The life cycle of Plasmodium falciparum is very complex, with an erythrocytic stage that involves the invasion of red blood cells and the survival and growth of the parasite within the host. Over the past several decades, numbers of studies have shown that proteins exported by P. falciparum to the surface of infected red blood cells play a critical role in recognition and interaction with host receptors and are thus essential for the completion of the life cycle of P. falciparum. However, little is known about long noncoding RNAs (lncRNAs). In this study, we designed a computational pipeline to identify new lncRNAs of P. falciparum from published RNA-seq data and analyzed their sequences and expression features. As a result, 164 novel lncRNAs were found. The sequences and expression features of P. falciparum lncRNAs were similar to those of humans and mice: there was a lack of sequence conservation, low expression levels, and high expression coefficient of variance and co-expression with nearby coding sequences in the genome. Next, a coding/noncoding gene co-expression network for P. falciparum was constructed to further annotate the functions of novel and known lncRNAs. In total, the functions of 69 lncRNAs, including 44 novel lncRNAs, were annotated. The main functions of the lncRNAs included metabolic processes, biosynthetic processes, regulation of biological processes, establishment of localization, catabolic processes, cellular component organization, and interspecies interactions between organisms. Our results will provide clues to further the investigation of interactions between human hosts and parasites and the mechanisms of P. falciparum infection.
In this study, the effects of wild-type and deletion mutant hepatitis C virus (HCV) core proteins on the induction of immune responses in BALB/c mice were assessed. p2HA-C145-S23, encoding a core protein with the C-terminal 46 amino acids truncated, significantly produced stronger antibody and cellular responses than p2HA-C191-S23. The induction of immune responses by p2HA-C145-S23 was dose dependent. However, increasing the doses or repeated administration did not enhance immune responses by the wild-type core protein. In addition, p2HA-C191-S23 was apparently able to interfere with the priming of specific immune responses by p2HA-C145-S23 when the two were coadministered. These results demonstrated that the wild-type HCV core protein itself could inhibit the priming of immune responses in the course of a DNA vaccination, whereas the truncated HCV core protein could provide potential applications for the development of DNA-and peptide-based HCV vaccines.
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