Research from the National Institutes of Health finds a common
and apparently harmless virus appears to significantly hinder
early stages of HIV infection in laboratory grown human tissue.
"Future research could lead to new drugs that can better help the
immune system to fend off HIV, and may even lead to new
strategies for designing a vaccine against HIV," said Duane
Alexander, director of the National Institute of Child Health and
Human Development, the organization which led the research.
Scientists, however, strongly recommend against AIDS patients
running out to get infected with the apparently helpful germ --
human herpesvirus 6 or HHV-6 -- especially as it may enhance
human immunodeficiency virus growth in the later stages of the
"Before these approaches could be developed and tested, any
attempts to use HHV-6 to slow down HIV infection are risky and
premature," cautioned lead researcher Leonid Margolis.
Human herpesvirus 6 is common throughout the world. It does not
seem to cause any illness in adults, although infants infected
with the germ may develop a mild rash that disappears within
Margolis and his colleagues worked with lab-grown human tonsil
tissue they infected with both HIV and HHV-6. They found human
herpesvirus 6 dramatically suppressed the growth of the HIV
variants that dominate the early stages of infection.
Both early and late stage variants of HIV bind to molecules
called receptors that poke out of the surfaces of cell membranes.
Molecules on the surface of HIV bind to immune cell receptors
much as keys fit in locks, allowing the virus to fuse with cells
and infect them.
Early stage versions of HIV bind to a receptor known as CCR5.
People infected with these germs may not show any outward sign of
disease for a long period. Late stage variants of HIV, however,
are associated with the rapid decline of the immune system. They
bind to a different receptor, CXCR4.
The scientists discovered human herpesvirus 6 dramatically slows
down the growth of early stage HIV by triggering the release of
large amounts of a biochemical called RANTES. This molecule
apparently blocks the CCR5 receptor, essentially acting like a
plug so HIV cannot come in.
On the other hand, the late-stage HIV variants that use CXCR4
appeared to reproduce slightly more rapidly in the presence of
HHV-6. This increase in growth rate did not, however, approach
Recent studies suggest a number of infections appear to hinder
HIV, among them the apparently harmless GBV-C virus and the
microbes that cause the potentially lethal illness scrub typhus.
Jack Stapleton, senior researcher behind the GBV-C findings, said
the technique of using living human tissue represented a major
advance, as it allowed Margolis' team to identify the mechanism
behind human herpesvirus 6's anti-HIV effect.
"If the trigger for that mechanism can be identified, the next
step would be try to mimic that effect to create a drug,"
Stapleton said in an interview with United Press International.
"In theory, the ability of HIV to resist a drug that acts on the
cell may be lower than the ability of HIV to resist drugs that
act on the virus as current types of HIV medicine do."