Tag: HIV

A Step Closer to a Once-off Treatment for HIV

HIV invading a human cell
HIV invading a human cell: Credit NIH

Researchers from Tel Aviv University have demonstrated success of a novel technology that may be developed into a one-time vaccine to treat people with HIV and AIDS. Using CRISPR technology, the researchers engineered B cells that in turn stimulate the immune system to produce HIV-neutralising antibodies.

Published in Nature, the study was led by Dr Adi Barzel and PhD student Alessio Nehmad and conducted in collaboration with additional researchers from Israel and the US.

“Based on this study,” said Dr Barzel, “we can expect that over the coming years we will be able to produce a medication for AIDS, additional infectious diseases and certain types of cancer caused by a virus, such as cervical cancer, head and neck cancer and more.”

He explains that the treatment can become a kind of permanent medication, lingering in the body to fight the virus. “We developed an innovative treatment that may defeat the virus with a one-time injection, with the potential of bringing about tremendous improvement in the patients’ condition. When the engineered B cells encounter the virus, the virus stimulates and encourages them to divide, so we are utilising the very cause of the disease to combat it. Furthermore, if the virus changes, the B cells will also change accordingly in order to combat it, so we have created the first medication ever that can evolve in the body and defeat viruses in the ‘arms race’.”

When they mature, the antibody-generating B cells move into the blood and lymphatic system and from there to the different body parts.

Dr Barzel explained: “Until now, only a few scientists, and we among them, had been able to engineer B cells outside of the body. In this study, we were the first to do this within body and then make those cells generate the desired antibodies. The genetic engineering is conducted with viral carriers derived from viruses that were also engineered. We did this to avoid causing any damage, and solely bring the gene coded for the antibody into the B cells in the body.”

“Additionally, in this case we have been able to accurately introduce the antibodies into a desired site in the B cell genome. All lab models that had been administered the treatment responded, and had high quantities of the desired antibody in their blood. We produced the antibody from the blood and made sure it was actually effective in neutralising the HIV virus in the lab dish.”

Source: Tel Aviv University

Innate Immune System Detects HIV-1 with a Two-step Strategy

HIV invading a human cell
HIV invading a human cell: Credit NIH

Scientists have now uncovered how the innate immune system detects even very small amounts of HIV-1. The findings, published in Molecular Cell, reveal a two-step molecular strategy that jolts the innate immune response into action when exposed to HIV-1. This has important implications for developing new HIV treatments and vaccines, as well as helping understand the innate immune response in other contexts such as Alzheimer’s.

“This research delineates how the immune system can recognise a very cryptic virus, and then activate the downstream cascade that leads to immunological activation,” says Sumit Chanda, PhD, professor in the Department of Immunology and Microbiology. “From a therapeutic potential perspective, these findings open up new avenues for vaccines and adjuvants that mimic the immune response and offer additional solutions for preventing HIV infection.”

The innate immune system is activated before the adaptive immune system, which is the body’s secondary line of defense that involves more specialised functions, such as generating antibodies. One of the innate immune system’s primary responsibilities is recognizing between “self” (our own proteins and genetic material) and foreign elements (such as viruses or other pathogens). Cyclic GMP-AMP synthase (cGAS) is a key signaling protein in the innate immune system that senses DNA floating in a cell. If cGAS does detect a foreign presence, it activates a molecular pathway to fight off the invader.

However, because HIV-1 is an RNA virus, it produces very little DNA – so little, in fact, that scientists have not understood how cGAS and the innate immune system are able to detect it and distinguish it from our own DNA.

Scripps Research scientists discovered that the innate immune system requires a two-step security check for it to activate against HIV-1. The first step involves a protein called polyglutamine binding protein 1 (PQBP1), which recognises the HIV-1 outer shell as soon as it enters the cell and before it can replicate. PQBP1 then coats and decorates the virus, acting as an alert signal to summon cGAS. Once the viral shell begins to disassemble, cGAS activates additional immune-related pathways against the virus.

The researchers were initially surprised to find that two steps are required for innate immune activation against HIV-1, as most other DNA-encoding viruses only activate cGAS in one step. This is a similar concept to technologies that use two-factor authentication, such as requiring users to enter a password and then respond to a confirmation email.

This two-part mechanism also opens the door to vaccination approaches that can exploit the immune cascade that is initiated before the virus can start to replicate in the host cell, after PQBP1 has decorated the molecule.

