Virus latency

Virus latency is a unique survival strategy used by certain pathogenic viruses. During this phase, a virus enters a dormant state within a host cell. This period is known as the lysogenic part of the viral life cycle. While the virus is latent, it stops producing new virus particles. However, the viral genome is not destroyed or removed from the body. Instead, it remains inside the host indefinitely. This allows the virus to persist without the host being reinfected by outside sources. Latency is a type of persistent infection, but it is different from a chronic infection.

There are two primary mechanisms that viruses use to achieve this state. The first is called episomal latency. In this method, the viral genes exist as distinct objects within the cell. They may be linear or lasso-shaped structures. These genes float freely in the cytoplasm or the nucleus. One advantage of this method is that the virus might avoid certain cellular defenses. For example, it may not need to enter the nucleus. This can help it avoid triggering an interferon response through specific pathways. However, episomal latency is more vulnerable to degradation. Cellular enzymes called ribozymes can attack these floating viral genes.

The second mechanism is known as proviral latency. This occurs when a virus integrates its genome directly into the host cell's DNA. This integrated genome is called a provirus. This method offers a major advantage for the virus's survival. When the host cell divides, the provirus is automatically copied along with the cell's own DNA. This makes the virus nearly impossible to remove without killing the host cell. The main disadvantage is that the virus must enter the nucleus to perform this integration. This requires specific packaging proteins to help the virus reach its destination.

Many different virus families utilize these different methods. The Herpesviridae family, which includes the chickenpox virus, uses episomal latency. These viruses establish themselves in neurons, or nerve cells. For instance, the herpes simplex virus (HSV) can fuse with DNA in nerve ganglia. It can also reactivate if the chromatin, or the material holding the DNA, loosens due to stress. Another member of this family is the cytomegalovirus (CMV). CMV establishes latency in myeloid progenitor cells. It often reactivates during periods of inflammation, sepsis, or critical illness.

Other viruses, like HIV, are famous for using proviral latency. HIV is a highly studied example of this mechanism. It uses an enzyme called reverse transcriptase to turn its RNA genome into a DNA copy. This DNA then integrates into the host's genome. This allows HIV to hide from the immune system for many years. Scientists refer to these hidden areas as viral reservoirs. These are specific tissues or cell types, like resting CD4-positive T cells, that hold the virus. Because the virus is so well-hidden in these reservoirs, it is very difficult to cure with current antiretroviral drugs.

To stay hidden, viruses must actively maintain their latent state. They often express specific genes that are only active during latency. These latency-associated genes help protect the viral genome from being digested by the cell. Some viral products can even stop the cell from undergoing apoptosis, which is programmed cell death. For example, the herpes simplex virus uses latency-associated transcripts (LATs). These transcripts interfere with the host's ability to trigger cell death. By doing this, the virus ensures the host cell lives long enough to protect the viral code.

Reactivation is the process where a latent virus wakes up and begins producing new progeny. This is known as the lytic part of the life cycle. Various external factors can trigger this change. For humans, stress, high body temperatures, or even sunlight can act as activators. When a herpes simplex virus reactivates, it may cause a minor annoyance like a cold sore. However, latency can also have more serious consequences. If a virus integrates into a host gene in a way that causes uncontrolled cell division, it can lead to cancer. This has been seen with the human papilloma virus, which can lead to cervical cancer.