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Rotavirus is the main cause of acute diarrhea in children up to five years of age. In this regard, probiotics are commonly used to treat or prevent gastroenteritis including viral infections. The anti-rotavirus effect of Bifidobacterium longum and Chlorella sorokiniana, by reducing viral infectivity and improving IFN-type I response, has been previously reported. The present study aimed to study the effect of B. longum and/or C. sorokiniana on modulating the antiviral cellular immune response mediated by IFN-γ, IL-10, SOCS3, STAT1, and STAT2 genes in rotavirus-infected cells. To determine the mRNA relative expression of these genes, HT-29 cells were treated with B. longum and C. sorokiniana alone or in combination, followed by rotavirus infection. In addition, infected cells were treated with B. longum and/or C. sorokiniana. Cellular RNA was purified, used for cDNA synthesis, and amplified by qPCR. Our results demonstrated that the combination of B. longum and C. sorokiniana stimulates the antiviral cellular immune response by upregulating IFN-γ and may block pro-inflammatory cytokines by upregulating IL-10 and SOCS3. The results of our study indicated that B. longum, C. sorokiniana, or their combination improve antiviral cellular immune response and might modulate pro-inflammatory responses. [ABSTRACT FROM AUTHOR]

Hypoxia-inducible factor -1 (HIF-1) is a transcriptional factor that regulates the expression of several glycolytic genes. The white spot syndrome virus (WSSV) induces a shift in glycolysis that favors viral replication in white shrimp Litopenaeus vannamei. HIF-1 is related to the pathogenesis of the WSSV infection through the induction of metabolic changes in infected white shrimp. Although the WSSV infection is associated with metabolic changes, the role of HIF-1 on key glycolytic genes during the WSSV infection has not been examined. In this work, we evaluated the effect of HIF-1α silencing on expression and activity of glycolytic enzymes (Hexokinase-HK, phosphofructokinase-PFK and pyruvate kinase-PK) along with the glucose transporter 1 (Glut1), regulatory enzymes (glucose-6-phosphate dehydrogenase-G6PDH and pyruvate dehydrogenase-PDH), and metabolic intermediates of glycolysis (glucose-6-phosphate-G6P and pyruvate). The expression of Glut1 increased in each tissue evaluated after WSSV infection, while HK, PFK and PK gene expression and enzyme activities increased in a tissue-specific manner. G6PDH activity increased during WSSV infection, and its substrate G6P decreased, while PDH activity decreased and its substrate pyruvate increased. Silencing of HIF-1α blocked the WSSV-induced Glut1 and glycolytic genes upregulation and enzyme activity in a tissue-specific manner. We conclude that HIF-1 regulates the WSSV-induced glycolysis through induction of glycolytic genes contributing to glucose metabolism in tissues of infected shrimp. Also, the inhibition, and activation of regulatory genes are likely to decrease the availability of the raw materials essential for WSSV replication and increase oxidative metabolism., (Copyright © 2019 Elsevier Ltd. All rights reserved.)