“While the adaptive immune system has been a main focus for HIV research and vaccine development, our discoveries clearly show the critical role the innate immune response plays in detecting the virus,” said Sunnie Yoh, PhD, first author of the study and senior staff scientist in Chanda’s lab. “In modulating the narrow window in this two-step process – after PQBP1 has decorated the viral capsid, and before the virus is able to insert itself into the host genome and replicate – there is the potential to develop novel adjuvanted vaccine strategies against HIV-1.”

By shedding light on the workings of the innate immune system, these findings also illuminate how our bodies respond to other autoimmune or neurodegenerative inflammatory diseases. For example, PQBP1 has been shown to interact with tau – the protein that becomes dysregulated in Alzheimer’s disease – and activate the same inflammatory cGAS pathway. The researchers will continue to investigate how the innate immune system is involved in disease onset and progression, as well as how it distinguishes between self and foreign cells.

Source: Scripps Research Institute

HIV Infection Found to Accelerate Ageing Process

HIV Infecting a T9 Cell. Credit: NIH

Within just two to three years of infection, HIV causes an “early and substantial” impact on ageing in infected people, accelerating epigenetic changes and telomere shortening associated with normal ageing, according to a study in iScience.

The findings suggest that new HIV infection may act to reduce an individual’s life span by five years compared to an uninfected person.

“Our work demonstrates that even in the early months and years of living with HIV, the virus has already set into motion an accelerated ageing process at the DNA level,” said lead author Elizabeth Crabb Breen, a professor emerita at UCLA. “This emphasises the critical importance of early HIV diagnosis and an awareness of ageing-related problems, as well as the value of preventing HIV infection in the first place.”

In previous studies, HIV and antiretroviral treatment has been observed to accelerate age-related conditions such as cardiovascular and renal disease, grail and cognitive impairment.

Researchers analysed stored blood samples from 102 men collected six months or less before they became infected with HIV and again two to three years after infection. They compared these with matching samples from 102 non-infected age-matched men taken over the same time period. All the men were participants in the Multicenter AIDS Cohort Study, an ongoing US study initiated in 1984.

The study examined how HIV affects epigenetic DNA methylation. Epigenetic changes are those made in response to the influence of outside factors such as disease that affect how genes behave without changing the genes themselves.

Five epigenetic measures of ageing were analysed – four of them are epigenetic ‘ clocks’, each of which uses a slightly different approach to estimate biological age acceleration in years, relative to chronologic age. The fifth measure assessed telomere length, which shorten with age and cell divisions.

Compared to non-infected controls, HIV-infected individuals showed significant age acceleration in each of the four epigenetic clock measurements – ranging from 1.9 to 4.8 years – as well as telomere shortening over the period beginning just before infection and ending two to three years after, in the absence of highly active antiretroviral treatment.

“Our access to rare, well-characterised samples allowed us to design this study in a way that leaves little doubt about the role of HIV in eliciting biological signatures of early ageing,” said senior author Professor Beth Jamieson. “Our long-term goal is to determine whether we can use any of these signatures to predict whether an individual is at increased risk for specific ageing-related disease outcomes, thus exposing new targets for intervention therapeutics.”

Study limitations included having only men as participants, with few non-white participants. The sample size was also too small to take into consideration later effects of highly active antiretroviral treatment or to predict clinical outcomes. Additionally, there presently is no consensus on what is normal ageing or how to define it, the researchers wrote.

Source: UCLA

How Kaposi Sarcoma-associated Herpesvirus Evades the Immune System

Kaposi sarcoma on the skin of an AIDS patient. Credit: National Cancer Institute

A study published in Cell Reports has identified a protein in the cancer cell’s nucleus as a critical agent keeping Kaposi sarcoma-associated herpesvirus (KSHV) dormant and hidden from the immune system. The virus, in the same family as Epstein-Barr virus, is linked to AIDS-related Castleman’s disease and cancers such as Kaposi sarcoma.

Up to 50% of the population in some parts of Africa are affected with KSHV, though not everyone with KSHV will develop Kaposi sarcoma. Those who do typically have a weakened immune system due to HIV infection, organ transplant, being older or other factors.

The introduction of antiretroviral therapy significantly reduced AIDS-related Kaposi sarcoma prevalence in Western countries; however, in sub-Saharan Africa, the disease continues to have a poor prognosis.

On entry into a human cell the virus causes a hidden infection in the nucleus: the virus simply latches onto parts of the cell’s chromosomes without replicating.

