HIV is a common cause of kidney failure, and because of this, approximately 900 HIV-infected patients start dialysis each year in the United States. Kidney transplantation has recently become a therapeutic option for these patients, and the survival rate of HIV-infected transplant recipients with undetectable HIV in the blood is similar to that of non-HIV-infected transplant recipients. For unknown reasons, however, organ rejection is more common in HIV-infected transplant recipients.
To investigate this issue, Guillaume Canaud, MD, PhD (Necker Hospital, in Paris, France) and his colleagues assessed all 19 of HIV-positive patients in their center who received kidney transplants between June 1, 2006, and October 31, 2011. Genetic analyses demonstrated that HIV infection occurred in 68% of the HIV-positive recipients' new organs even in the absence of any detectable HIV in their blood.
Biopsy experiments revealed two different forms of infection. In the first case, podocyte cells - which constitute the barrier through which blood is filtered in the kidneys - are the main target of HIV, and infection is associated with certain clinical signs of kidney dysfunction. In the second case, HIV infects tubular cells within the kidney, with fewer clinical manifestations.
The researchers also developed a new and simple urine test to detect HIV infection in the kidneys, which could be a promising non-invasive method for diagnosing problems in HIV-positive transplant recipients.
"This study is going to change the way of thinking of nephrologists and will certainly modify the approach of kidney transplantation in HIV patients, giving new hope to patients," said Dr. Canaud.
According to an accompanying editorial by Peter Stock, MD (University of California, San Francisco), the noninvasive urine test that detects early HIV-1 infection will help clinicians identify donor and recipient factors associated with recurrent HIV kidney disease. "It is less clear what intervention may control the reinfection, although identification of donor and/or recipient factors associated with early reinfection may provide some clues," he wrote.
Admittedly, Mandela paid very little attention to the country's growing AIDS burden when he became president in 1994. It was only once he had left office that he grew much more vocal and active in the fight against HIV/AIDS, and his involvement inspired scientists, activists and other political leaders to do more, noted Robert Soudré, the conference chairperson.
When UNAIDS Executive Director Michel Sidibe took up his position in 2009, he decided to hold his first official event in Khayelitsha, the township outside Cape Town, where Mandela had visited AIDS lobby group the Treatment Action Campaign and international medical charity Médecins Sans Frontières (MSF) in 2002.
"This was when he started to challenge the status quo; and this was where he also started talking about integrating TB and HIV at a time when we were still not doing this... he was a pathfinder," Sidibe told journalists ahead of the opening ceremony on 7 December.
MSF had recently begun providing free antiretrovirals (ARVs) at a public health clinic in Khayelitsha, despite the South African government's refusal to introduce HIV treatment in the public sector. "These were truly dark times," recalled singer and UNAIDS Goodwill Ambassador Annie Lennox. AIDS was so stigmatizing, no-one wanted to acknowledge its existence, rumours and misinformation about the disease were rife, and the high number of AIDS-related deaths was overwhelming, she said.
Mandela's decision to put on a t-shirt emblazoned with the words "HIV Positive" when he met activists in Khayelitsha was a turning point. The head of South Africa's National AIDS Council, Dr Fareed Abdullah, was a director general in the Western Cape health department, the first province to defy national government by offering ARVs to HIV-positive pregnant women, and he recalled the impact of Mandela's gesture. "With Nelson Mandela behind us – doctors, nurses and people living with HIV – then who could be against us?"
According to Abdullah, Nelson Mandela also worked behind the scenes to get the government to change South Africa's heavily discredited HIV policy. He clashed with his successor, Thabo Mbeki, over Mbeki's denialist views, which questioned the link between HIV and AIDS.
After the South African government finally announced in 2003 that it would introduce free HIV treatment at state facilities, Mandela invited musicians such as Annie Lennox and Alicia Keys to perform at the launch of his 46664 campaign to raise awareness of the global pandemic.
Lennox admitted that when Mandela invited her and other artists to Robben island and told them that AIDS was a genocide affecting mainly women and children, she was "ashamed" at how little she knew about the condition.
Another key moment came in 2005, when Mandela became one of the first leaders in the region to openly acknowledge the impact of AIDS on their family by disclosing that his only surviving son had died of an AIDS-related illness – an announcement still viewed as taboo in most communities.
Africa has come a long way since then. "Even the cynics and sceptics cannot say we are not making progress," Sidibe commented. New infections have fallen by 38 percent in sub-Saharan Africa, and AIDS-related deaths by more than 34 percent, since 2001.
