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Efficient mitigation strategies to prevent spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are required before achieving population immunity through vaccines. Inspired by the negatively charged nature of SARS-CoV-2 aerosols, in the present study, we demonstrate a virus blocking textile (VBT) which repulse SARS-CoV-2 respiratory particles based on Coulomb force. Also, we demonstrate that human body triboelectric energy harvesting can be a promising powering source for continuous, highly efficient blocking of VBT. We found that contact and separation between human body and surround materials can generate a peak-to-peak current of 259.6 μA at most and it charges VBT and a 0.25-μF capacitor to 180 V in 134 seconds. Further, through acrylic chamber study which mimics respiratory contact using SARS-CoV-2 aerosols, we found that VBT repulses SARS-CoV-2 aerosols and virus copies in VBT is 13-times reduced. As a result, 99.95% of SARS-CoV-2 is blocked at the flow rate of 0.5 m/s. These findings provide the first technology that prevents spread of virus based on repulsive Coulomb force and triboelectric energy harvesting. Funding Information: This work was financially supported by the Nano Material Technology Development Program (2020M3H4A1A03084600), the Basic Science Research Program (2021R1A2C2010990) and the Bio & Medical Technology Development Program (2021M3A9I2080490) through the National Research Foundation of Korea (NRF) funded by Ministry of Science and ICT. Declaration of Interests: The authors declare no competing interests.

Despite the worldwide effect of the Coronavirus disease 2019 (COVID-19) pandemic, the underlying mechanisms of fatal viral pneumonia remain elusive. Here, we show that critical COVID-19 is associated with enhanced eosinophil-mediated inflammation when compared to non-critical cases. In addition, we confirm increased Th2-biased adaptive immune responses, accompanying overt complement activation, in the critical group. Moreover, enhanced antibody responses and complement activation is associated with disease pathogenesis as evidenced by formation of immune complexes and membrane attack complexes in airways and vasculature of lung biopsies from six fatal cases, as well as by enhanced hallmark gene set signatures of FcγR signaling and complement activation in myeloid cells of respiratory specimens from critical COVID-19 patients. These results suggest that SARS-CoV-2 infection may drive specific innate immune responses, including eosinophil-mediated inflammation, and subsequent pulmonary pathogenesis via enhanced Th2-biased immune responses, which might be crucial drivers of critical disease in COVID-19 patients., Graphical Abstract, Kim et al. find that critical COVID-19 is associated with enhanced eosinophil-mediated inflammation when compared to non-critical cases. Increased Th2-biased immune responses, accompanying overt complement activation, are seen in the critical group. These findings suggest that enhanced eosinophil-mediated inflammation and dysregulated humoral responses might be drivers of severe COVID-19.

Despite the worldwide effect of the Coronavirus disease 2019 (COVID-19) pandemic, the underlying mechanisms of fatal viral pneumonia remain elusive. Here, we conducted kinetic profiling of respiratory leukocytes and associated inflammatory mediators to show that severe COVID-19 is associated with delayed but enhanced eosinophilic inflammation when compared to mild cases. In addition, we confirmed increased Th2-biased adaptive immune responses, accompanying overt complement activation, in the severe group. Moreover, enhanced antibody responses and complement activation was associated with disease pathogenesis as evidenced by formation of immune complexes and membrane attack complexes in airways and vasculature of lung biopsies from a fatal case, as well as by enhanced hallmark gene set signatures of FcgR signaling and complement activation in myeloid cells of respiratory specimens from severe COVID-19 patients. We also observed expression of viral antigen in lung epithelial and endothelial cells without producing viruses during late stage of COVID-19, indicating abortive viral infection which may further fuel antibody responses and aggravate immune-complex-mediated inflammation. These results suggest that SARS-CoV-2 infection may drive scripted specific innate immune responses, including eosinophilic inflammation, and subsequent pulmonary pathogenesis via enhanced Th2-biased immune responses, which might be crucial drivers of severe pneumonia in COVID-19 patients.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne disease caused by SFTS virus (SFTSV) infection. Despite a gradual increase of SFTS cases and high mortality in endemic regions, no specific viral therapy nor vaccine is available. Here, we developed a single recombinant plasmid DNA encoding SFTSV genes, Gn and Gc together with NP-NS fusion antigen, as a vaccine candidate. The viral antigens were fused with Fms-like tyrosine kinase-3 ligand (Flt3L) and IL-12 gene was incorporated into the plasmid to enhance cell-mediated immunity. Vaccination with the DNA provides complete protection of IFNAR KO mice upon lethal SFTSV challenge, whereas immunization with a plasmid without IL-12 gene resulted in partial protection. Since we failed to detect antibodies against surface glycoproteins, Gn and Gc, in the immunized mice, antigen-specific cellular immunity, as confirmed by enhanced antigen-specific T cell responses, might play major role in protection. Finally, we evaluated the degree of protective immunity provided by protein immunization of the individual glycoprotein, Gn or Gc. Although both protein antigens induced a significant level of neutralizing activity against SFTSV, Gn vaccination resulted in relatively higher neutralizing activity and better protection than Gc vaccination. However, both antigens failed to provide complete protection. Given that DNA vaccines have failed to induce sufficient immunogenicity in human trials when compared to protein vaccines, optimal combinations of DNA and protein elements, proper selection of target antigens, and incorporation of efficient adjuvant, need to be further investigated for SFTSV vaccine development., Author summary Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne infection endemic to East Asia including China, Korea, and Japan. Gradual rise of disease incidence and relatively high mortality have become a serious public health problem in the endemic countries. In this study, we developed a recombinant plasmid DNA encoding four antigens, Gn, Gc, NP, and NS, of SFTS virus (SFTSV) as a vaccine candidate. In order to enhance cell-mediated immunity, the viral antigens were fused with Flt3L and IL-12 gene was incorporated into the plasmid. Immunization with the DNA vaccine provides complete protection against lethal SFTSV infection in IFNAR KO mice. Antigen-specific T cell responses might play a major role in the protection since we observed enhanced T cell responses specific to the viral antigens but failed to detect neutralizing antibody in the immunized mice. When we immunized with either viral glycoprotein, Gn protein induced relatively higher neutralizing activity and better protection against SFTSV infection than Gc antigen, but neither generated complete protection. Therefore, an optimal combination of DNA and protein elements, as well as proper selection of target antigens, might be required to produce an effective SFTSV vaccine.

Severe fever with thrombocytopenia syndrome is a tick-borne viral disease, with a high mortality rate that was first reported in China in 2009. Scrub typhus is an acute febrile illness caused by Orientia tsutsugamushi, a bacterium transmitted to humans through chigger mite bites. Severe fever with thrombocytopenia syndrome and scrub typhus are endemic to South Korea. To investigate evidence of severe fever with thrombocytopenia syndrome virus (SFTSV) infection or mixed infection with scrub typhus in South Korea, we examined 2,329 sera samples collected from patients presenting from November 1, 2000, to November 1, 2003, for the diagnosis of rickettisal diseases at Seoul National University, Seoul, South Korea. We found retrospective evidence of SFTSV infection or mixed infection with scrub typhus in South Korea in 2000-2003. Severe fever with thrombocytopenia syndrome virus infections in South Korea occurred before previously reported cases and were more concurrent with those in China. It is important to consider SFTSV infection in patients with scrub typhus.