Category: COVID

Acute respiratory distress syndrome (ARDS) is a result of a viral pneumonia caused by the SARS coronavirus 2 (SARS-CoV-2) infection. Viral pneumonia and ARDS symptoms coexist in their presentations, making severe COVID-19 a hybrid condition. >R<

In patients who are severely sick, acute respiratory distress syndrome (ARDS) is a condition in which oxygen levels drop, fluid accumulates in the lungs, and positive pressure ventilation is required. Lung tissue damage from an unchecked inflammatory reaction is the cause of ARDS.

Fluid escapes into alveoli in ARDS because the epithelial cells lining the alveoli are no longer securely linked together. The gas exchange is halted as soon as the alveoli fill up with the spilled fluid. As a result, the amount of oxygen in the air is reduced, while the amount of carbon dioxide in the air increases.

In critical care units, ARDS goes unnoticed much too often. As many as 42% of patients with COVID-19 pneumonia and 61%–81% of those needing intensive care develop acute respiratory distress syndrome (ARDS). After the beginning of symptoms, the median time to intubation in Singaporean patients is 8.5 days. There have been earlier cases of ARDS developing on days 8 or 9 after the beginning of symptoms. Because of this, individuals with COVID19 infection should be closely monitored for the emergence of ARDS. >R<

Apart from the genetic component, there are several environmental and lifestyle factors that increase the susceptibility to ARDS, as well as some medical conditions: air pollution, age, right ventricular dysfunction, immunosuppression, alcohol abuse, and smoking can all contribute to ARDS.

Your report includes genetic components involved in a number of different viral recognition patterns in the body that recognize the virus and then trigger several different mechanisms of inflammatory cytokine release.

The body’s innate immune response must be managed so that it does not overwhelm it. Patients with COVID-19 may have “a variety of immunological reactions” as well as “the generation of cytokine storms in the body,” which may be linked to their very ill state if their infected lung cells aren’t removed.

Coronaviruses are a large and diverse viral family. They have a wide host range, including humans.

Coronaviruses cause both COVID-19 and SARS. SARS-CoV is the virus that causes SARS, whereas COVID-19 is caused by SARS-CoV-2.

Human coronaviruses typically cause mild respiratory infections such as the common cold. Human coronaviruses account for 10 to 30% of upper respiratory tract infections in adult individuals. >R<

SARS is the name given to the respiratory sickness caused by SARS-CoV. SARS is an abbreviation for severe acute respiratory syndrome.

It was discovered for the first time in 2003.

From late 2002 to mid-2003, there was a worldwide SARS outbreak. During this time, almost 8,000 people became infected with the virus, and 774 died. >R<

One of the initial indications of SARS is fever. Other symptoms may accompany this, such as: cough, malaise, or exhaustion; aches and pains in the body;
shortness of breath and headaches.

Respiratory symptoms can deteriorate, resulting in serious symptoms advancing quickly, leading to pneumonia or respiratory failure.

COVID-19 and SARS are comparable in many aspects.

Both are coronavirus-caused respiratory illnesses that are transmitted by respiratory droplets produced when a person with the virus coughs or sneezes. 

The transmission can also occur through contact with objects or surfaces containing the virus. >R<

Both infections can lead to potentially serious illness, sometimes requiring oxygen or mechanical ventilation can have worsening symptoms later in the illness.

Both of these coronaviruses have similar at-risk populations, including older persons and those with pre-existing medical issues.

The novel coronavirus also shares 79 percent of its genomic sequence with the SARS virus. >R<

Although SARS-CoV-2 is more closely related to bat coronaviruses in general, the receptor binding site is more comparable to SARS-CoV.

SARS-CoV-2 and SARS-CoV use the same host cell receptor, according to a new study. It was also shown that the viral proteins needed for host cell entrance attach to the receptor with the same tenacity in both viruses – they have similar affinity. >R<

Despite these similarities, there are also some significant distinctions between the two:

SARS cases were often more severe. It is estimated that 20 to 30 percent of people with SARS needed respiratory support and ventilation. >R<

The fatality rate of SARS is higher than that of COVID 19. 

The expected mortality rate is around 10%, with mortality rates as high as 45% in particular patient populations. >R<

SARS-CoV-2 seems to be more easily transferred than SARS-CoV. 

One theory is that the volume of viral load is greatest in the nose and throat of patients who have COVID-19 immediately after symptoms emerge.

With contrast, in SARS, virus loads peaked relatively late in the infection.

People infected with COVID-19 seem to shed the virus earlier than people infected with SARS, although there haven’t been any confirmed cases of SARS CoV transmission prior to the onset of symptoms.

In another study, researchers compared the part of the viral protein that binds to the host cell receptor. The study also discovered that SARS-CoV-2 has a receptor binding site that binds to the host cell receptor more strongly than SARS-CoV. >R<

On the point of cross immunity to SARS CoV-2 because of an earlier acquired immunity to other coronaviruses, previous studies have found that about 40–50% of the population has cross-reactive T-cells, most likely as a result of another coronavirus exposure in the past.

According to German research, even if COVID-19 patients did not produce antibodies, the majority of them elicited a T-cell response.

The study also discovered that T-cells from previous coronavirus exposure cross-reacted with SARS-CoV2 in about 80% of the control group (patients without COVID-19). Although this cross-reactivity may not provide complete immunity for everyone, it may help to alleviate symptoms. >R<

TLR7 (toll like receptor 7) is an innate immune system sensor  in charge of finding single-stranded RNA and it is therefore one of the ways that our immune systems recognise SARS-CoV-2 as a pathogen.

TLR7, an immune system-related gene, was found to have an uncommon mutation in a genetic investigation of young individuals in their 20s and 30s, with severe instances of COVID-19 (one of which resulted in death) .>R<

Most often a loss in TLR7 function may decrease viral protection and increase severity of viral infections. An overactive TLR7, however, may increase chances of developing lupus. 

There are common genetic variants which ca either decrease or increase TLR7 function.

The TLR7 genetics seem to have a severe, inhibitory impact on the production of Interferon type I which can cause much lower antiviral response of the innate immune system and impair its’ key role in fighting off viral infections at the right time.

TLR7 mutations proven to have this effect are most likely the reason why only a small subset of the young and healthy population end up as severe Covid-19 cases. /R/

When researchers examined some of the B cells from young and otherwise healthy males with severe Covid-19, it turned out that these patients’ B cells failed to respond to stimulation of TLR7. This could also potentially help to explain why most of younger patients who end up with severe Covid-19, are male. /R/, /R/