Nevertheless, there is still work to be done. Although 7.6 million people are now on treatment in Africa, 14 million more are still waiting for life-prolonging medicines. Children with HIV are still falling through the treatment cracks, and it is "unacceptable" that countries are still experiencing problems with drug supplies, causing frequent shortages and stockouts, Sidibe said.
Vulnerable groups such as men who have sex with men, injecting drug users, and prisoners are still being criminalized and marginalized in most countries, and are often unable to access basic HIV services, the conference heard.
But there are still many diseases for which vaccines do not yet exist. Moreover, strategies that have previously led to the successful development of vaccines are unlikely to work against more complex bacteria or viruses, such as HIV, which have evolved multiple mechanisms to evade the immune system.
The history of vaccinology is one in which biomedical and technological advances usher in the "next generation" of vaccines. In the 1950s, a breakthrough that enabled viruses to grow in tissue cultures led to the development of both live attenuated vaccines and inactivated vaccines for measles, polio, and other diseases. In the 1980s, recombinant DNA technology led to the development of vaccines against hepatitis B and human papillomavirus.
Around the turn of the century, the first sequencing of the human genome led to "reverse vaccinology." This approach, whereby computational analysis of a pathogen's genome enables identification and screening of a great many more potential vaccine targets than was previously possible, was used in the successful development of a vaccine against meningitis B.
The past decade has already yielded major advances in structure-assisted vaccine discovery, synthetic biology, systems biology and immune monitoring. However, successfully translating these advances into the development of next-generation vaccines continues to be impeded by gaps in our understanding of the human immune response that protects against specific bacteria, viruses or parasites.
That is why I, along with eight fellow scientists, have proposed the establishment of a new human-immunology-based clinical-research initiative, the Human Vaccines Project. In February 2014, leading scientists and public-health specialists will gather in La Jolla, California, to craft a scientific plan to identify, prioritize, and, most important, solve the major problems currently hindering development of vaccines against diseases such as AIDS, tuberculosis, and malaria.
Such a project would represent a paradigm shift in vaccine development. The current process is long (often spanning decades from concept to licensing), has a low probability of success (because of the limitations of animal models in predicting immune response and efficacy in humans), and is costly (often requiring hundreds of millions of dollars to develop a single vaccine).
Consider this: In just the past few years, many candidate vaccines against HIV, dengue, herpes, tuberculosis and staphylococcus aureus have failed, at a cost of more than $1 billion. Investing that amount over the next decade in a coordinated effort to address the major questions facing vaccine development would rapidly accelerate our search for effective solutions, implying a transformative impact on individual and public health.
HIV presents perhaps the greatest challenge, because the virus leverages its extensive genetic variability to hide from the immune system. Using recent advances, however, scientists have now identified highly conserved regions of this variable virus, determined their molecular structure, and begun designing next-generation vaccine candidates to elicit antibodies that target these regions to prevent HIV infection. But HIV vaccine development, like that for several other diseases, is still impeded by the limitations of what animal models can tell us about how to elicit the necessary immune responses in humans.
Two recent advances could accelerate vaccine development and reduce its costs dramatically. In synthetic biology, the rapid engineering of nucleic acid-based vaccines means more candidates move more quickly from concept to trial. In systems biology, high-throughput technologies have increased the number of genetic and immunologic parameters assessed in trials. This approach has helped predict the efficacy of potential new-generation vaccines against yellow fever and influenza within days of immunization, compared with the usual time frame of months or years.
Vaccines already prevent the deaths of 2 million to 3 million people every year, pre-empt human suffering, lighten the burden placed on health care systems and enable more rapid economic and social development. Models show that adding even a partly effective AIDS vaccine to the current range of prevention and treatment procedures could dramatically lower the rate of HIV infection.
As the Nobel Peace Prize laureate Desmond Tutu, one of the world's great campaigners against HIV/AIDS, wrote recently: "We must make the most of scientific advances over the last half-century, which have made vaccines for other preventable diseases the most powerful and cost-effective health care investment that currently exists."
That is the idea behind the Human Vaccines Project - a concept that would have been unimaginable even a decade ago. Today, technological advances in vaccine discovery and immune monitoring allow us realistically to explore this potentially game-changing approach to disease prevention. February's gathering in California may take us a giant step closer to a world without deadly and debilitating infectious diseases.
