Page 274 - Review of Medical Microbiology and Immunology ( PDFDrive )

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CHAPTER 33 Host Defenses
receptors on the cells of the resistant species. For example,
body may be produced against the original virus than
some people are resistant to HIV infection because they
against the current one. It appears that the immunologic
lack one of the chemokine receptors that mediate entry of
the virus into the cell. However, by far the most important
memory cells can respond to the original antigenic expo-
sure to a greater extent than to the subsequent one. This
type of defense is acquired immunity, either actively
acquired by exposure to the virus or passively acquired by
1
the transfer of immune serum. Active immunity can be
influenza virus, who, when exposed to the A type, pro-
2
duced large amounts of antibody to A but very little anti-
elicited by contracting the actual disease, by having an
body to the A virus. It is also the underlying cause of
inapparent infection, or by being vaccinated. was observed in people with antibodies to the A type of
2
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severe hemorrhagic dengue fever (see Chapter 42). This
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phenomenon has two practical consequences as well:
1. Active Immunity
(1) attempts to vaccinate people against the different influ-
Active immunity, in the form of both antibodies and cyto-
toxic T cells, is very important in the prevention of viral
(2) epidemiologic studies based on measurement of anti-
diseases. The first exposure to a virus, whether it causes an
body titers may yield misleading results.
How does antibody inhibit viruses? There are two main
inapparent infection or symptomatic disease, stimulates the
production of antibodies and the activation of cytotoxic T
mechanisms. The first is neutralization of the infectivity of
cells. The role that antibodies and cytotoxic T cells play in
the virus by antibody binding to the proteins on the outer
the recovery from this first infection is uncertain and may
vary from virus to virus, but it is clear that they play an
prevent the interaction of the virus with cell receptors, and
essential role in protecting against disease when exposed to
(2) it can cross-link the viral proteins and stabilize the virus
the same virus at some time in the future. surface of the virus. This binding has two effects: (1) It can
so that uncoating does not occur. The virus therefore can-
The duration of protection varies; disseminated viral
not replicate. Furthermore, antibody-coated virus is more
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rapidly phagocytized than normal virus, a process similar
infections such as measles and mumps confer lifelong
immunity against recurrences, but localized infections
to the opsonizing effect of antibody on bacteria. Antibody
such as the common cold usually impart only a brief
immunity of several months. IgA confers protection
can be recovered by dissociating the virus–antibody com-
against viruses that enter through the respiratory and gas-
plex. Incomplete, also called “blocking,” antibody can inter-
trointestinal mucosa, and IgM and IgG protect against
fere with neutralization and form immune complexes,
viruses that enter or are spread through the blood. The
which are important in the pathogenesis of certain diseases.
lifelong protection against systemic viral infections such as
Some viruses, such as herpesviruses, can spread from cell
to cell across intercellular bridges, eluding the neutralizing
the childhood diseases measles, mumps, rubella, and
chickenpox (varicella) is a function of the anamnestic (sec-
Antibodies that interfere with the adherence (adsorp-
ondary) response of IgG. For certain respiratory viruses
tion and penetration) of viruses to cell surfaces are called
such as parainfluenza and respiratory syncytial viruses, the
neutralizing antibodies. Note that neutralizing antibody is
IgA titer in respiratory secretions correlates with protec- effect of antibody.
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directed against the surface proteins of the virus, typically
tion, whereas the IgG titer does not. Unfortunately, protec-
the proteins involved with the interaction of the virus with
tion by IgA against most respiratory tract viruses usually
receptors on the surface of the host cell. Antibodies formed
lasts less than 5 years.
The role of active immunity in recovery from a viral
antigen of hepatitis B virus) do not neutralize the infectivity
infection is uncertain. Because recovery usually precedes
of the virus.
the appearance of detectable humoral antibody, immuno-
globulins may not be important. Also, children with agam-
The second main mechanism is the lysis of virus-
infected cells in the presence of antibody and complement.
maglobulinemia recover from measles infections normally
and can be immunized against measles successfully, indi-
Antibody binds to new virus-specific antigens on the cell
cating that cell-mediated immunity plays an important
degrades the cell membrane. Because the cell is killed
role. This is supported by the observation that children
with congenital T-cell deficiency are vulnerable to severe
before the full yield of virus is produced, the spread of virus
infections with measles virus and herpesviruses. T cells are surface and then binds complement, which enzymatically
is significantly reduced.
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Lysis of virus-infected cells is also caused by cytotoxic T
important in recovery from many but not all viral
lymphocytes. These CD8-positive T cells recognize viral
illnesses.
antigen only when it is presented in association with class I
The protection offered by active immunity can be
affected by the phenomenon of original antigenic sin. This
term refers to the observation that when a person is
cells by three methods: (1) by releasing perforins, which
exposed to a virus that cross-reacts with another virus to
make holes in the cell membrane of the infected cells; (2) by
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