\n– Potential treatment<\/a>
\n– The uncertainty of herd immunity<\/a>
\n– Scientific philanthropy boost<\/a>
\n– The distance between dental research and treatment<\/a>
\n<\/div>\n
Recent studies also suggest that COVID-19 can cause more serious complications and even make other diseases more likely to occur, such as diabetes, when the body does not properly metabolize sugar (glucose) molecules in the blood. This is a worrying scenario for scientists and raises the question of whether everyone who has overcome COVID-19\u2014more than 16 million people worldwide to date, of which 3 million are in Brazil\u2014can really be considered cured simply for having survived the initial infection. “As a result, it is possible that the number of deaths is indirectly much higher than estimated,” says infectious disease specialist Marcus Vin\u00edcius Lacerda, from the Dr. Heitor Vieira Dourado Foundation for Tropical Medicine in Manaus. \u201cMany patients who have recovered from COVID-19 and been discharged from hospital may later die of complications related to the infection. These deaths will not be counted in the pandemic figures, even if they are related.\u201d<\/p>\n
The statistics available do not yet paint a clear picture of this new chapter of the pandemic. It is also difficult to estimate a patient’s risk of developing long-term symptoms after overcoming the acute phase of COVID-19, or how long these symptoms might last. Scientists do not know what factors contribute to the risk of a person infected by the novel coronavirus developing more serious complications after the acute stage. Most studies following individuals considered cured of the disease are in the early development stages or are still ongoing. It is no coincidence that most evidence of post\u2013COVID-19 syndrome has come from research in the first countries hit by the pandemic between December 2019 and February 2020, such as Italy. A study published in the Journal of the American Medical Association<\/em> (Jama<\/em>) in July found that 87.4% of 143 patients admitted to a hospital in Rome with COVID-19 were still exhibiting symptoms two months after being discharged.<\/p>\n The most common problem identified by the researchers was shortness of breath (dyspnea). This complication results from the formation of fibrosis\u2014small scars\u2014in the lung tissue, which makes the organ less flexible, reducing its ability to exchange gases and oxygenate the body. Pulmonary fibrosis is more frequently seen in the most severe cases of COVID-19, caused directly by the virus as well as indirectly as a consequence of an unregulated inflammatory response in the affected area. Fibrosis can also occur as a result of spending a long time in an ICU breathing with the assistance of a mechanical ventilator. \u201cThe risk of fibrosis in the lungs varies according to the patient’s age, preexisting conditions, or even individual genetic factors,\u201d explains Dolhnikoff. “What is clear is that a portion of the affected population develop these scars, which have an impact on their quality of life.”<\/p>\n Kika Carvalho<\/span><\/a> SARS-CoV-2 can also infect the cells that line the inner wall of blood vessels, altering the coagulation mechanism and leading to hypercoagulability, with an increased chance of thrombi that can cause infarctions and hemorrhages in the heartKika Carvalho<\/span><\/p><\/div>\n Long-term complications can also extend beyond the lungs. In Germany, a study published in the journal Jama Cardiology<\/em> in July evaluated 100 patients between 45 and 53 years of age. All of them recovered from COVID-19. Ten weeks after diagnosis, however, 78% of them had developed cardiac abnormalities due to inflammation in the heart.<\/p>\n In Brazil, at least two studies are monitoring patients who have survived the disease and the long-term impacts on their health. One is being conducted by Marcus Lacerda and his team, who in July started collecting data from 800 patients discharged from hospitals in Manaus after testing negative for the disease. “We will track those who die after leaving hospital and identify the causes of their deaths,” he explains. The aim is to estimate the incidence of certain health problems in people considered cured, and to compare these numbers with people who have not had COVID-19. \u201cWe are also going to monitor those who survive but go on to develop other illnesses or complications, to look for possible relationships between them and COVID-19.