Men with low T-cells need
medicine to fight PCP
Gay men with fewer than 200 helper T-
cells need medicine to prevent Pneumocystis
cariini pneumonia, PCP, even if these men are
otherwise healthy, say researchers from the
Multi-Center AIDS Cohort Study. In
addition, men with more than 200 T-cells
need medicine to prevent PCP if they also
have thrush, fever, night sweats, weight loss,
or other symptoms of HIV infection. These
doctors reached their conclusions after
studying over 5,000 gay men for over four
years. Otherwise healthy men with more than
200 T-cells rarely got PCP. The doctors
recommend that gay men infected with HIV
have T-cell tests done every six months. Men
who have T-cells that drop below 200 should
take medicine to prevent PCP. The CDC
recommends either monthly aerosolized
Pentamidine treatments or daily oral
medication to help prevent PCP.
Reference: J. Phair and others. The risk of
PCP among men infected with HIV-1. The
New England Journal of Medicine. Jan. 18,
1990, pg: 161-63.
days, four of the six men no longer had HIV
cultured from their blood; and five of the six
men had lower blood levels of p24 — a sign
that less of the HIV was reproducing.
Although these early results show promise, it
is too soon to know whether rsCD4 decreases
the likelihood of developing an opportunistic
infection.
Reference: R. Gerety and others. Human
recombinant soluble CD4 therapy. Lancet.
Dec. 23130,1989, pg: 1521.
Recombinant CD4 prevents
infection
In laboratory experiments, a new drug
called recombinant soluble CD4 or rsCD4
prevented HIV from infecting two kinds of
white blood cells called monocytes and
macrophages. These two kinds of white blood
cells can harbor HIV and lead to further
infection of T-cells. RsCD4 also prevented
HIV inside of monocytes and macrophages
from spreading to T-cells. RsCD4 is an
artificial form of the handle where HIV
attaches to T-cells and other kinds of white
blood cells. RsCD4 works by fooling HIV
into attaching to rsCD4 rather than the real
CD4 on the surface of T-cells, monocytes and
macrophages.
Reference: M. Harbison and others.
Effects o f recombinant soluble CD4 on HIV-1
infection of monocyte!macrophages. Journal
of Infectious Diseases. Jan. 1990, pg: 1-5.
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HIV hinge may explain infection
BY
JEFFREY
Z U R L I N D E N
KS may be sexually transmitted
Kaposi’s sarcoma, or KS, may be caused
by a virus or another kind of germ that is
passed from person to person during sex, say
doctors at the Centers for Disease Control.
Although they have not identified the germ
that they believe causes KS, these doctors
think the statistics offer proof. Until the AIDS
epidemic, KS was rare. Today approximately
15 percent of people with AIDS have KS, but
gay men are more likely than IV-drug users to
have KS. Gay men in California and New
York are also more likely to have KS than are
men who live in the midwest In addition, the
percentage of gay men with AIDS who have
KS has decreased since the beginning of the
epidemic. Since the epidemic began, many
more gay men — even men who are
infected with HIV — use condoms. Condoms
and other safe-sex practices may prevent the
spread of the germ that causes KS in people
who are already infected with HIV.
Reference: V. Beral and others. Kaposi’s
sarcoma among persons with AIDS: a
sexually transmitted disease? Lancet. Jan.
20,1990, pg: 123-27
Recombinant CD4 shows
promise
Six men with AIDS received daily
injections of a new drug called recombinant
soluble CD4 also known as rsCD4. After 28
~
Scientists in England may have discovered
the key that allows HIV to attach to and infect
fresh cells. According to these researchers, the
piece of HIV that glues to a T-cell must first
break into a hinge to fit into that T-cell. In
order to make a hinge, HIV uses a substance
called protease. Drugs called protease
inhibitors could stop HIV from making hinges
and could prevent HIV from infecting fresh
cells.
Reference: P. Stephens and others. A
chink in HIV’s armour? Nature. Jan. 18,
1990, pg: 219.
New substance prevents HIV
from multiplying
In test-tube experiments, substances
known as protease inhibitors prevented HIV
from reproducing and infecting fresh cells. To
multiply, HTV must first divide large pieces
of virus into small building blocks that are
rearranged into packages that infect fresh
cells. A substance called protease chops the
immature large pieces into mature small
pieces. Protease inhibitors, in turn, prevent
protease from working, thus protease
inhibitors prevent HIV from maturing into a
form that can infect new cells. These
scientists have found two powerful substances
that block protease. They hope that these new
protease inhibitors will not harm healthy cells
and may eventually be used to treat people
who are infected with HIV.
Reference: T. Meek and others. Inhibition of
HIV-1 protease in infected T-lymphocytes by
synthetic peptide analogues. Nature. Jan. 4,
1990, pg: 90-92.
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