scholarly journals Epidemiological Profile of COVID-19 in Brazil and Worldwide

Author(s):  
Carla De Freitas ◽  
Gabriela Calanca ◽  
Elias Jirjoss Ilias ◽  
Arthur Sousa Bezerra

Introduction: COVID-19, caused by the new coronavirus or SARSCoV-2, has a high capacity for dissemination, which brings about an emergency scenario in public health. It manifests itself in a multifaceted manner, with a great variability in the profile of the affected population, which may be associated with biological, social and economic factors. Objective: To know the epidemiological profile of the population affected by COVID-19, in order to promote better assistance.   Methods: This is a literature review, starting in 2020, using the SciELO, PubMed, Google Scholar, DATASUS databases and the website of the Brazilian Institute of Geography and Statistics (IBGE).   Results: Studies show a higher prevalence of SARS-CoV-2 infection in men, in the age group after the fourth decade of life and among whites.   Discussion: The first studies showed a prevalence of coronavirus infection in males. One of the hypotheses drawn was that men present more cardiopulmonary diseases and smoke more. Another study shows that women's lower susceptibility to infection is due to the X chromosome and sex hormones, which are essential for the innate and adaptive immune response. As for the age group, most studies show a higher prevalence after the fourth decade of life, due to increased expression of angiotensin 2 receptors (ACE2), hormonal changes in aging and associated comorbidities.   Conclusion: Studies show with greater assertiveness a predominance of involvement by COVID-19 in males, individuals from the fourth decade of life and in whites. However, it is important to investigate the epidemiological profile in order to offer better assistance and prevention.

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Franca Rosa Guerini ◽  
Matteo Cesari ◽  
Beatrice Arosio

AbstractThe risk of serious complications and the fatality rate due to COVID-19 pandemic have proven particularly higher in older persons, putting a further strain in healthcare system as we dramatically observed.COVID-19 is not exclusively gerophile (géro “old” and philia “love”) as young people can be infected, even if older people experience more severe symptoms and mortality due to their greater frailty. Indeed, frailty could complicate the course of COVID-19, much more than the number of years lived. As demonstration, there are centenarians showing remarkable capacity to recover after coronavirus infection.We hypothesize that centenarian’s portfolio could help in identifying protective biological mechanisms underlying the coronavirus infection.The human leukocyte antigen (HLA) is one of the major genetic regions associated with human longevity, due to its central role in the development of adaptive immune response and modulation of the individual’s response to life threatening diseases. The HLA locus seems to be crucial in influencing susceptibility and severity of COVID-19.In this hypothesis, we assume that the biological process in which HLA are involved may explain some aspects of coronavirus infection in centenarians, although we cannot rule out other biological mechanisms that these extraordinary persons are able to adopt to cope with the infection.


2006 ◽  
Vol 13 (2-4) ◽  
pp. 109-123 ◽  
Author(s):  
Luis J. Jara ◽  
Carmen Navarro ◽  
Gabriela Medina ◽  
Olga Vera-Lastra ◽  
Francisco Blanco

The relationship between immune-neuroendocrine system is firmly established. The messengers of this connection are hormones, neuropeptides, neurotransmitters and cytokines. The immune-neuroendocrine system have the capacity to synthesize and release these molecules, which, in turn, can stimulate or suppress the activity of immune or neuroendocrine cells by binding to receptors. In fact, hormones, neuropeptides and neurotransmitters participate in innate and adaptive immune response.Autoimmune rheumatic diseases (ARD) are characterized by aberrant production of pro-inflammatory cytokines, which are a potent activator of the HPA axis. In consequence, high levels of pro-inflammatory hormones such as estrogens and prolactin, and low levels of glucocorticoids, an anti-inflammatory hormone, have been described in the active phase of ARD. In addition, high levels of pro-inflammatory hormones and cytokines have also been frequently detected in organ involvement of patients with ARD, suggesting an abnormal local neuroendocrine immune interaction. There is evidence that hormonal changes may appear before the symptomatic phase of the disease. Therefore, it is possible that a pro-inflammatory hormone favors the rupture of tolerance, which is a key feature of autoimmune diseases. The interactions between the immune-neuroendocrine system have a major impact on our understanding of the pathogenic mechanisms, diagnosis and therapy of ARD.


2021 ◽  
Vol 14 (2) ◽  
pp. e240496
Author(s):  
Isabelo Sicsic Jr ◽  
Andres R Chacon ◽  
Moe Zaw ◽  
Kori Ascher ◽  
Alexandre Abreu ◽  
...  