Copyright: Project Syndicate, 2013.
*The author is senior vice president and chief scientific officer of the International AIDS Vaccine Initiative.
In his last years, increasingly frail though he was, Nelson Mandela became one of the world's most important and effective campaigners against HIV/Aids. It was a difficult issue to take on because it pitched him into opposition with his own government. Believing that public confrontation would be unhelpful, he chose his words carefully; they were no less powerful for that.
By 2000, South Africa was the worst-affected country on the planet, with an HIV prevalence rate among 15- to 49-year-olds of 24.5%: more than 4 million people, and rising fast.
Things had got to this pass on Mandela's watch. As early as 1992, however, he had given a speech deploring the social conditions that led to the easy spread of Aids, from poverty and overcrowding to the low status of women and a migratory labour system that meant men were away from home for months and frequented sex workers. He talked even then of ending stigma and encouraging condom use.
But while Mandela recognised that Aids was a growing problem, and increased the funding to fight it, he had many pressing concerns during his presidency. There are indications that, with hindsight, he regretted not having done more while in power. During the 1994 election, he told the BBC: "I wanted to win, and I didn't talk about Aids." Once he was president, he said, he "had not time to concentrate on the issue".
Thabo Mbeki took over as president in 1999, as civil society groups, and the Treatment Action Campaign in particular, were becoming vociferous. Their demand for drug treatment for people with HIV coincided with Mbeki's growing interest in dissident theories about Aids. A few scientists, branded mavericks by the rest, argued there was no proof Aids was caused by a virus. They said it was a disease of poverty and that the antiretroviral drugs by then keeping people alive in rich countries were toxic.
Mandela's most significant contribution to the fight against Aids may have been his intervention at the international Aids conference in Durban in July 2000. The meeting had become a rally of those who wanted life-saving treatment for Africans with HIV. The powerful speeches of Edwin Cameron, a judge with HIV, and a small boy called Nkosi Johnson, who died a couple of years later, brought it to the world's attention. Mandela closed the meeting with a speech that changed the Aids agenda.
The conference was, he said, "the one event where every word uttered, every gesture made, has to be measured against the effect it can and will have on the lives of millions of real human beings all over this continent and planet".
A dispute had been raging on the edge of the conference, he said, that was distracting attention "from the real life-and-death issues we are confronted with as a country, a region, a continent and a world". That dispute must be put on the back burner, he said. Nobody was totally in the right or in the wrong.
He praised the integrity of Mbeki and the establishment scientists before issuing a passionate and powerful demand that the world should get on with using the tools that had been shown to save lives: information, life skills, abstinence, safe sex and condoms. He also called for action to prevent mother to child transmission, which involved the use of the controversial drugs.
It was a watershed moment that rallied world opinion to the side of action and muted the opposition of the South African government to treatment. Mbeki would no longer discuss his doubts and, although progress was painfully slow, a treatment plan was agreed in principle and there began to be some access to drugs within the public sector.
The speech marked the beginning of Mandela's total commitment to the battle against HIV/Aids. He continued to avoid confrontation with the government but used his influence in subtle ways. In 2002 he paid a very public visit to the Aids activist Zackie Achmat, who had refused to take antiretroviral drugs until the government made them generally available in South Africa.
As Mandela grew older and more fragile, he gave up all engagements except those at which he was invited to speak on Aids. It became the most important work of his foundation and he launched a charity, to which he gave his Robben Island prison number, 46664, to raise awareness and funds through huge international concerts. Some of the world's most famous artists and bands performed free, from Queen – whose lead singer, Freddie Mercury, died of Aids – to Beyoncé, the Corrs and the Eurythmics. Bono and Bill Clinton became two of his best allies in the cause. Mandela and Clinton were co-chairs of the advisory board of the International Aids Trust.
In January 2005, the cause became personal. Mandela's last surviving son, Makgatho, died in a Johannesburg hospital at 54. Within hours, Mandela had publicly announced that his son's death was from Aids-related complications. Although it later emerged that Makgatho had had pancreatic cancer, he was also HIV positive and on antiretroviral drugs, which would have made him more vulnerable to the disease.
Mandela had been unaware of his son's HIV status until the previous June, six months before his death. Telling the world that Makgatho had died of Aids was a deliberate and brave defiance of the stigma that still surrounded the illness, and the message to his people that he intended to give was reinforced by the Mbeki's presence at the funeral.
