A new study from Lund University in Sweden has opened the way for new approaches to slowing the development of AIDS in HIV-1-infected patients. It is hoped that this could lead to better treatment methods and preventive measures to combat HIV and AIDS.
The findings have just been published in the distinguished scientific journal New England Journal of Medicine.
The most common type of the virus that causes AIDS -- HIV-1 -- is less aggressive when it infects a person already carrying the milder HIV-2. The study looked at how the disease developed in those who had been infected with HIV-1 and those who were infected with both HIV-1 and HIV-2.
"The moderating effect of HIV-2 was extremely strong. The time it took to develop AIDS was around 50 per cent longer for those infected with both strains than for those only carrying the HIV-1 virus. The unusually large difference makes me, as a researcher, very optimistic that it will be possible to identify new and significant approaches that can be taken to combating the development of AIDS," says Joakim Esbjörnsson, a virologist at Lund University.
"The unique thing about our study, which has been carried out over 20 years, is that we have been able to follow healthy individuals from when they were infected with HIV-1 only or both HIV-1 and HIV-2 through the entire course of the disease, and to make comparisons of how the infection has developed over time," says Hans Norrgren, doctor in infectious diseases and researcher at Lund University and Skåne University Hospital.
An observation that was linked to an early stage of HIV infection was a difference in the genetic diversity of the HIV. It is well-known that different strains of HIV co-exist during the course of the infection and that the genetic difference between them increases the closer to AIDS the infection comes. This genetic difference was lower early on in the disease among people with a dual infection than among those with only HIV-1 infection, which gave them a better starting point from which the development of AIDS was delayed.
The researchers have also studied the levels of CD4+ T cells -- helper cells with a key role in the immune system that are attacked and destroyed by the HIV virus. Patients with dual infection were also seen to be at an advantage in this. They had a higher number of CD4+ T cells throughout the period of infection. It took longer to reach critically low levels of CD4+ T cells, and thus also longer before the infection developed into AIDS.
"Our results suggest that HIV-2 can activate cellular reactions which naturally check the development of AIDS. If we can map these, I think we can also uncover entirely new mechanisms that are key to the slower development of the disease. In the long run, this could lead to better preventive measures and treatments," says Patrik Medstrand, Professor of Virology at Lund University.
Behind the findings lies a unique 20-year follow-up of 4 700 people in Guinea-Bissau in West Africa.
"Our work is the result of many people's work over many years, in particular the staff of the National Public Health Laboratory in Guinea-Bissau and the police health station in the capital Bissau, who have carried out the practical work of examining the study participants, taking samples and conducting laboratory analyses," says Fredrik Månsson, a doctor in infectious diseases in Malmö and one of the researchers behind the study.
West Africa is the only region where the milder strain of HIV, HIV-2, is found on a large scale. Like the globally dominant and more aggressive HIV-1, HIV-2 is an infection that can lead to AIDS. However, fewer of those infected with HIV-2 develop AIDS, only around 25-30 per cent of those who do not receive treatment.
- Joakim Esbjörnsson, Fredrik Månsson, Anders Kvist, Per-Erik Isberg, Salma Nowroozalizadeh, Antonio J. Biague, Zacarias J. da Silva, Marianne Jansson, Eva Maria Fenyö, Hans Norrgren, Patrik Medstrand. Inhibition of HIV-1 Disease Progression by Contemporaneous HIV-2 Infection. New England Journal of Medicine, 2012; 367 (3): 224 DOI: 10.1056/NEJMoa1113244
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