Epidemiologic studies show that viral infections in developed countries are the most common cause of acute disease that does not require hospitalization. In developing countries, viral diseases also exact a heavy toll in mortality and permanent disability, especially among infants and children. Emerging viral diseases such as those due to HIV, ebola virus and hantavirus, appear regularly. Now that antibiotics effectively control most bacterial infections, viral infections pose a relatively greater and less controlled threat to human health. Some data suggest that the already broad gamut of established viral diseases soon may be expanded to include other serious human ailments such as juvenile diabetes, rheumatoid arthritis, various neurologic and immunologic disorders, and some tumors.

Viruses can infect all forms of life (bacteria, plants, protozoa, fungi, insects, fish, reptiles, birds, and mammals); however, this section covers only viruses capable of causing human infections. Like other microorganisms, viruses may have played a role in the natural selection of animal species. A documented example is the natural selection of rabbits resistant to virulent myxoma virus during several epidemics deliberately induced to control the rabbit population in Australia. Indirect evidence suggests that the same selective role was played by smallpox virus in humans. Another possible, though unproved, mechanism by which viruses may affect evolution is by introducing viral genetic material into animal cells by mechanisms similar to those that govern gene transfer by bacteriophages. For example, genes from avirulent retrovirus integrated into genomes of chickens or mice produce resistance to reinfection by related, virulent retroviruses. The same relationship may exist for human retroviruses, since human leukemia-causing retroviruses have been reported.
Viruses are small, subcellular agents that are unable to multiply outside a host cell (intracellular, obligate parasitism). The assembled virus (virion) is formed to include only one type of nucleic acid (RNA or DNA) and, in the simplest viruses, a protective protein coat. The nucleic acid contains the genetic information necessary to program the synthetic machinery of the host cell for viral replication. The protein coat serves two main functions: first, it protects the nucleic acid from extracellular environmental insults such as nucleases; second, it permits attachment of the virion to the membrane of the host cell, the negative charge of which would repel a naked nucleic acid. Once the viral genome has penetrated and thereby infected the host cell, virus replication mainly depends on host cell machinery for energy and synthetic requirements.
The various virion components are synthesized separately within the cell and then assembled to form progeny particles. This assembly type of replication is unique to viruses and distinguishes them from all other small, obligate, intracellular parasites. The basic structure of viruses may permit them to be simultaneously adaptable and selective. Many viral genomes are so adaptable that once they have penetrated the cell membrane under experimental conditions, viral replication can occur in almost any cell. On the other hand, intact viruses are so selective that most virions can infect only a limited range of cell types. This selectivity exists largely because penetration of the nucleic acid usually requires a specific reaction for the coat to attach to the host cell membrane and some specific intracellular components.