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Abstract

Rubella virus (RV) causes severe congenital defects when acquired during the first trimester of pregnancy. RV cytopathic effect has been shown to be due to caspase-dependent apoptosis in a number of susceptible cell lines, and it has been suggested that this apoptotic induction could be a causal factor in the development of such defects. Often the outcome of apoptotic stimuli is dependent on apoptotic, proliferative and survival signaling mechanisms in the cell. Therefore we investigated the role of phosphoinositide 3-kinase (PI3K)-Akt survival signaling and Ras-Raf-MEK-ERK proliferative signaling during RV-induced apoptosis in RK13 cells. Increasing levels of phosphorylated ERK, Akt and GSK3β were detected from 24-96 hours post-infection, concomitant with RV-induced apoptotic signals. Inhibition of PI3K-Akt signaling reduced cell viability, and increased the speed and magnitude of RV-induced apoptosis, suggesting that this pathway contributes to cell survival during RV infection. In contrast, inhibition of the Ras-Raf-MEK-ERK pathway impaired RV replication and growth and reduced RV-induced apoptosis, suggesting that the normal cellular growth is required for efficient virus production.

Co-Infection of the Hepatitis C Virus With Other Blood-Borne and Hepatotropic Viruses Among Hemophilia Patients in Poland

“…Inactive carriers represent the largest group of chronic HBV-infected patients. This condition is diagnosed according to the lack of HBeAg and the presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based tests, normal ALT levels, and minimal or no necroinflammation, minor fibrosis, or even normal histology on biopsy (32, 33). …”

Prior Corneal Scarification and Injection of Immune Serum are Not Required Before Ocular HSV-1 Infection for UV-B-Induced Virus Reactivation and Recurrent Herpetic Corneal Disease in Latently Infected Mice

“…21,55,56 Despite evidence that clinical recurrent HSK is due to virus reactivation from latency, 57,58 most pre-clinical animal studies investigating the immune mechanisms that orchestrate recurrent HSK have used primary acute infection of mice, 59–66 because spontaneous HSV-1 reactivation, virus shedding in tears, and recurrent HSK either does not occur at all or occurs at very low levels in mice. 16,17 Only a handful of pre-clinical studies have employed a mouse model of induced recurrent herpetic corneal disease. 21,56,67 …”

“…9,12,15 However, in contrast to humans, recurrent HSV shedding and recurrent herpetic disease does not occur in mice because HSV spontaneous reactivation is either extremely rare or does not occur. 16,17 Thus, studying mechanisms that control HSV-1 reactivation and recurrent herpetic eye disease in mice requires a clinically reliable method of inducing viral reactivation that leads to HSK in a significant proportion of eyes. 18–23 Euthanizing the mouse and removing and explanting latently infected TG into tissue culture media is a commonly used method of inducing reactivation of HSV-1, but this has the obvious disadvantage of being an ex vivo system with no possibility of determining virus shedding and recurrent eye disease.…”

Nerve Growth Factor Withdrawal-mediated Apoptosis in Naïve and Differentiated PC12 Cells through p53/Caspase-3-dependent and -independent Pathways

“…Because programmed cell death follows an orchestrated sequence of events, temporal markers of apoptosis occur in stages (45,46). Early apoptosis coincides with subtle membrane disruptions, leading to a change of topology in the bilayer, so that phosphatidylserines that mostly reside in the cytoplasmic leaflet can also be detected in the outer leaflet (47).…”