appropriate signals. Following infection by a sarcoma virus
They may become immortal and able to divide indefinitely
and intergration of the provirus into the host genome, the
in culture. In the animal this may lead to leukemias or
overexpression of the incorporated oncogene, or expression
of a mutated oncogene that continuously induces the cell to
multiply, results in transformation of the infected cell. The
incorporation of cellular oncogenes into a retrovirus is an
accident that results from recombination of the viral genome
with a cellular mRNA encoding an oncogene. The oncogene
replaces viral genes in the genome and almost all sarcoma
Viruses must be able to pass from one infected organ-
viruses are defective, unable to undergo a complete replica-
ism to another if they are to persist. The spread of specific
tion cycle without a helper. In nature sarcoma viruses are
viruses will be considered together with their other attributes
able to cause a tumor in the animal in which they arise but
in the chapters that follow, but it is useful to consider virus
are not passed on, and thus die out. The subject of sarcoma
epidemiology in overview at this point. The tissues infected
viruses will be covered in more detail in Chapter 6, after a
by a virus and the seriousness of the disease caused by it
discussion of the genome organization of retroviruses and
are attributes that determine in part the mechanism of spread
the details of their replication.
of a virus. Thus, knowledge of the epidemiology of a virus
Many DNA viruses also encode proteins that are capable
is important for understanding the biology of its replication
of transforming cells. These viral oncogenes induce cycling
and pathology.
in infected cells, providing an environment suitable for the
We can discriminate several general ways in which
replication of the viral DNA. Whereas the cellular oncogenes
animal viruses are spread: oral­fecal, airborne, blood-
present in sarcoma viruses serve no function in viral replica-
borne (including viruses that are spread by bloodsucking
tion, the viral oncogenes in DNA viruses are essential for
arthropods), sexual, and congenital. We can also distin-
viral replication. If the cell is not induced to enter S phase,
guish human viruses that have humans as their major or
the virus replicates poorly or not at all. Infection of a cell by
only host (referred to here as human viruses), and viruses
a DNA virus normally leads to the death of the cell caused
that are also associated with other animals (referred to as
by replication of the virus. Thus, although transformed, the
infected cell does not survive. However, if the virus is un-
Viruses spread by an oral­fecal route are disseminated by
able to undergo a complete lytic cycle, either because it is
ingestion of contaminated food or water. Infection begins in
defective or because the cell infected is nonpermissive or
the gut, and it may or may not spread to other organs. Many
semipermissive, the cell may survive as a transformed cell
of these viruses cause gastroenteritis. Virus is excreted in
if the early (transforming) genes continue to be expressed.
feces or urine to continue the cycle. Such viruses are usually
We return to the subject of viral oncogenes in Chapter 7,
fairly stable outside the organism because they may have to
because they are an ingredient of the replication cycle of
persist in an infectious form for long periods of time before
DNA viruses.
being ingested by the next victim.
Transformation of cells is accompanied by a number of
Airborne or respiratory viruses are spread when virus
phenotypic changes. Cells maintained in culture are normally
present in the respiratory tract is expelled as aerosols or in
derived from solid tissues and require anchorage to a solid
mucus. Infection begins when contaminated air is inhaled or
substrate as well as a supply of nutrients, including growth
when virus present in mucosal secretions, for example, on
factors, for growth. Transformed cells have a decreased
doorknobs or on a companion's hands, is contacted and the
requirement for a solid substrate and may have lost such a
virus is transferred to mucosal surfaces in the nose, mouth,
requirement entirely, and thus may grow in soft agar or in
or eyes. These viruses are often unstable outside the body
liquid culture. They have decreased requirements for growth
and spread usually requires close person-to-person con-
factors and will continue to divide in medium with lowered
tact. Infection begins on mucosal surfaces in the nose, the
amounts of such factors. They grow to higher densities in
upper respiratory tract, or the eye. Many of these viruses are
culture than do normal cells, and tend to pile up in mul-
restricted to growth in the upper respiratory tract and cause
tilayers on the surface of the culture dish (loss of contact
respiratory disease, but some are able to spread to other
inhibition or density-dependent growth). Transformed cells
organs and cause disseminated disease.
may be immortal and able to divide indefinitely in culture,
Blood-borne viruses establish a viremia in which
whereas normal cells stop dividing after a limited number of
infectious virus circulates in the blood. Some are trans-
divisions. Many of these changes in growth properties are
mitted by bloodsucking arthropods, which act as vectors,
reflected in changes in their cytoskeleton, their metabolism,
whereas others are transmitted by exposure to contami-
and in their interactions with the extracellular matrix.
nated blood or other bodily fluids. Arboviruses (e.g., yel-
Lymphocytes, which do not require anchorage for
low fever virus, genus Flavivirus, family Flaviviridae) can
growth, can also be transformed by the appropriate viruses.
replicate in both arthropods, such as ticks or mosquitoes,
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