A man from London has become the second person in the world to be cured of HIV, doctors say.
Adam Castillejo is still free of the virus more than 30 months after stopping anti-retroviral therapy, reports BBC.
He was not cured by the HIV drugs, however, but by a stem-cell treatment he received for a cancer he also had, the Lancet HIV journal reports.
The donors of those stem cells have an uncommon gene that gives them, and now Mr Castillejo, protection against HIV.
In 2011, Timothy Brown, the "Berlin Patient" became the first person reported as cured of HIV, three and half years after having similar treatment.
What is the treatment?
Stem-cell transplants appear to stop the virus being able to replicate inside the body by replacing the patient's own immune cells with donor ones that resist HIV infection.
Adam Castillejo - the now 40-year-old "London Patient" who has decided to go public with his identity - has no detectable active HIV infection in his blood, semen or tissues, his doctors say.
It is now a year after they first announced he was clear of the virus and he still remains free of HIV.
Lead researcher Prof Ravindra Kumar Gupta, from the University of Cambridge, told BBC News: "This represents HIV cure with almost certainty.
"We have now had two and a half years with anti-retroviral-free remission.
"Our findings show that the success of stem-cell transplantation as a cure for HIV, first reported nine years ago in the Berlin Patient, can be replicated."
But it will not be a treatment for the millions of people around the world living with HIV.
The aggressive therapy was primarily used to treat the patients' cancers, not their HIV.
And current HIV drugs remain very effective, meaning people with the virus can live long and healthy lives.
Prof Gupta said: "It is important to note that this curative treatment is high-risk and only used as a last resort for patients with HIV who also have life-threatening haematological malignancies.
"Therefore, this is not a treatment that would be offered widely to patients with HIV who are on successful anti-retroviral treatment."
But it might offer hope of finding a cure, in the future, using gene therapy.
How does it work?
CCR5 is the most commonly used receptor by HIV-1 - the virus strain of HIV that dominates around the world - to enter cells.
But a very small number of people who are resistant to HIV have two mutated copies of the CCR5 receptor.
This means the virus cannot penetrate cells in the body it normally infects.
Researchers say it may be possible to use gene therapy to target the CCR5 receptor in people with HIV.
It is the same receptor the now jailed Chinese scientist He Jiankui worked on when he created the world's first gene-edited babies.
Is it a permanent cure?
The tests suggest 99% of Mr Castillejo's immune cells have been replaced by donor ones.
But he still has remnants of the virus in his body, as does Mr Brown.
And it is impossible to say with absolute certainty his HIV will never come back.
Mr Castillejo told the New York Times: "This is a unique position to be in, a unique and very humbling position.
"I want to be an ambassador of hope.
"I don't want people to think, 'Oh, you've been chosen.'
"No, it just happened.
"I was in the right place, probably at the right time, when it happened."
Prof Sharon Lewin, from the University of Melbourne, Australia, said: "Given the large number of cells sampled here and the absence of any intact virus, is the London Patient truly cured?
"The additional data provided in this follow-up case report is certainly encouraging but unfortunately, in the end, only time will tell."
Australian researchers on Friday said they have replicated a crucial brain process that pointed to a potential pathway in slowing the development of Alzheimer's disease.
Overcoming the loss of a process in the brain called "RNA editing" may slow the progress of the major neurological condition and other synaptic disorders, the University of Technology Sydney said in a statement late Friday.
"RNA editing" is a genetic mechanism that modifies proteins essential in the connection between brain nerve cells called synapses, it said. RNA editing is deregulated in the brains of Alzheimer's disease patients, but whether that can cause disease is unknown.
University researchers "replicated this deregulated process in the brains of mice, and discovered it led to the loss of synapses, as occurs in Alzheimer's". Alzheimer's is a progressive, irreversible neurological disorder and the most common form of dementia, with most patients older than 65.
"Understanding mechanisms leading to synapses loss is essential to understand how patients suffering from Alzheimer's disease start losing their memory capacities and how to prevent this from happening," said Professor Bryce Vissel, senior author of the findings published in scientific journal Molecular Brain.
"Our study is extremely important because we now have shown a mechanism that can lead to loss of synapses as occurs in Alzheimer's disease."
Dr Gary Morris, a scientist who contributed to the study, said that because "synapses are important for learning, the loss of these synapses leads to memory loss".
"Our study suggests that if we can overcome the loss of RNA editing in the brain, we may potentially be able to slow the disease."
Vissel said the researchers' next step is "to see if they can rescue synapses and memory deficits in Alzheimer's disease by overcoming the loss of RNA editing in the Alzheimer's brain".
"We have good reason to think that this could ultimately be a highly beneficial approach for solving Alzheimer's and potentially other neurodegenerative diseases such as Parkinson's," Vissel said.
A newly-discovered part of our immune system could be harnessed to treat all cancers, say scientists and reports BBC.
The Cardiff University team discovered a method of killing prostate, breast, lung and other cancers in lab tests.
The findings, published in Nature Immunology, have not been tested in patients, but the researchers say they have "enormous potential".
Experts said that although the work was still at an early stage, it was very exciting.
What have they found?
Our immune system is our body's natural defence against infection, but it also attacks cancerous cells.
The scientists were looking for "unconventional" and previously undiscovered ways the immune system naturally attacks tumours.
What they found was a T-cell inside people's blood. This is an immune cell that can scan the body to assess whether there is a threat that needs to be eliminated.
