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Home / NewTech / "Koala AIDS" research shows that genome development is in action – Technology News, Firstpost

"Koala AIDS" research shows that genome development is in action – Technology News, Firstpost



Wild Koalas afflicted with a deadly retrovirus fight the disease on a genetic level.

The KoRV-A retrovirus infected the marsupial for the first time from hundreds to thousands of years ago, from northern Australia and into southern expansion, and may have its origins in bats.

It is linked to the koala immune system Deficiency syndrome (KIDS) is similar to AIDS in humans, but is less potent than AIDS and makes the animals susceptible to deadly cancers and secondary infections such as chlamydia, rendering them infertile.

<img class = "size-full wp-image-7481981" src = "https://images.firstpost.com/wp-content/uploads/2019/10/david-clode-CIMk0FSOrAE-unsplash.jpg" alt = "Koala AIDS research shows that genome evolution is in action [19659007] A koala hangs on a tree.

It is feared that these unfortunate events, if uncontrolled, ultimately lead to death

Retroviruses work by inserting their genome into a host genome, but unlike HIV, KoRV-A also enters the germ cells of the animal, producing sperm and eggs, meaning that it has been passed down through generations

Such pathogenic infections of germ cells are very rare, but recent research suggests they are a major driver Evolution: The last time that it took place in our human ancestors was three million years ago, and a whopping eight percent our genome comes from old n viruses.

Sometimes the viruses are co-opted for useful purposes, including the development of the placenta in our ancestors of mammals about 100 million years ago.

In a new article that was published Thursday in the journal Cell a team of scientists from the University of Massachusetts Medical School and the University of New York has published a report Queensland revealed a kind of "genome immunity "in newly infected koalas.

This contrasts with fighting the infection by the immune system, as animals normally fight disease.

Their findings suggest that germ cells recognize a major step in the viral life cycle and turn it against the intruder to suppress genome infection by detecting the difference between their own cells and the virus.

"And it seems to work, but not very well," said William Theurkauf of UMass Medical School and the newspaper's lead author to AFP.

A first answer

Theurkauf drew the analogy of a man who has contracted the flu: they will feel themselves ill as their body struggles against the disease. Without the initial immune response, all infections would eventually lead to death.

A second reaction phase, in which specialized small ribonucleic acids (RNAs) develop, plays a crucial regulatory role in various processes and is produced to eliminate the virus.

  A mother koala cuddles with her baby.

A koala mother cuddles with her baby.

"So we see the first reaction," said Theurkauf. "The question is, can we find koalas that have turned on in the next phase, in which they really shut it down?"
It is unclear whether this has already happened in some Koalas or, if not, how long it will take the way to develop the reaction. Otherwise, the virus could be "a mechanism of extinction," he added.

The northern population that first became infected is the most likely, and the team plans to investigate it next.

People might one day intervene to accelerate evolution through genetic engineering instead of waiting for the koalas to get there by themselves – even though science is still a long way off.

In the meantime, however, koalas are a living example of "something that every organism on the planet has gone through," said co-author Zhiping Weng, also at UMass Medical School.

"Animals are infected by retroviruses that invade the germ line cells, which multiply and proliferate in the chromosomes, altering the organization and function of the host genome, and continuing the process until the intruder is tamed by the host," he said Weng. "At the end of this infection cycle, the host has changed."

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