Loss of smell in COVID 19, its Mechanism an What are the Olfactory Nerves?

 Loss of smell in COVID 19, its Mechanism and What are the Olfactory Nerves? Define COVID 19:

Loss of Smell in COVID

Define COVID 19:

A respiratory condition brought on by the SARS-CoV-2 virus that is extremely contagious. SARS-CoV-2 is believed to be transmitted from person to person through droplets expelled during coughing, sneezing, or talking by an infected person. A less common method of transmission is by touching one's mouth, nose, or eyes after touching a surface that has the virus on it. Fever, coughing, and breathing difficulties are among COVID-19's most typical signs and symptoms. Additionally, possible symptoms include weakness, muscle aches, chills, headaches, sore throats, runny noses, nausea or vomiting, diarrhea, and a loss of taste or smell. The SARS-CoV-2 virus can cause mild to severe signs and symptoms, which typically show up 2 to 14 days after exposure.

Even if they show no symptoms, some people can still spread the virus. Most COVID-19 patients recover without the need for special care. However, some people are more susceptible to serious illnesses. Older adults and those with serious health issues like diabetes, cancer, heart, lung, or kidney disease, as well as those with weakened immune systems are at higher risk. Organ failure and potentially fatal pneumonia are examples of serious illnesses. Treatment for COVID-19 and SARS-CoV-2 infection prevention are the subjects of research. Likewise known as coronavirus disease 19.

COVID effects on Sense of Smell:

The impact of COVID-19 on different kinds of brain cells as well as other long-lasting neurological effects, like "brain fog," headaches, and depression.

Our ability to detect smells is mediated by a group of nerve cells called "olfactory sensory neurons" that are housed in the olfactory bulb, a structure rising up at the back of the nose. These neurons respond to odor molecules that we exhale through our noses thanks to tiny hair-like projections that extend into the mucus-covered nasal lining.

The medical term for this is “anosmia”. Serious consequences of only mild COVID disease - none of the test subjects had had a severe course. Research teams from all over the world are on the trail of the causes: Sars-Cov2 apparently damages the very nerve cells in the nose through which we perceive smells. It has long been known that the virus attacks the support cells of these neurons. Therefore, the olfactory cells lack nutrients, they are no longer optimally supplied.

Mechanism:

• Studies revealed that immune cells, such as microglia and T cells, which detect and fight infection, flooded into the area where the virus was present near nerve impulses (neurons) in the olfactory tissue. Even though the virus cannot infect them, such cells release cytokines, which alter the genetic exercise of olfactory nerve cells, according to the study's authors. The team theorizes that immune signaling persists in the brain in a way that decreases the activity of genes required for the development of olfactory receptors, where t lymphocyte activity would quickly dissipate in other scenarios.
• Loss of smell without a stuffy nose, as seen with other infections like the common cold, is one distinctive symptom of COVID-19 infection, according to researchers. Most of the time, the smell loss is temporary and lasts only a few weeks, but for more than 12 percent of COVID-19 patients, olfactory dysfunction continues as hyposmia, a persistent loss of smell, or altered perception of the same smell (parosmia).
• The current authors investigated the molecular effects of SARS-CoV-2 infectious disease in golden hamsters and in olfactory tissue obtained from 23 human autopsies to gain insight into COVID-19-induced smell loss. Hamsters serve as a good example because they are mammals that rely more on smell than humans do and are more prone to nasal cavity infections.
• The study's findings add to the body of knowledge that has been accumulated over many years about the complex 3D relationships involved in the process that activates genes, where certain DNA chains loop around to form long-range interactions that allow the stable reading of genes. As part of the "nuclear architecture," some genes function in open, active chromatin "compartments" (protein structures that house the genes), whereas others are compacted and closed.
• Experiments conducted for the current study supported previous findings that SARS-CoV-2 infection and the immune response to it reduce the ability of chromosomal DNA chains to be open and active and to loop around to activate gene expression. The research team found continuous and prevalent deregulations of olfactory receptor building in both hamster and human olfactory nerve cell tissue. According to other published work by these authors, recurring inflammatory cell reactions in the nasal cavity may affect emotions and cognitive function, which is consistent with long COVID, and olfactory nerve cells are wired into sensitive brain regions.
• Studies in hamsters with time-lapse recordings showed that down-regulation of olfactory neuron receptors persisted even after temporary changes that might have an impact on smell had naturally recovered. This, according to the authors, implies that COVID-19 causes longer-lasting disruption in the chromosomal control of gene expression, possibly resulting in a form of "nuclear memory" that prevents the transcription of the olfactory receptor from returning even after SARS-CoV-2 has been eradicated.
• Dr. never claims that it has important ramifications to realize that the sense of smell depends on "fragile" genomic interactions between chromosomes. "If olfactory gene expression stops each time the immune system reacts in specific ways that disrupt inter-chromosomal contacts, then the loss of smell may act as the "canary in the coal mine," giving early warnings that the COVID-19 virus is causing damage brain tissue before other symptoms present and suggesting new ways to treat it."
• The team is currently testing whether giving steroids to hamsters with long COVID can restore and restrain harmful immune reactions (an inflammatory condition) to protect nuclear architecture as a next step.

A short introduction to Olfactory Nerves:

Olfactory nerves (I) are unique sensory nerves that are responsible for the smell. They begin in the olfactory epithelium's receptors and exit at the olfactory bulbs after passing through the olfactory foramina in the cribriform plate of the ethmoid bone. The epithelia that line the superior nasal conchae, superior nasal septum, and roof of the nasal cavity contain specialized neurons known as olfactory receptors (see Fig. 10.2). The cribriform plate is penetrated by axons that combine to form 20 or more "bundles". The bundles are a portion of the olfactory nerves, which travel only a short distance before entering the olfactory bulbs. On either side of the crista, Galli is these masses of neurons or bulbs. Inside the olfactory bulbs, olfactory afferents synapse. Along thin olfactory tracts, postsynaptic neuron axons continue to the cerebral cortex. Only the olfactory nerves, which do not pass through the thalamus, are directly connected to the cerebrum.

The olfactory nerve, which carries the sense of smell, is a solely sensory nerve. The olfactory mucosa beneath the roof of the nasal cavity is where its receptors are found. The olfactory fibers enter the senses of smell bulb in the olfactory groove after crossing the base of the skull through the cribriform plate's olfactory foramina. The frontal lobe's medial inferior surface is where the olfactory tract, which travels posteriorly, courses after the olfactory bulb. The anterior perforated substance is where the olfaction tract enters the brain, where it is in close vicinity to the optic tract and initiatives to the olfactory cortex.