The difference is this one could attack a wide range of cancers.
"There's a chance here to treat every patient," researcher Prof Andrew Sewell told the BBC.
He added: "Previously nobody believed this could be possible.
"It raises the prospect of a 'one-size-fits-all' cancer treatment, a single type of T-cell that could be capable of destroying many different types of cancers across the population."
How does it work?
T-cells have "receptors" on their surface that allow them to "see" at a chemical level.
The Cardiff team discovered a T-cell and its receptor that could find and kill a wide range of cancerous cells in the lab including lung, skin, blood, colon, breast, bone, prostate, ovarian, kidney and cervical cancer cells.
Crucially, it left normal tissues untouched.
T-cells attack cancer cells
Exactly how it does this is still being explored.
This particular T-cell receptor interacts with a molecule called MR1, which is on the surface of every cell in the human body.
It is thought MR1 is flagging the distorted metabolism going on inside a cancerous cell to the immune system.
"We are the first to describe a T-cell that finds MR1 in cancer cells - that hasn't been done before, this is the first of its kind," research fellow Garry Dolton told the BBC.
Why is this significant?
T-cell cancer therapies already exist and the development of cancer immunotherapy has been one of the most exciting advances in the field.
The most famous example is CAR-T - a living drug made by genetically engineering a patient's T-cells to seek out and destroy cancer.
CAR-T can have dramatic results that transform some patients from being terminally ill to being in complete remission.
However, the approach is highly specific and works in only a limited number of cancers where there is a clear target to train the T-cells to spot.
And it has struggled to have any success in "solid cancers" - those that form tumours rather than blood cancers such as leukaemia.
The researchers say their T-cell receptor could lead to a "universal" cancer treatment.
So how would it work in practice?
The idea is that a blood sample would be taken from a cancer patient.
Their T-cells would be extracted and then genetically modified so they were reprogrammed to make the cancer-finding receptor.
Source: BBC Research
The upgraded cells would be grown in vast quantities in the laboratory and then put back into the patient. It is the same process used to make CAR-T therapies.
However, the research has been tested only in animals and on cells in the laboratory, and more safety checks would be needed before human trials could start.
What do the experts say?
Lucia Mori and Gennaro De Libero, from University of Basel in Switzerland, said the research had "great potential" but was at too early a stage to say it would work in all cancers.
"We are very excited about the immunological functions of this new T-cell population and the potential use of their TCRs in tumour cell therapy," they said.
Daniel Davis, a professor of immunology at the University of Manchester, said: "At the moment, this is very basic research and not close to actual medicines for patients.
"There is no question that it's a very exciting discovery, both for advancing our basic knowledge about the immune system and for the possibility of future new medicines."
Israeli researchers have discovered a method to rejuvenate the kidneys, which has the potential to eliminate the need for dialysis in the future, Israel's Sheba Medical Center said Wednesday.
In a study published in the journal Cell Reports, researchers from the center showed that it is possible to rejuvenate the kidneys and improve their function using the patient's own stem cells.
Previously, it was found that the adult kidney can constantly renew itself over time through the activity of colonies of cells that function to replace lost and degenerated cells in the kidney.
In the current study, the team developed a new technology that allows the extraction of such healthy kidney cells from diseased kidneys.
These cells are expanded into large numbers within a laboratory environment, and by generation of three-dimensional cultures called "kidney spheres", they show improved function to generate new kidney tissue and replace lost cells.
The cells are administered into the kidney, allowing them to rebuild it, positively influence neighboring cells and improve the kidney's function.
Because the newly developed technology relies on the patient's own cells, it circumvents problems associated with immune rejection.
This treatment, successfully tested on mice, resulted in improved renal function in the treated mice.
The results are expected to be further studied in clinical trials in patients with renal failure.
Researchers from Australia's national science body have successfully genetically engineered mosquitoes that are resistant to spreading dengue virus.
The Commonwealth Scientific and Industrial Research Organisation (CSIRO) on Friday revealed that it has engineered the first breed of mosquitoes resistant to spreading all four types of the dengue virus.
Dengue fever is a mosquito-borne disease caused by the dengue virus. It affects 390 million people every year around the world and can cause death if left untreated, according to CSIRO.
Prasad Paradkar, a Senior Research Scientist with the CSIRO, said that the disease is at epidemic levels in tropical and subtropical regions worldwide, with outbreaks currently occurring in Bangladesh, Pakistan, Sri Lanka and the Philippines.
"There is a pressing global demand for effective strategies to control the mosquitoes that spread the dengue virus, as there are currently no known treatments and the vaccine that is available is only partially effective," he said in a media release.
"In this study we used recent advances in genetic engineering technologies to successfully genetically modify a mosquito, the Aedes aegypti, with reduced ability to acquire and transmit the dengue virus.
"This is the first engineered approach that targets all four dengue types, which is crucial for effective disease suppression."
According to the CSIRO more than half the world's population is at risk of infection and the disease currently costs the global economy 40 billion Australian dollars (27.5 billion U.S. dollars) every year.
The CSIRO collaborated with Omar Akbari from the University of California San Diego on the landmark breakthrough.
"This breakthrough work also has the potential to have broader impacts on controlling other mosquito-transmitted viruses," Akbari said.
"We are already in the early stages of testing methods to simultaneously neutralise mosquitoes against dengue and a suite of other viruses such as Zika, yellow fever and chikungunya."