VIRAL INFECTION
AND DISEASE
Viruses are obligate
intracellular parasites that use many of the host cell’s biochemical mechanisms
and products to sustain their viability. A mature virus (virion) can exist
outside a host cell and still retain its infective properties. However, to reproduce, the virus must enter the host cell, take over the host
cell’s mecha-nisms for nucleic acid and protein synthesis, and direct the host
cell to make new viral particles.
Viruses are composed of one
or more strands of a nu-cleic acid (core) enclosed by a protein coat (capsid).
Many viruses possess an outer envelope of protein or lipoprotein. Viral cores
can contain either DNA or RNA; thus, viruses may be classified as DNA viruses
or RNA viruses. Further classification is usually based on morphology, cellular
site of viral multiplication, or other characteristics.
Examples of DNA viruses and
the diseases that they produce include adenoviruses (colds, conjunctivitis);
hepadnaviruses (hepatitis B); herpesviruses (cytomega-lovirus, chickenpox,
shingles); papillomaviruses (warts); and poxviruses (smallpox). Pathogenic RNA
viruses in-clude arborviruses (tick-borne encephalitis, yellow fever);
arenaviruses (Lassa fever, meningitis); or-thomyxoviruses (influenza);
paramyxoviruses (measles, mumps); picornaviruses (polio, meningitis, colds);
rhab-doviruses (rabies); rubella virus (German measles); and retroviruses
(AIDS).
Although the specific details
of replication vary among types of viruses, the overall process can be
described as consisting of five phases: (1) attachment and penetra-tion, (2)
uncoating, (3) synthesis of viral components, (4) assembly of virus particles,
and (5) release of the virus. An overview of the viral replication cycle is
shown in Figure 50.1.
Infection begins when specific receptor sites on the virus recognize corresponding surface proteins on the host cell. The virus penetrates the host membrane by a mechanism resembling endocytosis and is encapsulated by the host cell’s cytoplasm, forming a vacuole. Next, the protein coat dissociates and releases the viral genome, usually into the host cell’s nucleus.
Following the release of its
genome, the virus synthesizes nucleic acids and proteins in sequence. In DNA
viruses, the first genes to be transcribed are the im-mediate–early genes.
These genes code for regulatory proteins that in turn initiate the
transcription of the early genes responsible for viral genome replication.
After the viral DNA is replicated, the late genes are transcribed and
translated, producing proteins required for the assembly of the new virions.
RNA viruses have several major strate-gies for genome replication and protein
expression. Certain RNA viruses contain enzymes that synthesize messenger RNA
(mRNA) using their RNA as a template; others use their own RNA as mRNA. The
retroviruses use viral reverse transcriptase enzymes to produce DNA using viral
RNA as a template. The newly synthesized DNA integrates into the host genome
and is transcribed into mRNA and genomic RNA for progeny virions.
Following their production,
the viral components are assembled to form a mature virus particle. The viral
genome is encapsulated by viral protein; in some cases (e.g. adenovirus,
poliovirus), it is not encapsulated. In certain viruses, such as the
poxviruses, multiple mem-branes surround the capsid. Release of the virus from
the host cell may be rapid and produce cell lysis and death. A slower process
resembling budding may allow the host cell to survive.
Three basic approaches are
used to control viral dis-eases: vaccination, antiviral chemotherapy, and
stimula-tion of host resistance mechanisms.Vaccination has been used
successfully to prevent measles, rubella, mumps, poliomyelitis, yellow fever,
smallpox, chickenpox, and hepatitis B. Unfortunately, the usefulness of
vaccines ap-pears to be limited when many stereotypes are involved (e.g.,
rhinoviruses, HIV). Furthermore, vaccines have lit-tle or no use once the
infection has been established be-cause they cannot prevent the spread of
active infections within the host. Passive immunization with human im-mune
globulin, equine antiserum, or antiserum from vaccinated humans can be used to
assist the body’s own defense mechanisms. Intramuscular preparations of im-mune
globulin may be used to prevent infection follow-ing viral exposure and as
replacement therapy in indi-viduals with antibody deficiencies. Peak plasma
concentrations of intramuscular immune globulins occur in about 2 days. In contrast,
intravenously administered immune globulin provides immediate passive immunity.
The chemotherapy of viral
infections may involve interference with any or all of the steps in the viral
replication cycle. Because viral
replication and host cell processes
are so intimately linked, the main problem in
the chemotherapy of viruses is finding a drug that is se-lectively
toxic to the virus. Stimulation of host resistance
is the least used of the antiviral intervention strategies.
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