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BackgroundAt the beginning of 2020, SARS-CoV-2 spread to all continents, and since then, mutations have appeared in different regions of the world. The appearance of more virulent mutations leads to asseverate that they are also more transmissible. We analyzed the lower and higher virulent SARS-CoV-2 epidemics to establish a relationship between transmissibility and virulence based on a mathematical model.MethodsA compartmental mathematical model based on the CoViD-19 natural history encompassing the age-dependent fatality was applied to evaluate the SARS-CoV-2 transmissibility and virulence. The transmissibility was measured by the basic reproduction number R0 and the virulence by the proportion of asymptomatic individuals. The model parameters were fitted considering the observed data from São Paulo State.ResultsThe numbers of severe CoViD-19 and deaths are three times higher, but R0 is 25% lower in more virulent SARS-CoV-2 transmission than in a less virulent one. However, the number of more virulent SARS-CoV-2 transmitting individuals is 25% lower, mainly due to symptomatic individuals’ isolation, explaining the increased transmission in lower virulence.ConclusionsThe quarantine study in São Paulo State showed that the more virulent SARS-CoV-2 resulted in a higher number of fatalities but less transmissible than the less virulent one. One possible explanation for the number of deaths surpassing that predicted by the low virulent SARS-CoV-2 infection could be the transmission of more virulent variant(s).

Background: The continuous SARS-CoV-2 transmission in several countries could contribute to the mutations' appearance. The circulation of more virulent variants may increase the number of severe CoViD-19 needing hospital care and fatalities hugely. Methods: The partial quarantine in São Paulo State and further relaxation associated with the mutations are explained by a mathematical model based on the CoViD-19 natural history encompassing the age-dependent fatality. The model parameters were fitted considering the observed data from São Paulo State. Results: The partial quarantine was explained by the less virulent SARS-CoV-2 transmission, but the relaxation alone could not explain the epidemic observed in São Paulo State. However, more virulent variants plus the transmission among isolated individuals explained the increased CoViD-19 fatalities. Conclusions: The model described the CoViD-19 epidemic in São Paulo State by considering the partial quarantine, relaxation and mutations. The model provided a potential epidemiological scenario in the absence of mass vaccination.

ABSTRACT. The aim of this study was to investigate the effect of leukocyte filtration on the P-selectin (CD62P) surface expression of apheresis platelets during the retention period. Ten bags of apheresis platelets stored for 1 day (0-24 h) and 10 bags of apheresis platelets stored for 2 days (24-48 h) were used for leukocyte filtration (experimental group). Ten bags of apheresis platelets with the corresponding retention periods but without filtration were used as a negative control (control group). Thereafter, 100 μL of platelet suspensions from apheresis platelets with or without leukocyte filtration were sampled before and after leukocyte filtration for the detection of CD62P surface expression by flow cytometry. No statistical difference in the CD62P (2015) surface expression of apheresis platelets was observed before and after leukocyte filtration (P > 0.05), neither did the CD62P surface expression exhibit any change among the different retention periods. Leukocyte filtration does not affect the CD62P surface expression of apheresis platelets stored for up to 2 days, which indicates that leukocyte filtration does not damage the activation of apheresis platelets within the retention period.

Platelets have been seen traditionally as fragments of blood mediating coagulation. However, evidence during malaria infection suggests that platelets also act against merozoites, an infectious form of malaria in the bloodstream, and megakaryocytes can release giant platelets with a larger volume than normal platelets. We propose a mathematical model to study the interaction between red blood cells, merozoites, and platelets during malaria infection. We analyzed two cases of the interaction of platelets with malaria infection. In the first one, we considered the isolated action of normal platelets and, in the second one, the joint antiparasitic action of both normal and giant platelets. Numerical simulations were performed to evaluate the stability of the equilibrium points of the system of equations. The model showed that the isolated antiparasitic action of normal platelets corroborates malaria infection control. However, the system can converge to a presence-merozoite equilibrium point, or an oscillatory behavior may appear. The joint antiparasitic action of both normal and giant platelets eliminated the oscillatory behavior and drove the dynamics to converge to lower parasitic concentration than the case of isolated action of normal platelets. Moreover, the joint antiparasitic action of platelets proved more easily capable of eliminating the infection.