By Jessica Davenport, Society of Biology
The Human Immunodeficiency Virus (HIV) has been in the news a lot over the past couple of weeks; from the functional cure of the two-year old child born with HIV, to the announcement that nanoparticles carrying bee venom can destroy HIV. But why is HIV so difficult for our immune systems to tackle?
A master of disguise
The human immune system is pretty great. Whenever a new threat, such as bacterial or viral infection, is detected the cells of the immune system undergo a series of selective divisions, making new cells which are better able to identify the threat, and then initiate the immune response. Following the infections, these cells remain as memory cells. The immune system has learnt how to recognise that particular enemy and, if it attacks again, the immune system is able to recognise and initiate its defences much more quickly, even years after the first encounter.
However, HIV is the master of disguise. Its replication process leads to multiple genetic errors and mutations, meaning that the molecules on its surface, which the cells of the immune system would normally recognise, differ significantly. It is able to evade the fast immune attack because the immune system has no memory of it.
Destroying the immune system
To make matters worse, HIV attacks specific immune cells which would normally protect us from infection. HIV most commonly targets T helper cells in order to replicate. The virus will use the host cell in order to produce viral proteins and assemble them into new viruses. Studies have shown that a single infected cell can release 10,000 – 100,000 viral particles over its life span.
During this primary infection stage, there is a marked drop in the numbers of T helper cells. This is caused by several different mechanisms. The virus may directly kill infected cells, and also cause multiple cells to fuse together. Proteins may detach from the surface of the viral particle and float freely in the blood. If the protein lands on a healthy T cell – the innocent bystander – it can set in motion a molecular chain reaction which will result in cell death. During the infection, killer T cells are also activated in order to destroy infected cells.
Once numbers of T helper cells drop below a critical level immunity to infection is lost. T helper cells play a crucial role in coordinating this immune response; they activate killer T cells to directly attack pathogens, and B cells to produce antibodies which mark the pathogen for destruction. When the immune system has been sufficiently weakened, the risk of getting an opportunistic infection from other bacteria or viruses rises significantly.
The recent discovery that nanoparticles loaded with bee venom are able to destroy HIV particles while leaving healthy cells unharmed marks an important step towards prevention of HIV transmission. However, any practical applications remain a long way off.