AcademiaNet: Prof. Larsson, how much closer do you think we are today, more than 30 years after the discovery of HIV, to eradicating AIDS?
Curing HIV infections as well as stopping them in the first place is a challenge, but I think we have moved much closer to eradicating AIDS. We have learnt so much about HIV and the damage it causes to infected individuals and also how it is transmitted. Most importantly, today, we have antiretroviral treatments that can control the infection to an extent that virus levels are kept at such a low level that an infected person can live with HIV and transmission to other individuals becomes unlikely.
However, in spite of this success with antiviral treatments, we still don’t have a vaccine. HIV is particularly malicious, because it targets the immune system, especially the CD4+ T cells, and destroys them. To make things worse, HIV is able to hide within immune cells for a very long time without being detected by the immune system or by antiviral treatments. This makes even the best antiviral treatment a therapy and not a cure: if one stops taking the medication, the infection will recur and new viruses will be produced.
The only way to ultimately eradicate HIV would be an effective vaccine. I have not given up hope yet that, one day, we will be able to develop a vaccine that will stop the spread of HIV.
What are you currently working on?
We are working on how HIV modulates immune cells such as dendritic cells and T cells to get a deeper understanding of the immune impairment induced by HIV in these cells. In addition, we aim to gain a better understanding of the events in the primary HIV infection of the genital mucosa and this is also explored in the setting of co-infection with the herpes virus HSV2, which is known to create an environment supporting HIV infection. The overall and long-term goal is to define new potential therapeutic targets.
What effects exactly does the virus exert on our immune cells?
In fact, HIV impairs immune cells in multiple ways. The virus first and foremost infects and kills CD4+ T cells. These T helper cells are part of the adaptive immune system and are important in controlling infections. In addition, HIV infection leads to chronic activation of the immune system. This impairs the function of other important immune cells such as dendritic cells, T cells, MAIT cells and NK cells, making the responses by these cells suboptimal and too weak to fight and clear the HIV infection as well as other infections and cancers.
You have also studied co-infection with HIV and tuberculosis. Why is the risk of contracting tuberculosis (TB) so much higher in HIV-positive individuals? What is being done to reduce tuberculosis-related deaths in HIV-positive individuals?
HIV changes TB pathogenesis by increasing the risk of disease after exposure to TB bacteria. This is due to the impaired immune response in the HIV-infected individuals. There is a correlation between the risk of contracting TB and the level of HIV-infected CD4 T cells. Today, several courses of action, which are recommended by the WHO, are taken to reduce the number of deaths among HIV-TB-infected individuals. These include prevention, testing for TB infection in individuals that show symptoms and treatment of TB disease.
Thank you for the interesting interview, Professor Larsson.
Questions were asked by Neysan Donnelly for AcademiaNet.