Researchers studied KSHV’s latent-lytic switch, a process in which the virus exits its dormancy state to replicate in the host cell. This replication phase, called the lytic cycle, ends with the disintegration of the cell and the release of the viruses, infecting neighbouring cells.

“The virus likes to stay silent as long as possible to avoid being detected by the body’s immune system,” said Professor Yoshihiro Izumiya, the study’s senior author.

The team sought to understand the mechanisms behind this latent-lytic switch and the role the host cell environment played in this process.

“Where the virus latches onto the host cell, how it manages to stay dormant, and what triggers its activation were very exciting and important puzzles to solve,” Prof Izumiya said.

The study identified where the virus genome could be found on the host genome.

Izumiya and his team profiled and analysed chromosomal interactions on three cancer cell lines naturally infected with KSHV, locating the virus’s preferred chromosome docking sites. The binding patterns, similar among the three cancer cell lines, showed a nuclear ecosystem that can attract and help keep the virus in its silent form.

The team also found that CHD4 (chromodomain helicase DNA binding protein 4) binds to the virus’s genomic elements. CHD4, a protein in the host cell’s chromosomes, suppresses the work of the gene responsible for viral replication. The study showed that CHD4 is a key regulator of the KSHV latency-lytic switch.

“The location where the virus genome attaches to the host chromosome is not random,” said Ashish Kumar, a postdoctoral researcher in Izumiya Lab and the paper’s first author. “Without having enriched CHD4 protein, the virus starts to replicate, kicking in a cell destructive mode. For the virus to select CHD4 among many other host proteins, CHD4 must play a unique and important role in host cells.”

Virology can help identify cellular proteins essential for cell homeostasis. Over millions of years, the virus’s genome developed to encode or assemble a small number of very efficient proteins, which strategically connect to host cell proteins to keep viral chromatin dormant and impact the host cell’s tumour suppression function.

“We used virology as an entry point to shed light on the function of CHD4 in gene regulation in general. During virus-host co-evolution, KSHV cleverly learned to hijack host proteins that can help keep the gene responsible for viral replication dormant.”

The researchers found a viral protein which could serve as the basis for a replication inhibitor. Since CHD4 is critical for cancer cell growth in a variety of cancers, they hope this virus-host interaction could inform cancer treatment research.

Source: University of California – Davis Health

New Drugs for Cryptococcal Meningitis Sorely Needed in SA

Brain scan image
Image source: Mart Production on Pexels

Despite the greater safety and efficacy of a new short course treatment for HIV-related cryptococcal meningitis (CM), access to the treatment in South Africa will be a challenge, according to a pair of articles by Spotlight.

Following positive results of a trial, the World Health Organization last week announced new recommendations for the treatment of CM, with a single high dose of L-AmB followed by two weeks of flucytosine and fluconazole.

Using L-AmB (AmBisome) and flucytosine for the treatment of CM will be a welcome change for South Africa, which has the world’s highest burden of the condition. This shorter course with fewer side effects than the current treatment involving amphotericin-B could save lives as well as clinical resources in the public sector, but at present the treatment is hamstrung by pricing and availability uncertainty, with a course of L-AmB currently only available at a steep cost.

Amphotericin B [deoxycholate] is a drug that doctors and nurses used to call ampho-terrible,” Amir Shroufi, Médecins Sans Frontières (MSF) Southern Africa board member told Spotlight.

He explained that “it’s a really nasty drug, doctors and nurses don’t like it because it can cause severe anaemia. It’s toxic to the kidneys, so it can cause kidney damage and even kidney failure… and the infusion line used for the drug can often become infected and it can cause inflammation of the veins where it’s going into the body.”

L-AmB is a “much better drug”, he said, with great benefits of administering it for one day as opposed to a week or two. The seriousness of CM meant hospitalisation will still be required, pointed out Dr Jacqui Miot, division director of the Wits Health Economics and Epidemiology Research office, but means that patients won’t be tethered to a drip and may be able to go home sooner.

Under the treatment regimen, a patient receives a single high dose of L-AmB on the first day of treatment, followed by a 14-day course of flucytosine and fluconazole pills.

For a 60kg patient at the recommended dosage, twelve 50mg vials of L-AmB are needed, which at Gilead’s promised access price would be R2 880. Key Oncologics’ currently charges R34 560 for 12 vials.

Even given the availability of L-AmB, Shrouifi warns that “whatever you’re doing, you have to have flucytosine. That’s your baseline, even if you’re giving liposomal amphotericin B, you have to have the flucytosine”.

