642
UNIT FOUR
TABLE
16.11
|
Autoimmune Disorders
Disorder
Symptoms
Antibodies Against
Glomerulonephritis
Lower back pain
Kidney cell antigens that resemble streptococcal bacteria antigens
Graves disease
Restlessness, weight loss, irritability, increased heart rate
and blood pressure
Thyroid gland antigens near thyroid-stimulating hormone receptor,
causing overactivity
Type I diabetes mellitus
Thirst, hunger, weakness, emaciation
Pancreatic beta cells
Hemolytic anemia
Fatigue and weakness
Red blood cells
Multiple sclerosis
Weakness, incoordination, speech disturbances, visual
complaints
Myelin in the white matter of the central nervous system
Myasthenia gravis
Muscle weakness
Receptors for neurotransmitters on skeletal muscle
Pernicious anemia
Fatigue and weakness
Binding site for vitamin B on cells lining stomach
Rheumatic fever
Weakness, shortness of breath
Heart valve cell antigens that resemble streptococcal bacteria antigens
Rheumatoid arthritis
Joint pain and deformity
Cells lining joints
Systemic lupus erythematosus
Red rash on face, prolonged fever, weakness, kidney
damage, joint pain
Connective tissue
Ulcerative colitis
Lower abdominal pain
Colon cells
as in the anus or vagina (see ±
gure 3.34). Then, the
virus enters macrophages, impairing this ±
rst line of
defense. In these cells and later in helper T cells, the
virus adheres with a surface protein, called gp120,
to coreceptors on the host cell surface, called CD4
and CCR5, discussed in the vignette to Chapter 3.
Once the virus enters the cell, a viral enzyme, reverse
transcriptase, catalyzes the construction of a DNA
strand complementary to the viral RNA sequence
(the virus has RNA as its genetic material). The initial
viral DNA strand replicates to form a DNA double
helix, which enters the cell’s nucleus and inserts
into a chromosome. The viral DNA sequences are
then transcribed and translated. The cell ±
lls with
pieces of HIV, which are then assembled into new
viral particles that eventually burst from the cell.
Once infected helper T cells start to rapidly
die, bacterial infections begin, because B cells
aren’t activated to produce antibodies. Much
later in infection, HIV variants arise that bind to
receptors called CXCR4 on cytotoxic T cells, kill-
ing them too. Loss of these cells renders the body
vulnerable to other infections and to cancers.
Viral Variabilty
HIV replicates quickly, and can hide, twisting and
altering its surface features in ways that evade
recognition and attack by antibodies or cytotoxic
T cells. The virus is especially prone to mutation,
because it cannot repair DNA replication errors.
The immune system cannot keep up; antibod-
Natural History of a Modern Plague
I
n late 1981 and early 1982, physicians from
large cities began reporting to the United States
Centers for Disease Control and Prevention
cases of formerly rare infections in otherwise healthy
young men. Infections prevalent in the general
population, such as herpes simplex and cytomega-
lovirus, were unusually severe in these young men.
Some infections were caused by organisms known
to infect only nonhuman animals. Other infections,
particularly pneumonia caused by the microor-
ganism
Pneumocystis jirovecii,
and a cancer, Kaposi
sarcoma, were known only in individuals whose
immune systems were suppressed (fig. 16B). The
bodies of the sick young men had become nesting
places for all types of infectious agents, including
viruses, bacteria, protozoa, and fungi. The infections
were
opportunistic,
which means that they took
advantage of a weakened immune system.
As the unusual infections spread, a portrait of
a lethal infectious disease emerged. Table 16B lists
how it is, and isn’t, spread.
Acquired immune defi-
ciency syndrome,
or AIDS, starts with recurrent fever,
weakness, and weight loss. This may begin years
after infection with the human immuno de±
ciency
virus (HIV) that causes AIDS. Then, usually after
another relatively healthy period, infections begin.
How HIV Ravages the Immune System
HIV infection gradually shuts down the immune
system. First, HIV crosses a mucosal barrier, such
16.1
CLINICAL APPLICATION
Immunity Breakdown: AIDS
FIGURE 16B
Prior to the appearance of
AIDS, Kaposi sarcoma was a rare cancer seen
only in elderly Jewish and Italian men and in
people with suppressed immune systems. In
these groups, it produces purplish patches
on the lower limbs, but in AIDS patients,
Kaposi sarcoma patches appear all over the
body and sometimes internally too. These
lower limbs display characteristic lesions.
ies against one viral variant are useless against
another. For several years, the bone marrow pro-
duces 2 billion new T and B cells a day, counter-
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