Few doubt the huge contribution Mandela made to the fight against Aids. After he stood down from the presidency, Mark Heywood, of the Treatment Action Campaign in South Africa, said: "I think Nelson Mandela has been one of the most important voices on Aids in South Africa and in the world. He has used his reputation and his energy to stress how fundamental this is to the future of our country and the developing world generally."
Although highly active antiretroviral therapy (HAART) kills human immunodeficiency virus (HIV) in the bloodstream, it does not completely eliminate it from the body because the virus can linger in infected cells and replicate.
Researchers from the Albert Einstein College of Medicine of Yeshiva University in New York presented their findings at the 99th Scientific Assembly and Annual Meeting of the Radiological Society of North America (RSNA) in Chicago, IL, this week.
Study leader Ekaterina Dadachova, professor of radiology and of microbiology & immunology, says although there has been enormous progress in HIV treatments that slow progression to AIDS, the search for a permanent cure continues.
She explains:"To combat HIV, we need a method that will completely eliminate all HIV-infected cells without damaging non-infected cells."
In radioimmunotherapy (RIT), which has been used for a while to treat cancer, antibodies charged with radioactive isotopes target and destroy cancer cells.
The antibody selects the particular type of cancer cell and the attached radioisotope delivers a lethal dose of radiation that kills the target cell, while leaving untargeted (healthy) cells unharmed.
HIV infection reduced to undetectable levels
In previous work, Prof. Dadachova had already managed to use the approach in the lab to target and destroy human immune cells infected with HIV.
At the meeting, she and her colleagues presented the results of a study in which they used the approach to treat blood samples from people infected with HIV.
The blood samples came from 15 HIV patients receiving HAART treatment at the AIDS Center at Montefiore, the University Hospital for Einstein College and academic medical center.
The results showed that RIT targeted and killed HAART-treated lymphocytes - types of white blood cells - and in most samples, reduced HIV infection to undetectable levels.
The team then went on to see if RIT could reach HIV-infected cells in the brain and central nervous system.
This would be a big step because current antiretrovirals do not cross the blood-brain barrier very well, which is why so many HIV patients treated with HAART often have severe mental impairment.
For this test, they used a lab model of the blood-brain barrier made with human cells and discovered that the same radioisotope-charged antibodies used in earlier experiments could destroy HIV-infected cells in the brain without damaging the barrier.
Prof. Dadachova says:"We found that radioimmunotherapy could kill HIV-infected cells both in blood samples that received antiretroviral treatment and within the central nervous system, demonstrating RIT offers real potential for being developed into an HIV cure."
In another study published recently in the Journal of Infectious Diseases, researchers from Lund University in Sweden describe how they found that an aggressive new HIV strain leads to AIDS more quickly than other current strains.
In a study appearing in PLoS Pathogens, Dr. Donald Forthal of UC Irvine and colleagues studied the mechanisms employed by the virus to cross genital tract tissue and establish infection. Since cervicovaginal fluid is acidic and HIV-1 in cervicovaginal fluid is likely coated with antibodies, they explored the effect of low pH and HIV-1-specific antibodies on transcytosis, the movement of HIV-1 across tight-junctioned epithelial cells.
The researchers found that the combination of HIV-1-specific antibodies and low pH enhanced transcytosis as much as 20-fold.
Virus that underwent transcytosis under these conditions was infectious, and infectivity was highly influenced by whether or not the antibody neutralized the virus. They observed enhanced transcytosis using antibody from cervicovaginal and seminal fluids and using transmitted/founder strains of HIV-1. Enhanced transcytosis was due to the Fc neonatal receptor (FcRn), which binds immune complexes at acidic pH and releases them at neutral pH. Finally, staining of human tissue revealed abundant FcRn expression on columnar epithelial cells of penile urethra and endocervix.
"A large part of the reason we lose wars against viruses that cause chronic infection is that immune cells called T cells get turned off," says Jonathan Schneck, M.D., Ph.D., a professor of pathology in the Johns Hopkins Institute for Cell Engineering, who led the study. "We've been trying for some time to find out why that is, and in our study we were able to identify a family of proteins called Sprouty, specifically Sprouty-2, as a culprit."
T cells, a type of white blood cell, are programmed to recognize and kill cells infected with a specific virus or other disease-causing agent. Doing so effectively requires a T cell to perform multiple functions - par for the course when the cells are fighting a fresh infection. But when infection drags on, as HIV does, T cells often become "exhausted," losing two or more functions, except among so-called "elite suppressors" - rare HIV-infected patients whose T cells never seem to tire.
