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Definition

Persistent infections are characterized as those in which the virus is not cleared but remains in specific cells of infected individuals. Persistent infections may involve stages of both silent and productive infection without rapidly killing or even producing excessive damage of the host cells. There are three types of overlapping persistent virus-host interaction that may be defined as latent, chronic and slow infection.
Pathogenesis

The mechanisms by which persistent infections are maintained involve both modulation of virus and cellular gene expression and modification of the host immune response. Reactivation of a latent infection may be triggered by various stimuli, including changes in cell physiology, superinfection by another virus, and physical stress or trauma. Host immunosuppression is often associated with reactivation of a number of persistent virus infections.

Persistent virus infections are discussed from the virus point of view in terms of the bodily sites in which the infection persists.
Glands and body surfaces are thought to be significant because they give the virus protection at the topographical level from immune
forces, and because they are appropriate sites for the shedding of virus to the exterior.
Germ cells are relevant sites because infection can thus be transmitted vertically from generation to generation in the host.
The central nervous system, however, is generally a 'dead end' from which there is no shedding to the exterior.
Persistence in blood may be relevant when continued arthropod transmission becomes possible.
Most persistent viruses infect lymphoreticular tissues, and this is interpreted by suggesting that it results in an impaired immune
response to the infecting virus, which in turn favours persistence.

The Course of Viral Infection

When a virus enters the host, there is an initial nonequilibrium phase of acute infection. During this phase, viral and immune strategies compete for dominance. Assuming the host survives, a decision point is reached at which the infection is either cleared or becomes chronic. This decision point may be reached very early in infection for viruses that can establish a latent infection, in which case the infection is permanent regardless of the course of acute infection. If recovery occurs, the immune system must reset by clearing the antigen and re-establishing immune homeostasis. If the balance shifts toward chronic infection, a new set of viral and host strategies interact to define a metastable equilibrium in which viral replication is held in check, but the virus is not cleared.

Another mode of virus infection is the latent phase, where the virus is ‘quiescent’ (a state in which the virus is not replicating). A combination of these stages, where virus replication involves stages of both silent and productive infection without rapidly killing or even producing excessive damage to the host cells, falls under the umbrella of a persistent infection. Reactivation is the process by which a latent virus switches to a lytic phase of replication.

Reactivation is the mechanism whereby a latent virus that has infected a host cell switches to a lytic stage, undergoing productive viral replication and allowing the virus to spread. Viral reactivation is associated with several stress factors [1], including viral infection (with other viruses), nerve trauma, physiologic and physical changes (e.g., fever, menstruation and exposure to sunlight) and immunosuppression (as in cytomegalovirus [CMV] disease).

A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. However, the viral genome is not fully eradicated. The result of this is that the virus can reactivate and begin producing large amounts of viral progeny without the host being infected by new outside virus, denoted as the lytic part of the viral life cycle, and stays within the host indefinitely

While viral latency exhibits no active viral shedding nor causes any pathologies or symptoms, the virus is still able to reactivate via external activators (i.e. sunlight, stress) to cause an acute infection