Biomedical Engineering Reference
In-Depth Information
Virion multiplication normally causes host cell damage or death, which is why virus
tend to establish milder infections in which cell death is more of an aberration than the
norm. Notable exceptions include HIV, Ebola virus, Hantavirus, and rabies virus; indeed,
some virus are capable of establishing forms of silent infection [5].
Their extreme dependence on the host cell makes virus distinct among other microor-
ganisms. A virus grows within a host cell and is viewed together with its host in case of
any consideration of pathogenesis, epidemiology, host defenses, or therapy. Specific con-
ditions for pathogenesis are imposed by the bilateral association between the virus and its
host. Rhinoviruses, for instance, require temperatures not exceeding 34°C. This environ-
ment restricts their growth to cells in the cool outer layer of the nasal mucosa, thereby pre-
venting their spread to areas of higher temperature in deeper cells [6].
Even though the virus is protected from some of the host's immune mechanisms by its
intracellular location, it is vulnerable because of its dependence on the host cell's synthetic
machinery. This state, however, may be altered by subtle physical and chemical changes
produced by the viral infection itself, including inflammation, fever, circulatory alter-
ations, and interferon [7].
The virus-host association is greatly influenced by the virus's epidemiologic properties
[8]. As an example, certain arthropod-borne virus in insects multiply only within a narrow
temperature range; as a result, it is only under specific seasonal and geographical condi-
tions that the virus are found. Transmissibility of virus in aerosols and food is determined
by other environmental conditions [9].
Virus replicate only within host cells, primarily utilizing many of the host cell's biosyn-
thetic processes, which makes them difficult targets for chemotherapy. The similarity of
host-directed and virus-directed processes makes it difficult to identify antiviral agents
with sufficient specificity to exert their effect on viral replication in infected cells rather
than on functions in uninfected host cells. Through experimentation, however, we are
learning that each virus may have specific steps of replication that can be used as targets
for selective, carefully aimed chemotherapeutic agents. Appropriate use of such drugs
requires a thorough knowledge of suitable targets, based on an in-depth understanding of
the virion's replication mechanisms and a correct diagnosis [10].
Successful vaccines are based on the knowledge of pathogenesis and immune defenses,
while comparable considerations govern treatment with interferon. Correct diagnosis,
prevention of the virion's spread in the environment, and effective treatment of the
disease are complex issues. Knowledge of the pathogenetic mechanisms by which a virus
enters, spreads, and exits the body is critical for antibody-containing immunoglobulin
treatment and requires knowing when a virus is susceptible to an antibody (for instance,
during viremic spread), and when a virus reaches target organs where the antibody may
be less effective [11]. Viral infections are among the most difficult and demanding situa-
tions that a physician must address. While tremendous progress has been made over the
past few decades, unfortunately, some of these issues still lack satisfactory solutions. More
aspects of medical virology are understood now than previously, while others are being
clarified gradually, and yet more are still obscure. Successful investigation and manage-
ment of their pathologic processes is based on the knowledge of the properties of virus
and the relationships they establish with their hosts [12].
21.1.1
Virion and Virus Structure
Virus are noncellular infectious agents consisting of a single type of nucleic acid (either
RNA or DNA) surrounded by a protein coat (see Figure 21.1). Lacking any independent
metabolism of their own and reproducing wholly within living host cells, simple virus are