Flucytosine is an old, off-patent medicine developed in the 1950s. Despite its age and its demonstrated efficacy in the landmark ACTA trial four years ago, flucytosine was only recently authorised for use in South Africa and is only slowly being rolled out.

Amir Shroufi warned that access to the life-saving medicine remains a major issue. “Doctors are not being given the tools they need to treat [CM],” he said. “The first tool they have to have is flucytosine and they still don’t have flucytosine. So, that’s the thing that needs to happen urgently, you know, tomorrow! Everyone with cryptococcal meningitis must get access to flucytosine.”

Like L-AmB, Mylan’s 250mg and 500mg flucytosine tablets were only registered recently, in December 2021. The Department of Health’s target price for a pack of 100 tablets is R1 500. Fortunately, it appears that the Clinton Health Access Initiative (CHAI) will be able to secure packs of 100 at R1 470 each for use in South Africa’s flucytosine access programme.

The next steps for rollout of flucytosine will be inclusion on the national essential medicines list and in CM treatment guidelines before tenders can be put out.

Source 1: Spotlight

Source 2: Spotlight

‘One-dose’ Course Effective for HIV-associated Cryptococcal Meningitis

HIV invading a human cell
HIV invading a human cell: Credit NIH

A new short course of treatment for HIV-associated cryptococcal meningitis is as effective as the longer, standard one, and is better tolerated, according to a real-world study in the New England Journal of Medicine.

The international study involved a randomised trial in southern and eastern Africa. This new ‘one-dose’ approach offers a practical, easier-to-administer and better tolerated treatment for HIV-associated cryptococcal meningitis in Africa, the researchers said.

Cryptococcal meningitis causes a serious disease in immunosuppressed people living with HIV, with around 180 000 cryptococcal meningitis-related deaths each year, mostly in sub-Saharan Africa. Current treatments are either a 7 or 14-day course of amphotericin-B, combined with either oral antifungal tablets or oral fluconazole.

This new trial investigated whether a single high dose of liposomal amphotericin-B (L-AmB, Ambisome) paired with two oral antifungals, fluconazole and flucytosine, was as effective at reducing deaths as the currently recommended WHO first-line treatment based on seven days of Amphotericin-B therapy.

Dr Melanie Alufandika-Moyo, study author and the lead research doctor at the Malawi-Liverpool Wellcome Unit, said: “Cryptococcal meningitis is the most common type of adult meningitis in much of Africa. Without effective treatment, infection progresses quickly, often resulting in deaths. Current treatment requires prolonged hospitalisation, intensive nursing care and costly laboratory monitoring which can be expensive for the healthcare system and the patient. Amphotericin-B can also cause kidney damage and blood problems.

“We urgently need new ways of treating the disease, so it’s fantastic that we were able to show a new streamlined treatment, requiring just one intravenous infusion, is as effective and less dangerous for patients.”

More than 800 adult patients with a first episode of HIV-associated cryptococcal meningitis, from five countries in southern and eastern Africa, took part in the trial.

Half received, and half received standard care. After 10 weeks, 25% (101/407) of people in the AmBisome arm died compared to 29% (117/407) in the control arm – this is among the lowest mortality rate reported from a major cryptococcal meningitis trial in Africa, despite more than a quarter of participants presenting with very severe disease.

Drug-related toxicity was significantly lower in the new ‘one-dose’ AmBisome arm. Anaemia occurred in 13% of AmBisome participants compared to 39% in the control arm, with more participants in the control arm needing blood transfusions. Far less drug related kidney toxicity was observed in the one dose AmBisome arm than in the control arm.

AmBisome, a liposomal formulation of amphotericin-B, was suspected to be an effective cryptococcal meningitis treatment as it is less toxic and can be given in large doses that remain in the brain for some time. A single, high-dose of AmBisome had previously been shown to be effective at clearing Cryptococcus from around the brain, which prompted the real-world trial.

Professor Tom Harrison from St George’s, University of London, who co-led the trial with Professor Joe Jarvis from the London School of Hygiene & Tropical Medicine and Botswana Harvard AIDS Institute Partnership, said: “These exciting results represent the culmination of a long programme of collaborative work to optimise antifungal drug combinations and reduce deaths from this terrible infection, and provide the strong evidence needed for policymakers to decide how cryptococcal meningitis should be treated going forward.

“Fortunately, with the support of advocates and funders, Ambisome and flucytosine are now becoming more available, which is essential to enable wide-scale implementation of this novel treatment regimen.”