To investigate the source of exhaustion, the Johns Hopkins team first sought a way to recreate that phenomenon in the laboratory. Yen-Ling Chiu, M.D., a graduate student in Schneck's laboratory, was able to simulate the effects of long-term chronic infection by growing influenza-fighting T cells and dosing them with large amounts of antigen, a type of molecule that, like a red flag waved at a bull, signals immune cells to attack. Doing this "made the T cells dysfunctional - they looked like exhausted T cells in HIV," Chiu says.
Chiu next looked for differences in proteins made in the dysfunctional cells compared to those in fresh T cells. It turned out, he says, that many of the proteins whose quantities were different between the two groups of cells were involved in a biochemical chain of events called the MAPK/ERK pathway. That pathway controls a variety of important processes, such as cell division. One of the proteins that was more abundant in the exhausted T cells than in the fresh T cells was Sprouty-2, which, other studies had shown, slows down the MAPK/ERK pathway. Suspecting that Sprouty-2 could be the culprit in T cell exhaustion, Chiu used a specially engineered virus to disable the Sprouty-2 gene in some T cells and found that they were more likely to retain all of their functions than were the cells with working Sprouty-2.
"It was a surprise to find T cell exhaustion controlled by such a central pathway, and especially that it worked in such a highly fine-tuned way, keeping some T cell functions going but not others," says Schneck.
Though the finding was intriguing, Schneck says, "the real test was whether it held up in blood samples from HIV patients." In one experiment, reducing the amount of Sprouty-2 in exhausted HIV-fighting T cells partially restored them, the researchers found. Drawing on the work of other groups, which had shown that reducing the amount of another protein, called PD-1, modestly improved the function of exhausted T cells, the research team next tried disabling both Sprouty-2 and PD-1 in the HIV-fighting cells. "That reversed the exhaustion completely," Schneck says.
"By identifying Sprouty-2 and related proteins as potential targets, these results support the idea that immunotherapy may someday lead to a functional cure for HIV-1 infection," says Joel Blankson, M.D., Ph.D., an associate professor in the Department of Medicine's Division of Infectious Diseases, who also took part in the study.
There are no known chemical compounds that can block Sprouty-2 in living animals, so Schneck's group plans to begin looking for one - a first step toward potentially developing new drugs based on the discovery. Schneck notes that they will also investigate whether Sprouty proteins cause exhaustion in T cells fighting other chronic infections, such as tuberculosis and hepatitis C.
In this regard, Government would continue to provide leadership that would ensure that pharmaceutical companies in the country meet the criteria for obtaining the necessary World Health Organization (WHO) pre-qualification to produce ARV locally.
Vice President Amissah-Arthur stated this during the national celebration of the 2013 World AIDS Day in Wa.
He noted that local production of ARVs was the most efficient means to get more people living with HIV on treatment.
In Ghana, the 2013 World AIDS Day is being celebrated under the sub-theme: "Getting to Zero: Accelerating the National HIV Response Towards the Millennium Development Goals (MDGs)".
Vice President Amissah-Arthur stressed Ghana's continued commitment to protecting the rights of persons living with HIV and ensuring the elimination of mother-to-child transmission of HIV in order to guarantee an HIV free generation in Ghana.
According to the Vice President, achieving less than five percent mother to child transmission of HIV by 2015 was the next important goal to be achieved.
The Government would work on closing the resource gap needed to help the country accelerate to zero new infections, zero stigma and discrimination and zero AIDS related deaths by 2015.
He said last year, Government took steps towards addressing the issue of cost as a barrier to accessing HIV treatment services and ultimately help Ghana get to zero AIDS related deaths.
The Ministry of Health was then instructed by Government to scrap the GHcedi 5.00 service charge paid by people living with HIV for treatment while the Ghana AIDS Commission was also asked to ensure that all persons living with HIV got registered onto the National Health Insurance Scheme (NHIS).
Vice President Amissah-Arthur noted that Government could not achieve the goals of the national response to HIV and AIDS alone.
He therefore called on communities, civil society organizations, the private sector, religious leaders and the general public to continue playing their roles as social partners to ensure that every section of the Ghanaian community was reached with HIV and AIDS information and services.
