ABSTRACT
OBJECTIVE: We aimed to characterize the temporal variation in coronavirus disease 2019 (COVID-19) infection and mortality as a possible tool to monitor and control the spread of this disease. METHODS: We analyzed cyclicity and synchronicity in cases of COVID-19 infection and time series of deaths using Fourier transform, its inverse method, and statistical treatments. Epidemiological indices (e.g., case fatality rate) were used to quantify the observations in the time series. The possible causes of short-term variations are reviewed. RESULTS: We observed that were both short-term and long-term variations in the COVID-19 time series. The short cycles were 7 days and synchronized among all countries. This periodicity is believed to be caused by weekly cycles in community social factors, combined with diagnostic and reporting cycles. This could also be related to virus-host-community dynamics. CONCLUSION: The observed synchronized weekly cycles could serve as herd defense by providing a form of social distancing in time. The effect of such temporal distancing could be enhanced if combined with spatial distancing. Integrated spatiotemporal distancing is therefore recommended to optimize infection control strategies, taking into account the quiescent and active intervals of COVID-19.
Subject(s)
COVID-19 , Humans , Infection Control , Physical Distancing , SARS-CoV-2ABSTRACT
OBJECTIVE: Coronavirus disease 2019 (COVID-19) shows a wide range of severity, ranging from an asymptomatic presentation to a severe illness requiring intensive care unit admission. Identification of a strategy to manage the severity of this disease will not only help to reduce its case fatality but also help to remove some of the burden from the already overwhelmed health care systems. While successful management of symptoms in general is important, identifying measures to modify the severity of the illness is a key factor in the fight against this pandemic. METHODS: This paper presents a short literature review to suggest a new treatment modality for COVID-19. RESULTS: COVID-19 is less severe and rarely fatal in children than in adults, which could be caused by greater fluctuations of plasma epinephrine in children. Our literature survey endorses this hypothesis according to both the epidemiological and immunological findings. CONCLUSION: Application of epinephrine pulses with a specific amplitude may be considered an intervention to minimize the severity of COVID-19.
Subject(s)
CD8-Positive T-Lymphocytes/drug effects , Circadian Rhythm/drug effects , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Epinephrine/therapeutic use , Pandemics , Pneumonia, Viral/drug therapy , Pneumonia, Viral/epidemiology , Adult , Age Factors , Asymptomatic Diseases , Biomarkers/blood , CD8-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/virology , COVID-19 , Child , Circadian Rhythm/immunology , Coronavirus Infections/immunology , Coronavirus Infections/virology , Drug Administration Schedule , Epinephrine/blood , Epinephrine/immunology , Humans , Immunity, Innate/drug effects , Models, Immunological , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , Prognosis , Severity of Illness IndexABSTRACT
The concept, molecular self-assembly, has a profoundly novel effect on thoughts and efforts related to medicine and pharmacology. This new style of thinking calls for a range of new researches based on new predictions about disease mechanisms (especially autoimmune diseases, endocrinopathies, and neoplasms) and relevant treatment strategies (superstructural pharmaceuticals). Thanks to this new point of view the most fundamental issue in physiology is the quest of how biological systems exert control on the self-assembly of their components and the most fundamental issue in pathology is the quest of how self-assembly of an undesired superstructure triggers a network of events that result in a particular disease state. Therefore, every disease (infectious or non-infectious) must have a superstructural disease agent (SDA). Sophisticated superstructures like bacteria and viruses are stable and long living and thus infectious but simpler SDAs are unstable and short living thus less infectious. Then we can see how diseases like sarcoidosis, currently classified as non-infectious, are indeed infectious. From this point of view, the fact that one viral infection is protective against a second viral infection can be seen as a superstructural drug that protects against a superstructural disease agent. So it becomes understandable how one opportunistic infection in a late-stage HIV-infected individual may cause de-establishment of HIV-infection in a long-term survivor.