Is COVID-19 a new disease?

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In a review recently published in Respiratory Medicine Lancet magazine by Osuchowski et al. (May 6th, 2021) the currently known pathophysiology of COVID-19 is known to describe the mechanistic characteristics that make COVID-19 different from many conditions previously thought to be similar.

Even considering the unprecedented scientific scrutiny aimed at severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) since the beginning of the pandemic, the scientific community is only in the early stages of understanding infectivity. and virus transmissibility, the mechanisms behind it. the acute respiratory manifestations frequently observed in severe cases and the associated persistent symptoms known as long COVID, the result of unregulated immunomodulation. Here are some of the key points of the review.

Comparison with other coronaviruses

The coronavirus family contains several human pathogens, being SARS-CoV-2 genetically similar to SARS-CoV, and somewhat less so with MERS-CoV.

The SARS-CoV mortality rate is almost 10% compared to the much lower rates reported for SARS-CoV-2, particularly once asymptomatic cases are counted. However, there were only about 8,000 cases of SARS-CoV in 2003. MERS-CoV had an even higher rate, about a third, although fortunately there were only about 2,500 cases in 2012.

The much wider SARS-CoV-2 transmissibility is thought to be related to the initial infection in the upper respiratory tract, with viral loads being observed to peak before the other. coronavirus.

There is a robust and long-term response of T cells to the SARS-CoV-2 challenge, and it has been shown to provide protective immunity against reinfection in most cases.

Antibody production typically correlates with T cell response, although a decoupled response has been reported in COVID-19, as the antibody response is strongly linked to the severity of the disease, with mild or asymptomatic cases that sometimes produce low or undetectable responses.

Cross-reactivity in the T cell response between SARS-CoV and SARS-CoV-2 has been shown, with about 20-50% of the population reportedly having cell responses. Pre-existing T SARS-CoV-2-related exposure to common human coronaviruses, four of which are common colds, while cross-reactivity of antibodies is rare.

Covid-19 severe

The authors advise caution with regard to common information cytokine storm induced by COVID-19, stating that while an increased systemic response is not questioned, it is in fact lower than that observed in other acute-induced acute respiratory disorder syndrome (ARDS).

Post-mortem lung studies have also found variable results and elevated cytokine levels similarly to influenza are observed. The ACE2 receptor can also be expressed more intensely in any part of the body than the lungs, i.e. the small intestine and heart. Although studies have shown that these organs are also affected, they have no potentially cytokine-related effects to almost the same degree.

Severe COVID-19 is associated with many thrombotic events in the lungs, endothelial inflammation, pleural effusion, and pulmonary edema induced by an unusual phenomenon called silent hypoxemia, where a patient has critically low oxygen pressure but appears to have only discomfort. mild respiratory. The reason for this condition is not yet fully apparent, nor is the mechanism by which SARS-CoV-2 extends from the upper to lower airways, which tends to distinguish between mild and severe COVID-19. .

The authors describe two currently preferred theories: aspiration of virus particles released by the upper airway or direct infection of the lower respiratory tract. via breathing.

Impact and conclusions

In summary, the authors state that a new infectious profile is evident in SARS-CoV-2. Some older coronaviruses, such as hCoV-229E or hCoV-NL63 (common colds), infect the upper respiratory tract and cause mild to moderate respiratory disease, while more highly pathogenic coronaviruses have been shown to be more prevalent. the lower respiratory tract, resulting in more severe pneumonia and ARDS.

SARS-CoV-2 shares the characteristics of each of these subspecies, infecting the upper respiratory tract and progressing to the lower airway and giving rise to ARDS only in severe cases.

Compared with SARS-CoV or influenza, COVID-19 disease is more common in multiorgan failure and thromboembolic events, and endothelial and epithelial infection also dominate SARS-CoV-2 infections, rather than alveolar-centered infections. .

Patients with COVID-19 also present with high but variable levels of proinflammatory cytokines over a longer period of time than those infected with influenza, although levels are often lower than those observed in patients with non-COVID-related ARDS. A deregulated host response is associated viral load the severity of the disease and evidence suggests that it is a poor response control by the host leading to severe COVID-19. SARS-CoV-2 appears to be associated with inducing this deregulation and generates a unique and still little known inflammatory profile.

Given the similarity of COVID-induced ARDS to ARDD by other means, the authors consider that many of the critical clinical responses used for those with severe SARS-CoV-2 infection were adequate, although they also emphasize that COVID-19 should be considered a new entity with different pathophysiology and should be studied without preconceptions based on other diseases.

Future research prioritized by the group includes establishing the molecular basis for the lower pathogenicity observed in SARS-CoV-2 than in SARS-CoV and the development of precise predictive thresholds for disease progression.

With regard to severe COVID-19 and the development of long-term COVID, the role of pre-existing and acquired T cell immunity in COVID-19 should be clarified and optimal anticoagulant and immunomodulatory strategies should be developed. to combat late-stage disease until better preventive measures can be put in place.





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