How Zika virus induces congenital microcephaly

Epidemiological studies show that in utero fetal infection with the Zika virus (ZIKV) may lead to microcephaly, an irreversible congenital malformation of the brain characterized by an incomplete development of the cerebral cortex. However, the mechanism of Zika virus-associated microcephaly remains unclear.

Combined analysis of human fetuses infected with Zika virus, cultures of human neuronal stem cells and mice embryos showed that ZIKV infection of cortical progenitors -stem cells for cortical neurons) controlling neurogenesis triggers stress in the endoplasmic reticulum -where some of the cellular proteins and lipids are synthesized in the embryonic brain, inducing signals in response to incorrect protein conformation.

When it reaches the brain, Zika virus infects neuronal stem cells, which will generate fewer neurons, and by inducing chronic stress in the endoplasmic reticulum, it promotes apoptosis-the early death of these neuronal cells. These two combined mechanisms explain why the cerebral cortex of infected fetuses becomes deficient in neurons and is therefore smaller in size.

 Researchers administered an inhibitors of protein-folding re-sponse in cortical progenitors and found that this inhibited the development of microcephaly in mice embryos infected with Zika virus. The defects observed are specific to an infection by ZIKV, as other neurotropical viruses of the flavivirus family- West Nile virus and yellow fever did not cause microcephaly, in contrast to Zika virus.
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Strong persistence of viral infection

Infections caused by viruses, such as respiratory syncytial virus, measles, parainfluenza and Ebola, are acute. These viruses cause disease quickly and live within a host for a limited time. But in some cases the effects of the infection, and presence of the virus can lead to chronic problems.

Viral infection leads to defective viral genomes, DVG which involved in triggering an immune response, can also kick off a molecular pathway that keeps infected cells alive. The study used a novel technique to examine the presence of DVGs on a cell-by-cell basis to show that DVG-enriched cells had strategies to survive during an immune-system attack.

Partial viral genomes are produced in infected cells when a virus begins to replicate rapidly, leading to defective versions that contain large deletions. DVGs are increasingly believed to be important components of viral infections.

DVGs are critical in stimulating an immune response to respiratory viruses, they are also critical for stimulating an immune response to the human virus RSV, the presence of DVGs in human respiratory samples from infected patients correlates with enhanced antiviral immune responses.

Researchers used a sophisticated technique that allowed them to differentiate full-length genomes from the partial genomes of DVGs at the single-cell level. They studied cells in culture infected with the Sendai virus, or with RSV, a virus that often affects infants and can lead to chronic respiratory problems.

To dig deeper into how the DVGs were influencing the course of infection, the researchers infected cells either with a version of the Sendai virus that lacked DVGs or one enriched in DVGs. The cells infected with the virus high in DVGs survived more than twice as long as those infected with virus lacking DVGs.

 Adding purified DVGs boosted the cells' survival time, indicating a direct role for the DVGs in promoting cell survival.
The results were similar in parallel experiments with RSV, suggesting that the pro-survival role of DVGs held across viral types.

The researchers next were curious to know what molecular pathways might enable the DVG-rich cells to avoid apoptosis. An analysis of highly-expressed genes in DVG-enriched cells compared to the cells with full-length viral genomes revealed that a host of pro-survival genes were activated in the DVG-rich cells.
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Breast milk can kill cancer

Breast milk is being used to fight cancer after scientists discovered it contains a substance that kills tumour cells.

Trials in patients with bladder cancer yielded good results and researchers believe the compound breast milk contains – nicknamed Hamlet – will also help tackle bowel cancer and cervical cancer.

Breast milk is better than chemotherapy because it does not destroy healthy cells. Professor Catharine Svanborg, who made the initial discovery, said ‘There’s something magical about Hamlet’s ability to target tumour cells and kill them.’

Human breast milk contained a protein called alpha-lactalbumin, which is transformed into a cancer-fighting agent when in the gut.

Prof Svanborg, an immunologist at Lund University in Sweden, made the chance discovery that the substance kills tumour cells when working on antibiotics.

New breast milk is a very good source of  antimicrobial agents. During one
experiment we needed human cells and bacteria to be present, and we chose human tumour cells for practical reasons.

‘To our amazement, when we added this compound of milk, the tumour cells died. The substance attacks cancer cells  in numerous ways – first evading the cell’s outer defences, then targeting the ‘power station’ mitochondria and the  nucleus.

These actions cut off the cell’s energy source and ‘programme’ it to commit suicide, in a process called apoptosis.
Early trials in patients with bladder cancer show those injected with Hamlet start shedding dead tumour cells in their urine within days.

Tomato extract prevents gastric cancer

A new study shows that whole tomato extracts from two different Southern Italy cultivars inhibit gastric cancer cell growth.

Gastric cancer developed from the lining of the stomach, common symptoms are: heart burn, nausea and abdominal pain.

Experiments analyzed whole tomato lipophilic extracts for their ability to tackle various neoplastic features of gastric cancer cell lines.

Extracts of both the San Marzano and
Corbarino tomato varieties were able to inhibit the growth and cloning behavior of malignant cells.

Treatment with the whole tomato extracts affected key processes within the cells preventing their migration ability, hindering cell cycle through the modulation of retinoblastoma family proteins and specific cell cycle inhibitors, and inducing cancer cell death through apoptosis.

Gastric cancer is the fourth most common type of cancer worldwide and has been associated with genetic causes, Helicobacter pylori infection, and eating habits, such as consumption of smoked and salted food. Different tomato components have also been analyzed for their ability to counteract tumor growth.