Professor Joe Jarvis, the lead author of the study, said: “The results of this trial have the potential to transform how cryptococcal meningitis is treated and the management of advanced HIV-related disease in sub-Saharan Africa. It has far fewer significant side effects, which is obviously hugely important, and has the potential to prevent a large number of deaths in low-resource settings by being both easier to administer and cost-effective.”

Study imitations included the current lack of access to Ambisome and flucytosine, the key components of this novel treatment regimen, in many low-resource settings. To address this, an additional five years funding has been received.

Source: London School of Hygiene and Tropical Medicine

Anti-HIV Antibodies Achieve Viral Suppression

HIV Infecting a T9 Cell. Credit: NIH

A trial has successfully used a novel treatment of anti-HIV antibodies to achieve viral suppression in several HIV patients. The results published in Nature, would enable a treatment not reliant on vigilant daily dosing and which could potentially reduce the body’s reservoir of HIV, something antiretroviral drugs cannot do. The antibody treatment could be used in combination with long-acting antiretrovirals, or alone after such medications have sufficiently brought down viral levels.

“The idea is that you would still be on HIV treatment, but instead of having to take a pill every day, with the long-acting versions of the antibodies, patients would be able to take infusions every six months,” said Professor Marina Caskey, who co-led the study.

In this trial, 18 participants received seven infusions of a pair of broadly neutralising antibodies over five months, while discontinuing their antiretroviral medications. Thirteen of these participants maintained viral suppression for at least five months, and in a few cases over a year, suggesting the antibodies are able to control viruses that are sensitive to the antibodies and prevent viral levels from rising to dangerous levels.

Besides suppressing the virus, antibody therapy may also have an effect on cells infected with HIV that cannot be eliminated by antiretroviral drugs. “Ultimately, with any treatment, we’d like to see a decline in the reservoir of infected T-cells, which fuel rebound when therapy is discontinued,” says Christian Gaebler, an assistant professor of clinical investigation in Nussenzweig’s lab and the study’s first author. After therapy, the team detected a decrease in the infected T-cells, specifically those that harbor intact viruses capable of replication. “It’s a promising finding that we hope to follow up on in future, larger studies,” Gaebler says.

The new study built on a previous, shorter trial in which participants had received three antibody infusions over six weeks. The researchers found that administering additional infusions was generally safe and well-tolerated, and the longer treatment period did not result in the emergence of new resistant variants.

Source: Rockefeller University

Why HIV Still Lingers in Patients’ Bodies

HIV invading a human cell
HIV invading a human cell: Credit NIH

Even with antiretroviral therapy, HIV still lingers in the body, preventing complete cure. Now, new research published in PLOS Pathogens, revealed a possible answer to why HIV persists in the body: a lack of a certain protein in HIV patients’ killer T cells. The discovery also explained why people with HIV have less risk of developing multiple sclerosis (MS).

Because this protein, CD73 is responsible for migration and cell movement into the tissue, the lack of the protein compromises the ability of killer T cells to find and eliminate HIV-infected cells, explained immunologist Shokrollah Elahi, lead researcher of the study.

“This mechanism explains one potential reason for why HIV stays in human tissues forever,” he said, adding that the research also shows the complexity of HIV infection.

“This provides us the opportunity to come up with potential new treatments that would help killer T cells migrate better to gain access to the infected cells in different tissues.”

After spending three years identifying the role of CD73, Elahi turned his focus to understanding potential causes for the drastic reduction. He found it is partly due to the chronic inflammation that is common among people living with HIV.

“Following extensive studies, we discovered that chronic inflammation results in increased levels of a type of RNA found in cells and in blood, called microRNAs,” he explained. “These are very small types of RNA that can bind to messenger RNAs to block them from making CD73 protein. We found this was causing the CD73 gene to be suppressed.”

This discovery also helps explain why people with HIV have a lower risk of developing MS, Elahi noted.

“Our findings suggest that reduced or eliminated CD73 can be beneficial in HIV-infected individuals to protect them against MS. Therefore, targeting CD73 could be a novel potential therapeutic marker for MS patients.”

Elahi said the research could next look into seeing how to turn on the CD73 gene in patients with HIV and off in those with MS.

