Johns Hopkins Gazette: January 9, 1995

HIV Survivor Could Provide Clues to Assist in AIDS Battle

By Marc Kusinitz

     Scientists at Hopkins and elsewhere have discovered
important clues that may explain the remarkable ability of a
woman infected with HIV-1 to suppress growth of the virus or the
emergence of AIDS for many years.
     The clues emerged from studies of a woman infected with
HIV-1 for 13 years but with little trace of the virus within her.
She has never developed AIDS-related diseases. The research group
is now studying four other HIV-infected long-term survivors who
also seem to have suppressed reproduction of HIV-1.
     "There are at least a handful of long-term survivors
infected with HIV who have never had symptoms and whose immune
systems appear to have suppressed the AIDS virus to the point
where it cannot be grown from the blood in the laboratory
setting, even when we use the best tricks we have for growing and
detecting HIV," said David Schwartz, assistant professor of
molecular microbiology and immunology at the School of Hygiene
and Public Health.
     "This knowledge could lead to development of improved AIDS
vaccines and therapies," Dr. Schwartz said. Dr. Schwartz is the
leader of the study, funded by the National Institutes of Health
and the American Foundation for AIDS Research.
     While there is a previous report of an infected donor and
several recipients of HIV-tainted clotting factor doing very well
years after infection, the present case differs in several key
respects, including the fact that the blood donor and two other
recipients have died of AIDS.
     The patient's children, breast-fed for one year after her
infection, and her husband remain negative for HIV, according to
the report, published in the December issue of AIDS Research and
Human Retroviruses.
     The woman, referred to as patient 3799, was infected by a
contaminated blood transfusion during childbirth in 1981, but has
never had HIV-associated diseases. Although her levels of CD4 T
cells, an important type of immune system cell, have been reduced
since they were first measured in 1988, they have held steady
over that period.
     "Since she was first studied in 1985, laboratory tests have
consistently shown that her immune system has been making
antibodies to HIV-1," Dr. Schwartz said. "This is strong evidence
that she is infected with the virus. Test-tube experiments   
showed a lower number of antibody-producing cells making
antibodies against HIV-1 compared to most other HIV-positive
     Nevertheless, in more than 30 separate attempts over the
past six years, researchers at Hopkins and other laboratories
around the country have never succeeded in isolating replicating
HIV from the patient's blood or bone marrow, despite using the
most sensitive and sophisticated methods available. They have
detected very small amounts of proviral DNA--genetic material
belonging to HIV-1--in her blood T cells.
     Because HIV-1 DNA gets into human genes inside infected
cells, researchers say it is possible the HIV-1 DNA they found
actually belongs to multiplying viruses living somewhere other
than the circulating blood (for example, lymph nodes, spleen or
thymus). Or it may belong only to "dead end" mutant viruses that
got into the DNA of those white blood cells and then were copied
along with the cells' own DNA during normal cell division.
     However, the Hopkins-led team reported clues that suggest
how the woman's immune system was able to suppress HIV-1
     First, the researchers found that certain cells, called
lymphocytes, were very active in killing immune system cells
infected with HIV-1.
     This is common among symptom-free HIV-positive individuals,
Dr. Schwartz said. Unusual, however, was that, in test-tube
experiments, the woman's lymphocytes multiplied when exposed to
parts of the protein coat of the AIDS virus. For reasons not well
understood, such proliferation is almost never seen among
infected people, even early in disease or during long
symptom-free intervals.
     The authors suggest that the patient  may have been able to
suppress all the AIDS viruses that infected her, as well as those
that developed through mutation since then. Only defective,
slow-growing viruses would have remained in her white cells,
occasionally making individual pieces of the virus. These pieces
of virus could then have stimulated the woman's immune system
even though they weren't full, active viruses.
     The reason that the level of CD4 cells is reduced, but
stable, might be due to indirect consequences of the immune
response to those pieces of viral protein. For example, the viral
pieces might have somehow caused the cells to self-destruct,
stick together and die, or become "innocent by-standers" when the
immune system attacked other infected white blood cells.

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