The public health response to coronavirus disease 2019 in China has illustrated that it is possible to contain COVID-19 if governments focus on tried and tested public health outbreak responses. 1,2 Isolation, quarantine, social distancing, and community containment measures were rapidly implemented. In China, patients with COVID-19 were immediately isolated in designated existing hospitals, and new hospitals were rapidly built to manage the increasing numbers of cases in the most affected areas. Home quarantine for contacts was initiated and large gatherings were canceled. Additionally, community containment for approximately 40 million to 60 million residents was instituted. A significant positive association between the incidence of COVID-19 cases and mortality was apparent in the Chinese response. 3 That is, the rapid escalation in the number of infections in China had resulted in insufficient health care resources, followed by an increase in mortality.The association of mortality with health care resources should provide guidance for resource-limited regions on how and when to prepare for possible local outbreaks. 3 In addition, lessons learned from the 2003 severe acute respiratory syndrome coronavirus (SARS-CoV) outbreak geared toward strengthening of public health systems will be helpful.
COVID-19 Preparedness in AfricaLeaders have 2 important responsibilities in times of crisis: to solve the immediate problem and keep it from happening again. 4 An African task force for coronavirus preparedness and response (AFTCOR) has been established,
van der Geest-Blankert Nannet , Wertheim Heiman . Strong associations and moderate predictive value of early symptoms for SARS-CoV-2 test positivity among healthcare workers, the Netherlands, March 2020. Euro Surveill. 2020;25(16):pii=2000508. https://doi.
Background
Excessive activation of immune responses in coronavirus disease 2019 (COVID-19) is considered to be related to disease severity, complications and mortality. The complement system is an important component of innate immunity and can stimulate inflammation, but its role in COVID-19 is unknown.
Methods
A prospective, longitudinal, single center study was performed in hospitalized COVID-19 patients. Plasma concentrations of complement factors C3a, C3c, and terminal complement complex (TCC) were assessed at baseline and during hospital admission. In parallel, routine laboratory and clinical parameters were collected from medical files and analyzed.
Results
Complement factors C3a, C3c and TCC were significantly increased in plasma of COVID-19 patients compared to healthy controls (p<0.05). These complement factors were especially elevated in ICU patients during the entire disease course (p<0.005 for C3a and TCC). More intense complement activation was observed in patients that deceased and in patients with thromboembolic events.
Conclusions
COVID-19 patients demonstrate activation of the complement system, which is related to disease severity. This pathway may be involved in the dysregulated pro-inflammatory response associated with increased mortality and thromboembolic complications. Components of the complement system might have potential as prognostic markers for disease severity and as therapeutic targets in COVID-19.
NK cells are rapid IFN‐γ responders to Plasmodium falciparum‐infected erythrocytes (PfRBC) in vitro and are involved in controlling early parasitaemia in murine models, yet little is known about their contribution to immune responses following malaria infection in humans. Here, we studied the dynamics of and requirements for in vitro NK responses to PfRBC in malaria‐naïve volunteers undergoing a single experimental malaria infection under highly controlled circumstances, and in naturally exposed individuals. NK‐specific IFN‐γ responses to PfRBC following exposure resembled an immunological recall pattern and were tightly correlated with T‐cell responses. However, although PBMC depleted of CD56+ cells retained 20–55% of their total IFN‐γ response to PfRBC, depletion of CD3+ cells completely abrogated the ability of remaining PBMC, including NK cells, to produce IFN‐γ. Although NK responses to PfRBC were partially dependent on endogenous IL‐2 signaling and could be augmented by exogenous IL‐2 in whole PBMC populations, this factor alone was insufficient to rescue NK responses in the absence of T cells. Thus, NK cells make a significant contribution to total IFN‐γ production in response to PfRBC as a consequence of their dependency on (memory) T‐cell help, with likely positive implications for malaria vaccine development.
These results underscore the value of early IFN-gamma responses to P. falciparum as a correlate of anti-parasite immunity, not only in this setting but also in the wider context of malaria, and support the development of malaria vaccines aimed at inducing such responses.
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