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HIV, the virus that causes AIDS, is the cause of one of the most far-reaching and destructive epidemics in modern times. Responsible for approximately 1.8 million deaths and more than 2.5 million new infections annually, HIV is a major public health concern, particularly in the developing world. HIV-1, the most common and virulent strain of the virus, has been studied extensively by researchers hoping to better understand the virus’s life cycle and develop treatments that disrupt its ability to infect and reproduce. One of the greatest barriers to effective treatment and clearance of HIV-1 is the virus’s astonishing capacity for immune evasion. From constant mutation to active subversion of the body's immune system, HIV is a particularly difficult pathogen to eliminate. In a paper published in PLoS: Pathogens in March of 2010, researchers from the Institut Pasteur examined one method by which HIV-1 is able to evade the natural killer (NK) cells of the innate immune system and establish a persistent infection, providing both a better understanding of HIV-1 immune evasion and a possible target for future HIV treatments.
Under normal conditions, viruses and virus particles are taken up by a subset of the host’s white blood cells known as dendritic cells (DCs). The DCs act as the immune system’s sentries, scouting the body’s tissues for foreign particles or pathogens and presenting them to other immune cells to stimulate a response. DC function is closely regulated by the interactions that take place with NK cells following infection. When inflammation occurs at the site of an infection or injuries, chemical signals known as chemokines cause NK cells to migrate to the infection site. Upon arrival, NK cells interact with DCs, sending signals that may cause the DCs to mature, and receive activating signals from the DCs. If an NK cell encounters a DC that has been infected by a virus or other intracellular pathogen, the NK cell will kill the infected cell by inducing a process known as apoptosis. When the infected DCs undergo apoptosis – also known as programmed cell death – the virus inside them can no longer replicate. This process is essential to the immune system’s ability to clear a virus from the body, particularly during the early stages of infection. However, previous research has suggested that HIV positive people are deficient in killing DCs that are infected with HIV-1, causing the infected DCs to act as a reservoir in which the virus can replicate without interference. In this paper, the researcher set out to determine the methods by which HIV-1 is able to prevent NK cells from killing infected DCs.