The novel coronavirus (SARS-CoV-2) has produced millions of infections and deaths worldwide. It is believed that adaptive immunity to the virus occurs although with variation in its pattern and duration. While uncommon, confirmed reinfection with the novel coronavirus has been reported. Telemedicine has emerged as a viable tool for the delivery of healthcare in lieu of in-person patient contact. The variable and occasionally rapid course of clinical disease raises safety concerns of using telemedicine in the clinical management of acute infection with the novel coronavirus. We present a case of novel coronavirus infection in an immunocompetent individual with obstructive sleep apnea (OSA) who failed to manifest an adaptive immune response to acute infection and was subsequently reinfected. The case highlights the use of telemedicine in managing novel coronavirus respiratory disease and the potential role of OSA as a disease facilitator.


2021 ◽  
Vol 12 (4) ◽  
pp. 45-57
Author(s):  
O. S. Groznova ◽  
V. A. Warriors ◽  
D. Donich ◽  
V. V. Vetrov ◽  
D. O. Ivanov

COVID-19 infection usually occurs in children in a mild form, but some of them in a delayed period (one or several weeks after acute infection with COVID-19) may develop a severe inflammatory disease with clinical manifestations similar to toxic shock syndrome (Kawasaki disease), classified as multisystem inflammatory syndrome in children (MISC). It is possible that the syndrome has only a temporary connection with the COVID-19 infection. In the future, new associations of such clinical manifestations with other infectious (or non-infectious) diseases may appear. But currently, all children in the described cohorts with MISC have an association with COVID-19 infection. It is believed that the syndrome is initiated by an excessive adaptive immune response with the formation of autoantibodies. Treatment is based on anti-inflammatory, including steroid therapy, the possible use of intravenous immunoglobulin, aspirin, interleukin 1 and 6 receptor antagonists. The article analyzes current views on Kawasaki-multisystem inflammatory syndrome in children in the delayed period of COVID-19 coronavirus infection in the aspects of diagnosis, pathogenesis, clinical manifestations (with a discussion of foreign and Russian studies) and approaches to therapy and possible prevention, including the possibility of using plasmapheresis in complex therapy.


2021 ◽  
Vol 23 (5) ◽  
pp. 1005-1016
Author(s):  
A. A. Artemenkov

The review article analyzes literature data on the issues of immune response dysregulation during aging. It has been shown that impairment of innate and adaptive immune response in elderly and senile people under the conditions of spreading the new coronavirus infection is an aggravating factor in the course of the disease and recovery. Neuro-immuno-endocrine changes occurring in the organs of immune system, immunocompetent cells, molecules and receptor formations involved into the arising immune response have been traced. The imbalance of the brain-intestine-microbiota axis is considered in sufficient details, where a significant role is attributed to the changes occurring in hypothalamic-adrenal system under participation of biogenic neurotransmitters and neuromodulators. It is shown that intestinal microbiota may be involved into the neurodegeneration events, due to toxic effects on the brain via the neuro-immuno-endocrine and metabolic pathways. The data are presented, which show that adrenaline, norepinephrine, dopamine and serotonin are involved in the immune response dysregulation, thus making this process similar to the changes that occur during the general adaptation syndrome and stress response of the body. On the other hand, the review notes that chronic stress during aging not only alters the activity of macrophages, lymphocytes and dendritic cells, but also increases the level of proinflammatory cytokines in blood, thereby affecting permeability of the blood-brain barrier. The article emphasizes that with body aging, a neuroendocrine sensory pathway of immune response dysregulation is gradually formed. In this regard, it is noted that the afferent nerve endings and neurons of the vagus, adrenergic and peptidergic nerves are involved into dysfunction of immune system by affecting the processes occurring not only in thymus, but also in the brain. However, it is obvious that the pathodynamic “dysadapting circuit” formed in the higher compartments of nervous system is also involved in dysregulatory immune responses during aging. Hence, the work concludes that the signaling networks of the body's regulatory systems (nervous, immune and endocrine) are closely interconnected throughout the lifetime, but with aging and penetration of antigens into the body, this interaction is easily disrupted at different levels of organization of living matter, thus leading to dysregulation.


2019 ◽  
Vol 21 (1) ◽  
pp. 7-19 ◽  

Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune responses may be pivotal drivers of AD pathogenesis. We reviewed microglia-related data from postmortem AD studies and examined supporting evidence from AD animal models to answer the following questions: i) What is the temporal sequence of immune activation in AD progression and what is its impact on cognition? ii) Are there discordant, "primed", microglia responses in AD vs successful cognitive aging? iii) Does central nervous system (CNS) repair in aging depend on recruitment of the elements of cellular adaptive immune response such as effector T cells, and can the recruitment of systemic immune cells ameliorate AD neuropathology? iv) How effective are the immune-system-based therapeutic approaches currently employed for the treatment of AD?


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