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DENV immune sera enhances ZIKV infection in primary human macrophages. Human sera containing DENV antibodies (DENV1-4 are serotype confirmed, Col are serotype unknown) or from healthy controls were diluted 1:10 to 1:10,000 and incubated with ZIKV. The sera are described in Table 1. Primary isolated human macrophages were infected either with ZIKV alone or with the ZIKV-sera mixtures. (a) DENV1 antibody-containing sera. (b) DENV2 antibody-containing sera. (c) DENV3 antibody-containing sera. (d) DENV4 antibody-containing sera. (e) DENV-antibody sera from Colombian individual 1. (f) DENV-antibody sera from Colombian individual 2. The infection was measured by qRT-PCR analysis at 48 h postinfection. Technical and biological replicates were done in triplicate. The data are pooled, and the error bars indicate standard deviation. Student's t-test and ANOVA were used for the statistical analysis. * P < 0.001. This figure has been modified from Londono-Renteria et al. 8 . Please click here to view a larger version of this figure.
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The recent emergence of the flavivirus Zika and neurological complications, such as Guillain-Barré syndrome and microcephaly in infants, has brought serious public safety concerns. Among the risk factors, antibody-dependent enhancement (ADE) poses the most significant threat, as the recent re-emergence of the Zika virus (ZIKV) is primarily in areas...
Citations
... A partial protective vaccine may also prime the immune system in some individuals that can mount a strong inflammatory response when infected, leading to enhanced severe symptoms. Another related possibility is ADE that was observed in various viral infections, including Dengue virus (Waggoner et al., 2020), influenza (Winarski et al., 2019), Zika virus (Asad et al., 2019), coronavirus (Negro, 2020;Wan et al., 2020), and Acinetobacter baumannii bacteria (Wang-Lin et al., 2019). ADE is a well-known mechanism that viruses or bacteria may infect susceptible cells by interacting with antibodies or complement components (Fc or complement receptors), leading to enhanced viral entry into host cells and/or higher replication rate. ...
Malaria is the most deadly parasitic disease, affecting hundreds of millions of people worldwide. Malaria parasites have been associated with their hosts for millions of years. During the long history of host-parasite co-evolution, both parasites and hosts have applied pressure on each other through complex host-parasite molecular interactions. Whereas the hosts activate various immune mechanisms to remove parasites during an infection, the parasites attempt to evade host immunity by diversifying their genome and switching expression of targets of the host immune system. Human intervention to control the disease such as antimalarial drugs and vaccination can greatly alter parasite population dynamics and evolution, particularly the massive applications of antimalarial drugs in recent human history. Vaccination is likely the best method to prevent the disease; however, a partially protective vaccine may have unwanted consequences that require further investigation. Studies of host-parasite interactions and co-evolution will provide important information for designing safe and effective vaccines and for preventing drug resistance. In this essay, we will discuss some interesting molecules involved in host-parasite interactions, including important parasite antigens. We also discuss subjects relevant to drug and vaccine development and some approaches for studying host-parasite interactions.
