Oxidative stress viral infections

Hemolysis is secondary to acute oxidative stress, such as oxidative drugs (primaquine, sulfonamides, anti-TB drugs), and more typically by viral or bacterial infections. 

JNKs can be activated by a large range of different stimuli, including kainic acid [47], microtubule-disrupting agents [48], double-stranded ribonucleic acid (RNA) [49], viral infections [49], tumor necrosis factors, interleukins [50], osmotic stress [51], and trophic factor withdrawal [30]. JNKs have also been reported to be activated by oxidative stress, particularly that induced by ultraviolet radiation [47], hypoxia [52], ischemia [53], hydrogen peroxide [30,54], peroxynitrite [55], malondialdehyde [56], and 4-hydroxynonenal [57]. 

The transcriptional factor NF-kB is a protein complex that controls the transcription of DNA. NF-kB is found in almost all animal cell types and is involved in cellular responses to different stimuli, e.g. stress, cytokines, free radicals, ultraviolet irradiation, oxidized low density lipoprotein (LDL) and bacterial or viral antigens. NF-kB plays a key role in regulating the immune response to infection and is widely used by eukaryotic cells as a regulator of genes that controls cell proliferation and cell survival. Biotin deficiency is associated with increased nuclear translocation of NF-kB, enhancing the transcriptional activity of antiapoptotic genes in human lymphoid cells (Rodriguez-Melendez et al. 2004). 

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