Mitochondria Dump Their Rubbish DNA, And It Could Be Costing Us Our Health

Researchers have discovered a key molecular process that may contribute to chronic inflammation as we age. If this process can be accurately targeted, it could unlock ways to stay healthier in our later years.

The discovery centers on the unique strands of DNA contained within our mitochondria, the power stations of our cells. By banishing their 'mtDNA' into the surrounding cytoplasm, mitochondria can cause inflammation. Yet just how or why this happens has never been well understood.

In this study, researchers led by a team from the Max Planck Institute for Biology of Ageing in Germany analyzed tissue samples from humans and test animals, using mice genetically engineered to be models of aging and disease.

Researchers have discovered a key molecular process that may contribute to chronic inflammation as we age. If this process can be accurately targeted, it could unlock ways to stay healthier in our later years.

The discovery centers on the unique strands of DNA contained within our mitochondria, the power stations of our cells. By banishing their 'mtDNA' into the surrounding cytoplasm, mitochondria can cause inflammation. Yet just how or why this happens has never been well understood.

In this study, researchers led by a team from the Max Planck Institute for Biology of Ageing in Germany analyzed tissue samples from humans and test animals, using mice genetically engineered to be models of aging and disease.

Past research has shown that deoxyribonucleotides become less abundant as we grow older, meaning there are fewer genetic building blocks in older cells and in tissues that are senescent, or effectively retired from active duty.

This latest investigation reveals that a lack of these building blocks causes mtDNA to pick up ribonucleotides instead, which may explain why mitochondria reject 'imperfect' copies of this molecule.

That rejection is potentially one of the key drivers behind the inflammation that comes with old age, and the negative health consequences associated with it – from certain types of cancer to neurodegenerative diseases like Alzheimer's.

 

This is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.   

https://gscrochetdesigns.blogspot.com. one can see my crochet creations  

https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes    

https://kneereplacement-stickclub.blogspot.com. for info on knee replacement

https://GSiyers home remedies.blogspot.com   is the latest addition to my blogs

 

Protein that helps HIV to evade the body's defence system discovered

Researchers have discovered the protein that helps HIV to evade the body's defense system, an advance that may help stop the deadly virus in its tracks.

When HIV-1 infects an immune cell, the virus travels to the nucleus so quickly there is not enough time to set off the cells alarm system.

Now, researchers  have discovered the protein that helps the virus travel so fast.

The researchers found that without this protein, the virus became stranded in the cytoplasm, where it was detected by the viral defense system.

"By preventing its normal movement, we essentially turned HIV-1 into a sitting duck for cellular sensors," said  an associate professor.

HIV-1 infects and kills immune system cells, including T cells and macrophages that were used in the study.

This cripples the immune system, making the patient vulnerable to common bacteria, viruses and other pathogens that are usually harmless in people with healthy immune systems.

After HIV-1 enters a cell, it has to work its way through the cytoplasm to the nucleus. Once inside the nucleus, HIV-1 takes control of the cell and makes additional HIV-1 copies.

However, getting through the cytoplasm is not easy. Cytoplasm consists of fluid that is thick with proteins and structures such as mitochondria.

"Something the size of a virus cannot just diffuse through the cytoplasm," said an author of the study published.

"It would be like trying to float to the bathroom in a very crowded bar. You need to have a plan," said the author.

HIV-1 is able to get to the nucleus quickly via tubular tracks called microtubules. The virus attaches itself to a molecular motor called dynein, which moves down the microtubule like a train car on tracks.

Researchers discovered the "ticket" HIV-1 needs to get on the train - a protein called bicaudal D2.

HIV-1 binds to bicaudal D2, which recruits the dynein molecular motor. The dynein then transports HIV-1 towards the nucleus.

The finding raises the possibility of developing a drug that would prevent HIV-1 from binding to bicaudal D2, thus stranding the virus in the cytoplasm.

This would not only prevent infection, but also give the cell time to turn on antiviral genes that would protect it and neighbouring cells from infection.

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.   

PS- THOSE INTERESTED IN RECIPES ARE FREE TO VIEW MY BLOG-                      

HTTP:GSEASYRECIPES.BLOGSPOT.COM/
FOR INFO ABOUT KNEE REPLACEMENT, YOU CAN VIEW MY BLOG-                                                                       

HTTP://KNEE REPLACEMENT-STICK CLUB.BLOGSPOT.COM/
FOR CROCHET DESIGNS
HTTP://MY CROCHET CREATIONS.BLOGSPOT.COM

Novel approach to track HIV infection

Scientists have developed a novel method of tracking HIV infection, allowing the behavior of individual virions -- infectious particles -- to be connected to infectivity.

The findings could help lead to the development of novel therapies for HIV prevention and treatment by providing a deeper understanding of the mechanisms of HIV's life-cycle.

It has become routine to visualize the movement and progression of individual virions in cells, but the relevance of these observations was previously unclear, as many virions are defective or do not progress to make further copies of themselves.

"This approach -- and the ability to say 'that virion infected that cell' -- will help bring clarity to the field," said principal investigator  a professor of cell and molecular biology. "It allows us to understand what the virus really needs to do to infect a cell. It gives us new details, like where in the cell it happens and the timing of specific events. The more we know about the virus, the better our chances are to stop it."

During the course of infection, HIV fuses onto a target immune cell and delivers its capsid -- a cone that holds the genetic material of the virus -- into the cell's cytoplasm. From there, the capsid disassembles through a process called "uncoating," which is crucial to the synthesis of viral DNA from its RNA genome and the hijacking of the cell's functions.

But the specific details of uncoating have been controversial, with two groups of thought. One believed that uncoating takes place late at pores, allowing factors to enter the nucleus. A second camp showed data suggesting that uncoating takes place early and in the cytoplasm.

In part, the uncertainty persisted because previous methods in HIV research have been unable to distinguish between viral particles that actually lead to infection of the cell, and those that are irrelevant.
In the current study, the team of scientists used a novel live-cell fluorescent imaging system that allowed them for the first time to identify individual particles associated with infection.

In this case, they utilized the approach to monitor how the HIV capsid uncoats in the cell at the individual particle level. They demonstrated that uncoating leading to infection occurs early in the cytoplasm, around 30 minutes after cell fusion.

The finding is just one example of novel discoveries about HIV that might now be possible with the imaging system.

"Being able to connect infectivity of individual particles and how they behave in the cell to infection -- which is what we really care about -- is going to have a big impact on the field," Hope said. "The system can now be used to resolve other controversies in HIV biology and to determine which potential targets for drug development are most relevant."

The study has implications in the wider field of virology research as well.

"Theoretically, you could apply this technique to the study of any fluorescently-tagged virus," explained the first author.

In future projects, the research team plans to continue to leverage the method to study infection in later stages of the HIV lifecycle.

"We want to understand all the details, from when the virus fuses, to the point where it integrates and starts to make new viruses, to the last phase," explained the researcher, also a professor of Obstetrics and Gynecology. "We need to understand what's going on, so we can find the Achilles' heel of the virus and use it as a drug target."

this is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.                                                                                                             https://gscrochetdesigns.blogspot.com. one can see my crochet creations                                   https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes                 https://kneereplacement-stickclub.blogspot.com. for info on knee replacement