Viral Infections

Effects of viruses can span short periods—days to weeks—or last for months or years. Because viruses invade host cells to replicate, they either diminish the function of those cells or destroy them. Cell death is a result of cytopathic effects and can occur immediately or over a period of time. A cytopathic effect is a virus-induced structural change in a host cell that results in cell death, either through lysis (rupture) or inability to reproduce. Two examples of cytopathic effects are particular changes in host cell shape and the fusion of adjacent host cells.

Most animal viruses are lytic—overproduction of new virus particles causes the cell to burst and die. Acute infections are attacked by the host's immune system, and the infections diminish after a short period (days or weeks). Many enveloped viruses, however, release virions through budding rather than lysis. Thus, the infected host cells live a long time or even indefinitely. This leads to persistent infections, which can last years. Examples of diseases caused by persistent viral infections include chronic hepatitis, AIDS (acquired immunodeficiency syndrome), and several illnesses triggered by herpesvirus.

Some animal viruses cause cancer. These viruses are labeled oncogenic, causing tumors to develop. With oncogenic viruses, the effect occurs in host cells. Such infections are considered to be transforming because they permanently damage the host cell's genetic material. Viral transformation is a change to the host cell's physiology, biochemistry, or genetics because of the introduction of viral genetic information. An oncogenic animal virus converts a normal cell into a tumor cell. One example of transformation is Burkitt's lymphoma, a tumor caused by the Epstein-Barr virus. Burkitt's lymphoma is common in children of New Guinea and central Africa.

Viral infections may also be latent, meaning there is a delay between the time of infection and host cell lysis. The virus can exist in a latent (inactive) state for some time. Cold sores (fever blisters) are the product of a latent infection by the herpes simplex virus. Another example is HIV, which can remain asymptomatic for years.

The viral life cycle that involves release of virions through host cell lysis is the lytic life cycle, which is common among most viruses. Many bacteriophages—viruses that infect bacteria—are also capable of following the lysogenic life cycle after their genetic material has been injected into host cells. Bacteriophages capable of the lysogenic life cycle incorporate their genetic material into the host cell's chromosome without destroying the cell. When this happens, viruses in the lysogenic cycle have entered lysogeny. Lysogeny is a state in which most viral genes in a host cell are dormant and the viral genome (provirus) and host chromosome are integrated and replicated together. Thus a provirus, or prophage, is the genome of a virus in the lysogenic life cycle that is incorporated and replicated with the host chromosome. Replication follows a different process and proceeds more slowly than in the lytic cycle, but it can continue within the same cell. The provirus also protects its host from infection by other lytic viruses. Lysogenic viruses, known as temperate viruses, can be hosted without damage until they re-enter the lytic cycle.

Sometimes lysogenic conversion occurs, the transfer of genetic information from one bacterial host cell to another by the hosted lysogenic virus. Because new genetic material is passed along, lysogenic conversion can influence the epidemiology (occurrence and control) of bacterial diseases. For example, the disease diphtheria is caused by a bacterium hosting the provirus that codes for the disease's toxin.

A well-studied temperate bacteriophage is the lambda (λ) virus. Lambda induces lysogeny in some strains of Escherichia coli (E. coli) bacteria. The incorporated lambda provirus is noninfectious and permits replication of the host cell DNA along with its own genetic material.

Repression of the lytic process in a bacteriophage can be inactivated, switching the virus to a lytic life cycle. Factors regulating the choice between lytic and lysogenic life cycles can be quite complex. One example is damage to the host cell's DNA, which signals the provirus to switch from the lysogenic to the lytic life cycle.