Source: University of Alberta

Generic Options for HIV Prophylactic Cabotegravir Locked Out, MSF Warns

Image of a syring for vaccination
Photo by Mika Baumeister on Unsplash

Médecins Sans Frontières (MSF) has warned that pharmaceutical company ViiV’s recent decision not to pursue voluntary licensing for the long-acting HIV prophylactic cabotegravir (CAB-LA) means that lower cost generic production in low- and middle-income countries (LMICs) is effectively locked out for countries like South Africa.

CAB-LA was approved for the prevention of HIV infection by the USFDA in December 2021, and ViiV currently charges $3700 (R55 000) per vial in the US ($22 200/R333 000 annually per person). The Clinton Health Access Initiative (CHAI) has shown that generic manufacturers could produce this drug for around $2.60 (R39) per vial (less than $20/R3000 per person per year). Although ViiV has publicly said they would provide CAB-LA for their at-cost price in many LMICs, they have yet to announce what that price is.

According to MSF, generic manufacturer prices are often much lower than the patented drug – and they can even produce complicated formulations like CAB-LA.  The generic equivalent [PDF] of ViiV’s paediatric formulation of the HIV drug dolutegravir costs 22 times less.

Amanda Banda, Infectious Diseases Policy and Advocacy Advisor of the MSF Access Campaign, said: “What good is HIV prevention if the people who need it can’t afford it? This is the most effective form of HIV prevention for vulnerable and marginalised communities and yet ViiV is delaying the ability of generic manufacturers to supply the drug, meaning that many people across low- and middle-income countries who would benefit from the medicine to prevent HIV infection won’t be able to access it. CAB-LA will need to be available at a price that is comparable to currently available oral PrEP if country treatment programs and donors are expected to scale up its use to the levels needed – and it’s hard to imagine that ViiV will make CAB-LA available at less than $40 (R600) per year.  ViiV needs to immediately sign a licensing deal with the Medicines Patent Pool so that more affordable generics can be produced, and more lives can be saved.”

Dr Tom Ellman, Head of MSF’s South African Medical Unit said: “We want to urgently make this drug available for people at high risk of HIV infection in our programs in sub-Saharan Africa – we don’t want a donation with many strings attached from the corporation; it is not the role of ViiV to control the use of a drug that is approved by the USFDA. We want ViiV to sell us this drug at an affordable price.”

Source: MSF

HIV Co-discover Dies

HIV Infecting a T9 Cell. Credit: NIH

Luc Montagnier, the French virologist credited as being a co-discoverer of the human immunodeficiency virus (HIV), has died aged 89. He jointly received the 2008 Nobel Prize was jointly awarded to Montagnier for his work in isolating the virus.

He was lauded for his crucial research, but in later life he was criticised for unscientific claims about autism and COVID.

Local news site FranceSoir reported that he died on Tuesday in Neuilly-sur-Seine “surrounded by his children”.

The virologist first began working on the virus in the early 1980s while at the Pasteur Institute in France. Montagnier and his team examined tissue samples from patients who had the mysterious new syndrome.

In 1983, Luc Montagnier’s team at the Pasteur Institute in Paris discovered HIV‑1. They cultured T cells from a lymph node biopsy from a 33-year-old homosexual French patient with symptoms that can precede AIDS (subsequently called pre-AIDS), such as lymphadenopathy. 
Finding that they had isolated a retrovirus, they were able to infect T cells from a healthy donor, but were unable to infect other cell types, including B cells and fibroblasts. 

The group concluded that this patient at risk for AIDS was infected with a T cell–tropic retrovirus; however they could only tentatively associate it with AIDS. In 2008, Luc Montagnier and Françoise Barré-Sinoussi from his team were awarded the Nobel Prize for the isolation and characterisation of HIV-1.

However, US scientist Robert Gallo published similar findings in the same edition of Science in which the Pasteur team had announced theirs. He later concluded that the virus caused Aids. This led to years of heated debate over who actually discovered HIV.

Gallo revealed in 1991 that the virus he found came from the Pasteur Institute the year before, and the two men publicly agreed in 2002 that Montagnier’s team discovered HIV, but that Gallo first showed its role in causing Aids.

However, when Montagnier and Barré-Sinoussi were awarded the Nobel Prize in 2008 for their work – alongside Harald zur Hausen for his work on cervical cancer – the committee made no mention of Gallo, which provoked controversy.

Later on, Montagnier attracted great criticism for a series of unscientific claims, including over the causes of autism and later over the origins of COVID.

French media first reported that he had died at the American hospital in Neuilly-sur-Seine on 8 February, and his death was officially declared by authorities some time later.

Source: BBC News