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Seaweed Infusion Responsible for the Inhibition of the AIDS Virus
From the Journals of AIDS Research and Therapy.... for those of you with an interest.
Inhibition of highly productive HIV-1 infection in T cells, primary
human macrophages, microglia, and astrocytes by Sargassum fusiforme
Elena E Paskaleva , Xudong Lin , Wen Li , Robin Cotter , Michael T
Klein , Emiliy Roberge , Er K Yu , Bruce W Clark , Jean-Claude
Veille , Yanze Liu , David Y-W Lee and Mario Canki
AIDS Research and Therapy 2006, 3:15 doi:10.1186/1742-6405-3-15
Published 25 May 2006
Abstract (provisional)
Background
The high rate of HIV-1 mutation and increasing resistance to
currently available antiretroviral (ART) therapies highlight the
need for new antiviral agents. Products derived from natural sources
have been shown to inhibit HIV-1 replication during various stages
of the virus life cycle, and therefore represent a potential source
of novel therapeutic agents. To expand our arsenal of therapeutics
against HIV-1 infection, we investigated aqueous extract from
Sargassum fusiforme (S. fusiforme) for ability to inhibit HIV-1
infection in the periphery, in T cells and human macrophages, and
ability to inhibit in the central nervous system (CNS), in microglia
and astrocytes.
Results
S. fusiforme extract blocked HIV-1 infection and replication by over
90% in T cells, human macrophages and microglia, and it also
inhibited pseudotyped HIV-1 (VSV/NL4-3) infection in human
astrocytes by over 70%. Inhibition was mediated against both CXCR4
(X4) and CCR5 (R5)-tropic HIV-1, was dose dependant and long
lasting, did not inhibit cell growth or viability, was not toxic to
cells, and was comparable to inhibition by the nucleoside analogue
2', 3'-didoxycytidine (ddC). S. fusiforme treatment blocked direct
cell-to-cell infection spread. To investigate at which point of the
virus life cycle this inhibition occurs, we infected T cells and CD4-
negative primary human astrocytes with HIV-1 pseudotyped with
envelope glycoprotein of vesicular stomatitis virus (VSV), which
bypasses the HIV receptor requirements. Infection by pseudotyped HIV-
1 (VSV/NL4-3) was also inhibited in a dose dependant manner,
although up to 57% less, as compared to inhibition of native NL4-3,
indicating post-entry interferences.
Conclusions
This is the first report demonstrating S. fusiforme to be a potent
inhibitor of highly productive HIV-1 infection and replication in T
cells, in primary human macrophages, microglia, and astrocytes.
Results with VSV/NL4-3 infection, suggest inhibition of both entry
and post-entry events of the virus life cycle. Absence of
cytotoxicity and high viability of treated cells also suggest that
S. fusiforme is a potential source of novel naturally occurring
antiretroviral compounds that inhibit HIV-1 infection and
replication at more than one site of the virus life cycle.
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