Human immunodeficiency virus (HIV) is the causative agent of AIDS (Acquired Immunodeficiency Syndrome), a disease which was first described in the United States in the early 1980s. Since its initial discovery, HIV/AIDS has risen to become a global pandemic, with over 30 million infected individuals worldwide.

In collaboration with members of the CHEETAH consortium and the NIGMS Specialized Centers for HIV/AIDS-Related Structural Biology, this project seeks to describe current understanding of the molecular mechanisms by which HIV gains entry to and exits from its target cells, an area of intense investigation by researchers around the globe.

Please note that the animation shown here is a work-in-progress, and will be further updated, refined and augmented over the coming years.  Additional animations will illustrate how antiretroviral drugs impact the life cycle, and how innate immunity can block HIV infection.

The HIV Life Cycle

How does HIV infection occur? This molecular animation depicts the process of how HIV infects a T cell and transforms the cell into a viral factory.

Click here to view a version of this animation without narration.

Download the HIV Life Cycle animation (narrated version, 523 MB)

Download the HIV Life Cycle animation (music-only version, 523 MB)

Animated and narrated by Janet Iwasa (Department of Biochemistry, University of Utah)
Music written and performed by Joshua Roman
Music recorded by Jesse Lewis (Immersive Music Project)

Restriction Factors

Restriction factors act as one of our first lines of defense against viral invaders. These proteins, which are produced by the host cell, can work to inhibit the replication of broad classes of viruses, including HIV. Different restriction factors can target different points of the HIV cell cycle, including entry, reverse transcription, and budding. However, HIV has evolved mechanisms to counter these host defenses. By understanding these interactions, researchers may be able to develop new therapeutics against HIV. 


APOBEC3G (A3G) is a protein that is produced by the host cell and is packaged into budding viruses. After these viruses infect a new host cell, A3G produces a large number of changes in the HIV genome, which causes the virus to become non-infectious due to catastrophic errors in its genetic sequence. This process is shown below, in the animation on the left.

Viral infectivity factor (Vif) and A3G 

As shown in the animation below (on the right), HIV counteracts A3G restriction by encoding a protein called viral infectivity factor (Vif). Vif hijacks the host’s molecular machinery and uses it to destroy A3G, preventing A3G from being packaged into new HIV virions.


The tripartite-motif protein 5 alpha (TRIM5α) is a restriction factor that can potently block viral replication and is found in most primates. Acting as part of the innate immune system, TRIM5α (colored purple) can bind to the HIV capsid shell (yellow) that coats and protects the viral genome. Studies have shown that TRIM5α is a potent inhibitor of HIV-1 in old world monkeys, making them immune to HIV-1. Human TRIM5α, however, is not as effective as blocking HIV-1, but is thought to mediate restriction against other viruses.

Structural studies have shown that TRIM5 can form a cage-like structure surrounding the capsid. There are three proposed mechanisms by which TRIM5 can inhibit HIV infection as shown in this animation.