Dr Angela El-Adas, Director General of the Ghana AIDS Commission explained that the World AIDS Day was a day set aside to rekindle the awareness of HIV and AIDS, renew their support to those living with and affected by HIV as well as commemorate friends and families who were lost to AIDS.
She said Ghana had chalked a lot of successes in the national response over the past years, saying the general adult prevalence for HIV had dropped by over 60 per cent in 10 years, from 3.6 per cent in 2003 to 1.37 per cent in 2012.
New HIV infections have also dropped from 26,000 per annum to less than 8,000 in 2012 while the number of AIDS related deaths had also declined significantly.
Dr. EL-Adas stated that the country had also reduced by 70 per cent the number of new HIV infections among children due to increased coverage of antiretroviral prophylaxis for pregnant women living with HIV.
She said from 31 per cent in 2009, the proportion of children born with HIV to positive mothers declined to nine per cent in 2012, adding that, Ghana was the only country in West and Central Africa to reduce mother-to-child transmission of HIV to this level.
Dr Ephraim Avea Nsoh, Upper West Regional Minister said the region was one of the regions with HIV prevalence rate of 1.2 per cent that was lower than that of the national average of 1.37 per cent.
He called for sustained efforts in order to reduce it further as a significant way of contributing to the achievement of the MDGs.
Speaking at the White House to mark World AIDS Day, the president said the United States would contribute $1 for every $2 pledged by other donors over the next three years to support The Global Fund, an international financing institution that fights AIDS, tuberculosis and malaria.
Obama also said he would redirect $100 million into a National Institutes of Health program to research a cure for HIV, the human immunodeficiency virus that causes AIDS.
"The United States should be at the forefront of new discoveries into how to put HIV into long-term remission without requiring lifelong therapies - or, better yet, eliminate it completely," Obama said at an event attended by Secretary of State John Kerry and software magnate Bill Gates, whose foundation has pledged up to $500 million for The Global Fund.
Obama also signed into law legislation authorizing an extension of a successful and popular program to combat AIDS worldwide, the President's Emergency Plan for AIDS Relief, known as PEPFAR.
PEPFAR funding has fallen 12 percent since 2010. Critics have accused Obama, a Democrat, of failing to show the same level of commitment to fighting AIDS as his Republican predecessor, Bush, who poured $15 billion into the program to combat AIDS worldwide.
Obama has argued that his administration has expanded the program's scope without increasing spending.
Globally, the United States is the largest donor to HIV efforts to fight HIV/AIDS in low and middle income countries, according to a report by the United Nations and the Kaiser Family Foundation. Overall donor government funding for HIV has remained at the about the same level since 2008, reflecting tighter budgets following the 2007-2009 financial crisis.
(Reporting By Mark Felsenthal; Editing by Cynthia Osterman)
The period from infection to development of AIDS was the shortest reported among HIV-1 types, at around five years.
There are over 60 different epidemic strains of HIV-1 in the world, and geographic regions are often dominated by one or two of these. If a person becomes infected with two different strains, they can fuse and a recombined form can occur.
"Recombinants seem to be more vigorous and more aggressive than the strains from which they developed", explained Angelica Palm, a doctoral student at Lund University.
The recombinant studied is called A3/02 and is a cross between the two most common strains in Guinea-Bissau, West Africa - 02AG and A3. It has previously been described by Joakim Esbjörnsson, a postdoctoral fellow at the University of Oxford, who is a co-author of the study.
So far, the new strain has only been identified in West Africa, but other studies have shown that the global spread of different recombinants is increasing. In countries and regions with high levels of immigration, such as the US and Europe, the trend is towards an increasingly mixed and complex HIV flora, unlike in the beginning of the epidemic when a small number of non-recombinant variants of the virus dominated. There is therefore reason to be wary of HIV recombinants in general.
"HIV is an extremely dynamic and variable virus. New subtypes and recombinant forms of HIV-1 have been introduced to our part of the world, and it is highly likely that there are a large number of circulating recombinants of which we know little or nothing. We therefore need to be aware of how the HIV-1 epidemic changes over time", said Patrik Medstrand, Professor of Clinical Virology at Lund University.
The research is based on a unique long-term follow-up of HIV-infected individuals in Guinea-Bissau, a project run by Lund University. In future research, Angelica Palm and her colleagues hope to be able to continue researching the characteristics of recombinant viruses and the presence of these among HIV carriers in Europe.
For health services, the new research results mean a need to be aware that certain HIV-1 types can be more aggressive than others, according to the research team.