the CD8+TRLs made it to the brain and subsequently released chemicals that directly protect against additional brain damage and inflammation.
In tests using mice, the recipients of a transfusion of pure CD8+TRLs fared better and recovered more quickly than the untreated mice over the course of five weeks. Following a stroke, the CD8+TRLs seem to serve as early responders, alerting and mobilising defences.
Gene Therapy For ALS Shows Potential
Gene therapy in ALS animal models was found to noticeably delay the development of the disease, according to research from the University of California San Diego School of Medicine. The mouse and rat models of ALS have a hereditary form, despite the fact that the majority of ALS cases have an unknown origin.
Synapsin-Caveolin-1 cDNA was delivered via an AAV-vector into the mice’s spinal cords as part of the treatment. The SynCav1 lengthened the mice’s lives by preserving and protecting spinal cord motor neurons. They suggest the possibility that SynCav1 could be used in innovative gene therapy for ALS and other CNS diseases.
A neurodegenerative condition called amyotrophic lateral sclerosis (ALS) is characterised by the gradual loss of motor neurons in the brain and spinal cord. It is deadly and has no known treatments.
Colorectal Tumours Now Have A New Therapeutic Target
A possible novel colorectal tumour treatment target has been discovered by researchers at the Tokyo University of Science.
Colorectal cancers can frequently result from inflammatory bowel disease (IBD), which encompasses Crohn’s disease and ulcerative colitis. IBD develops as a result of innate immunological receptors like C-type lectin receptors (CLRs). However, they also have a significant impact on pathogen defence and gut microbiota regulation.
Dendritic cell immunoreceptors (DCIRs), one of such CLRs, are in charge of preserving the immune and skeletal systems’ equilibrium. Researchers using mice discovered that mice without DCIR had less severe colitis and were less susceptible to the formation of colon tumours brought on by AOM-DSS. They discovered that employing the DCIR-binding antibody anti-NA2 targeting asialo-biantennary-N-glycans (NA2) reduced the symptoms of colitis and stopped the growth of colorectal tumours.
Two Viruses That Are Frequently Linked To Alzheimer’s
According to a study from Tufts University and the University of Oxford, some viral infections are linked to Alzheimer’s disease. Herpes simplex virus (HSV) and varicella-zoster virus (VZV), the latter of which is linked to chickenpox and shingles, can both be dormant in brain cells.
Researchers showed that VZV may activate HSV to create the foundation for the early stages of Alzheimer’s disease using 3D human tissue culture models that mimic the brain. When HSV-1, the most common type, is activated, tau and amyloid-beta proteins build up and are thought to play a role in Alzheimer’s disease. The Journal of Alzheimer’s Disease published their research.
According to a research associate in the Biomedical Engineering Department at Tufts, Dana Cairns, Ph.D., GBS12, their data reveals one pathway to Alzheimer’s disease, driven by a VZV infection that causes inflammatory signals that awaken HSV in the brain. While they found a connection between VZV and HSV-1 activation, other inflammatory brain processes may also awaken HSV-1 and cause Alzheimer’s disease.