\u201d<\/p>\n Kika Carvalho<\/span><\/a> Studies suggest that the novel coronavirus is capable of invading and damaging a range of neuronal cells, such as astrocytes and neurons, causing inflammation that can result in psychomotor agitation, delirium, and hallucinations months after the acute phase of COVID-19 passesKika Carvalho<\/span><\/p><\/div>\n A team led by physician Augusto C\u00e9sar de Oliveira, from the Em\u00edlio Ribas Institute of Infection Diseases in S\u00e3o Paulo, also started a study in July, in partnership with the Albert Einstein and S\u00edrio-Liban\u00eas hospitals in S\u00e3o Paulo, and Fortaleza General Hospital in Ceara. The objective is to assess the incidence of long-term neurological disorders in individuals infected with SARS-CoV-2. “We will analyze patients over the next six months,” explains the researcher. He says that since the beginning of the pandemic, clinical reports indicate a high incidence of headaches and mental confusion in people who have had COVID-19. “We initially thought this was associated with the acute phase of the disease, but the amount of people still suffering neurological problems after overcoming the disease is surprising.”<\/p>\n Oliveira cites a specific example: a middle-aged woman, with no pre-existing conditions, who was infected with the novel coronavirus and developed a moderate case of COVID-19. “She recovered from the illness, but four months after her first symptoms, she began experiencing cognitive and behavioral changes, such as memory lapses, difficulty concentrating, and feelings of agitation,” says the researcher. SARS-CoV-2 was found in the patient’s cerebrospinal fluid, which surrounds and protects the brain, \u201csuggesting that the virus is not only capable of invading the central nervous system, but of remaining there for a prolonged period of time, even after the primary symptoms of the disease have stopped.\u201d According to physician Jorge Casseb, a researcher at the S\u00e3o Paulo Institute of Tropical Medicine (IMT) at USP and one of the project\u2019s sub-coordinators, \u201cthese sequelae can cause potentially serious injuries over a patient\u2019s lifetime.\u201d<\/p>\n Dalcolmo, from FIOCRUZ, has been observing similar cases at his private practice. “I have patients who have overcome the acute phase, but almost a month later developed meningoencephalitis, inflammation that affects the brain and its protective membranes, called the meninges.” Some even tested negative for the virus after providing respiratory secretion samples for a RT-PCR test, considered the gold standard for COVID-19 diagnosis. Yet they later continued to suffer from the symptoms of the disease or developed more serious complications.<\/p>\n The situations observed by Oliveira and Dalcolmo raise an important question: is the virus still present in the bodies of patients with persistent symptoms or more serious complications months after the acute phase of the infection? There is apparently no pattern. Some still carry the virus, even if at lower levels, while others do not. Some experts also suggest that RT-PCR tests cannot detect the virus in other parts of the body, such as the central nervous system, where its effects can lead to the emergence of other diseases. In July, Lacerda and his team described the case of a teenager in Manaus who developed Guillain-Barr\u00e9 syndrome after being infected with the novel coronavirus. This immune disorder damages the myelin, a substance that lines the nerves, causing muscle weakness and in severe cases, total paralysis of the limbs, and even death.<\/p>\n All of these complications demonstrate the virus’s versatility and ability to invade different cell types. Like a key fitting into a lock, SARS-CoV-2 uses its S protein (S for spike) to bind to angiotensin-converting enzyme 2 (ACE2) on the surface of the cells that cover the lung. \u201cIt just so happens that the cells of the heart, the central nervous system, and several other organs also express ACE2, making practically all human tissue vulnerable,\u201d explains biomedic Marcelo Mori, from the Institute of Biology (IB) at the University of Campinas (UNICAMP). \u201cAfter invading the cells, the virus begins to multiply,\u201d says biochemist Jos\u00e9 Carlos Alves-Filho of the Ribeir\u00e3o Preto School of Medicine at USP. “After replicating a certain number of times, the copies break through the cell membrane and infect other cells, repeating the process.”<\/p>\n They can even infect monocytes, immune system cells produced in the bone marrow. Monocytes travel via the bloodstream and can differentiate into macrophages, immune cells that detect and engulf foreign particles and microorganisms. In a study published in the journal Cell Metabolism <\/em>in July, Mori and other researchers from UNICAMP’s COVID-19 task force found that SARS-CoV-2 multiplies faster inside these cells in patients with high blood glucose levels. Glucose is used by cells to produce energy. “In these cases, however, the virus appears to use it to replicate more quickly within the monocytes,” says the researcher. In response to the increasing viral load, monocytes release large amounts of proteins (cytokines) that aggravate the body\u2019s inflammatory response, and consequently the disease.<\/p>\n![\"\"](\"https:\/\/revistapesquisa.fapesp.br\/wp-content\/uploads\/2021\/02\/018-023_covid_sintomas_295-2-1140.jpg\")
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