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Register a new userDoes blood type affect the COVID-19 infection pattern?
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Among the many aspects that characterize the COVID-19 pandemic, two seem particularly challenging to understand: (i) the great geographical differences in the degree of virus contagiousness and lethality which were found in the different phases of the epidemic progression, and (ii) the potential role of the infected peoples blood type in both the virus infectivity and the progression of the disease. A recent hypothesis could shed some light on both aspects. Specifically, it has been proposed that in the subject-to-subject transfer SARS-CoV-2 conserves on its capsid the erythrocytes antigens of the source subject. Thus these conserved antigens can potentially cause an immune reaction in a receiving subject that has previously acquired specific antibodies for the source subject antigens. This hypothesis implies a blood type-dependent infection rate. The strong geographical dependence of the blood type distribution could be, therefore, one of the factors at the origin of the observed heterogeneity in the epidemics spread. Here, we present an epidemiological deterministic model where the infection rules based on blood types are taken into account and compare our model outcomes with the exiting worldwide infection progression data. We found an overall good agreement, which strengthens the hypothesis that blood types do play a role in the COVID-19 infection.
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Some ideas are presented about the physical motivation of the apparent capacity of generalized logistic equations to describe the outbreak of the COVID-19 infection, and in general of quite many other epidemics. The main focuses here are: the complex, possibly fractal, structure of the locus describing the contagion event set; what can be learnt from the models of trophic webs with herd behaviour.
We present a robust data-driven machine learning analysis of the COVID-19 pandemic from its early infection dynamics, specifically infection counts over time. The goal is to extract actionable public health insights. These insights include the infectious force, the rate of a mild infection becoming serious, estimates for asymtomatic infections and predictions of new infections over time. We focus on USA data starting from the first confirmed infection on January 20 2020. Our methods reveal significant asymptomatic (hidden) infection, a lag of about 10 days, and we quantitatively confirm that the infectious force is strong with about a 0.14% transition from mild to serious infection. Our methods are efficient, robust and general, being agnostic to the specific virus and applicable to different populations or cohorts.
SARS-CoV-2 has disrupted the life of billions of people around the world since the first outbreak was officially declared in China at the beginning of 2020. Yet, important questions such as how deadly it is or its degree of spread within different countries remain unanswered. In this work, we exploit the `universal growth of the mortality rate with age observed in different countries since the beginning of their respective outbreaks, combined with the results of the antibody prevalence tests in the population of Spain, to unveil both unknowns. We validate these results with an analogous antibody rate survey in the canton of Geneva, Switzerland. We also argue that the official number of deaths over 70 years old is importantly underestimated in most of the countries, and we use the comparison between the official records with the number of deaths mentioning COVID-19 in the death certificates to quantify by how much. Using this information, we estimate the fatality infection ratio (IFR) for the different age segments and the fraction of the population infected in different countries assuming a uniform exposure to the virus in all age segments. We also give estimations for the non-uniform IFR using the sero-epidemiological results of Spain, showing a very similar growth of the fatality ratio with age. Only for Spain, we estimate the probability (if infected) of being identified as a case, being hospitalized or admitted in the intensive care units as function of age. In general, we observe a nearly exponential growth of the fatality ratio with age, which anticipates large differences in total IFR in countries with different demographic distributions, with numbers that range from 1.82% in Italy, to 0.62% in China or even 0.14% in middle Africa.
In order to analyze the effectiveness of three successive nationwide lockdown enforced in India, we present a data-driven analysis of four key parameters, reducing the transmission rate, restraining the growth rate, flattening the epidemic curve and improving the health care system. These were quantified by the consideration of four different metrics, namely, reproduction rate, growth rate, doubling time and death to recovery ratio. The incidence data of the COVID-19 (during the period of 2nd March 2020 to 31st May 2020) outbreak in India was analyzed for the best fit to the epidemic curve, making use of the exponential growth, the maximum likelihood estimation, sequential Bayesian method and estimation of time-dependent reproduction. The best fit (based on the data considered) was for the time-dependent approach. Accordingly, this approach was used to assess the impact on the effective reproduction rate. The period of pre-lockdown to the end of lockdown 3, saw a $45%$ reduction in the rate of effective reproduction rate. During the same period the growth rate reduced from $393%$ during the pre-lockdown to $33%$ after lockdown 3, accompanied by the average doubling time increasing form $4$-$6$ days to $12$-$14$ days. Finally, the death-to-recovery ratio dropped from $0.28$ (pre-lockdown) to $0.08$ after lockdown 3. In conclusion, all the four metrics considered to assess the effectiveness of the lockdown, exhibited significant favourable changes, from the pre-lockdown period to the end of lockdown 3. Analysis of the data in the post-lockdown period with these metrics will provide greater clarity with regards to the extent of the success of the lockdown.
COVID-19 infections have well described systemic manifestations, especially respiratory problems. There are currently no specific treatments or vaccines against the current strain. With higher case numbers, a range of neurological symptoms are becoming apparent. The mechanisms responsible for these are not well defined, other than those related to hypoxia and microthrombi. We speculate that sustained systemic immune activation seen with SARS-CoV-2 may also cause secondary autoimmune activation in the CNS. Patients with chronic neurological diseases may be at higher risk because of chronic secondary respiratory disease and potentially poor nutritional status. Here, we review the impact of COVID-19 on people with chronic neurological diseases and potential mechanisms. We believe special attention to protecting people with neurodegenerative disease is warranted. We are concerned about a possible delayed pandemic in the form of an increased burden of neurodegenerative disease after acceleration of pathology by systemic COVID-19 infections.
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