643
CHAPTER SIXTEEN
Lymphatic System and Immunity
cals that destroy the recipient’s tissues. Antigens on cells
in scleroderma lesions match those that cause GVHD.
Mothers who have scleroderma and their sons have cell
surfaces more similar than those of unaffected moth-
ers and their sons. Perhaps the similarity of cell surfaces
enabled the fetal cells to escape destruction by the wom-
an’s immune system. Female fetal cells probably have the
same effect, but these cells cannot be distinguished from
maternal cells by the presence of a Y chromosome.
Perhaps other disorders considered autoimmune refl ect an
immune system response to lingering fetal cells.
PRACTICE
33
How are allergic reactions and immune reactions similar yet dif
erent?
34
How does a tissue rejection reaction involve an immune response?
35
How is autoimmunity an abnormal Functioning oF the immune
response?
stimulating antibody production. The resulting antibodies and
symptoms appear to be an autoimmune disorder. The pres-
ence of more than one genetically distinct cell population in
an individual is called microchimerism (“small mosaic”).
Microchimerism that refl ects the retention of cells from a fetus
may explain the higher prevalence of autoimmune disorders
among women. It is seen in a disorder called scleroderma,
which means “hard skin.”
Scleroderma, which typically begins between ages forty-
± ve and ± fty-± ve, is described as “the body turning to stone.”
Symptoms include fatigue, swollen joints, stiff ±
ngers, and
a masklike face. The hardening may affect blood vessels,
the lungs, and the esophagus. Clues that scleroderma is a
delayed response to persisting fetal cells include the follow-
ing observations:
It is much more common among women.
Symptoms resemble those of graft-versus-host disease
(GVHD), in which transplanted tissue produces chemi-
cells to Form. Entry oF a single virus into a single cell
can cause inFection, and so any vaccine must be
extremely powerFul and Fast-acting.
It may not be possible to devise an HIV vac-
cine. There are other ways to prevent HIV inFec-
tion, such as education about reducing risk
Factors, circumcising men, and giving pregnant
women antiretroviral drugs to prevent transmis-
sion to oFFspring. ±or people already inFected,
ing the million to billion new HIV particles that
inFected cells release daily.
So genetically diverse is the population oF
HIV in a human host that within days oF initial
inFection, viral variants can arise that resist drugs.
Combining drugs that act in dif
erent ways mini-
mizes the number oF viruses (“viral load”) and
delays symptom onset and progression. Classes
oF HIV/AIDS drugs target dif
erent points oF viral
vulnerability. The mechanisms oF action parallel
viral inFection. They block HIV From binding to T
cells, Fusing with the cell membrane, entering the
cell, replicating its genetic material once in the
cell, or processing its proteins to a Functional size.
More than 200 drugs are also used to treat AIDS-
associated inFections and cancers.
Viral variability has also stymied vaccine devel-
opment. Many candidates have Failed. Reasons
vary. Some trials did not go on For long enough to
see an ef
ect. Others did not accurately consider the
expected incidence oF inFection in the studied popu-
lation, critical to predicting the number oF expected
cases in a trial and Following enough patients to see
an ef
ect. Many people dropped out oF clinical trials
or Failed to comply with complex drug regimens.
Other reasons For the Failure to develop a vaccine
are scientiFic—a live vaccine is too dangerous; a
killed vaccine does not evoke a su²
cient immune
response; and insertion oF viral genetic material
into human chromosomes happens too Fast to raise
an antibody response, let alone enable memory
drugs work so well that For some individuals who
have access to them, HIV inFection and AIDS may
become chronic diseases.
The epidemic may have peaked. The Joint UN
Programme on HIV/AIDS estimates that incidence
worldwide is declining by 2.5 percent per year—but
this still projects 20 to 60 million new inFections by
the year 2028. Perhaps like other inFectious diseases,
AIDS will become less harmFul as time goes on.
TABLE
16B
|
HIV Transmission
How HIV Is Transmitted
Sexual contact, particularly anal intercourse, but also vaginal intercourse and oral sex
Contaminated needles (intravenous drug use, injection oF anabolic steroids, accidental needle stick
in medical setting)
During birth From inFected mother
Breast milk From an inFected mother
Receiving inFected blood or other tissue (precautions usually prevent this)
How HIV Is Not Transmitted
Casual contact (social kissing, hugging, handshakes)
Objects (toilet seats, deodorant sticks, doorknobs)
Mosquitoes
Sneezing and coughing
Sharing Food
Swimming in the same water
Donating blood
previous page 673 David Shier Hole's Human Anatomy and Physiology 2010 read online next page 675 David Shier Hole's Human Anatomy and Physiology 2010 read online Home Toggle text on/off