A study just published in the Journal of Biochemistry has
generated a great deal of press coverage because it reports that a compound
derived from bananas can inhibit HIV in a lab dish. The substance, a banana
lectin known as BanLec, was first discovered twenty years ago and shown to be a potent mitogen (a substance
which non-specifically stimulates T cell proliferation). The mechanism of HIV
inhibition appears related to its ability to bind to sugar molecules on the viral envelope, thereby blocking virus attachment and entry into target cells. This
mechanism is similar to the broadly neutralizing monoclonal antibody 2G12, although the paper reports that, unlike
2G12, BanLec can inhibit HIV isolates from clade C as well as clade B. The researchers
conclude that BanLec might be adapted for use in microbicides, but caution that
its mitogenic potential would have to somehow be stymied. Unfortunately many of
the press stories have missed this caveat, instead characterizing BanLec as
“naturally occurring” as if this is synonymous with safe. But the caveat is
crucial, because stimulation of T cell proliferation would carry the risk of
increasing susceptibility to HIV infection and causing other untoward
inflammation-related toxicities. A Google news search for “BanLec HIV” currently retrieves 156 results, a search for “BanLec mitogen” retrieves none.
J Biol Chem. 2010 Mar 19;285(12):8646-55. Epub 2010 Jan 15.
A Lectin Isolated from Bananas Is a Potent Inhibitor of HIV
Replication
Michael D. Swanson‡, Harry C. Winter§, Irwin J. Goldstein§ and
David M. Markovitz‡¶‖,1
From the ¶Department of Internal Medicine, Division of
Infectious Diseases, ‡Program in Immunology, ‖Cellular and Molecular
Biology Program, and
§Department of Biological Chemistry, University of Michigan Medical
Center, Ann Arbor, Michigan 48109
Abstract
BanLec is a jacalin-related lectin isolated from the fruit
of bananas, Musa acuminata. This lectin binds to high mannose carbohydrate
structures, including those found on viruses containing glycosylated envelope
proteins such as human immunodeficiency virus type-1 (HIV-1). Therefore, we
hypothesized that BanLec might inhibit HIV-1 through binding of the
glycosylated HIV-1 envelope protein, gp120. We determined that BanLec inhibits
primary and laboratory-adapted HIV-1 isolates of different tropisms and
subtypes. BanLec possesses potent anti-HIV activity, with IC50 values in the
low nanomolar to picomolar range. The mechanism for BanLec-mediated antiviral
activity was investigated by determining if this lectin can directly bind the
HIV-1 envelope protein and block entry of the virus into the cell. An
enzyme-linked immunosorbent assay confirmed direct binding of BanLec to gp120
and indicated that BanLec can recognize the high mannose structures that are
recognized by the monoclonal antibody 2G12. Furthermore, BanLec is able to
block HIV-1 cellular entry as indicated by temperature-sensitive viral entry
studies and by the decreased levels of the strong-stop product of early reverse
transcription seen in the presence of BanLec. Thus, our data indicate that
BanLec inhibits HIV-1 infection by binding to the glycosylated viral envelope
and blocking cellular entry. The relative anti-HIV activity of BanLec compared
favorably to other anti-HIV lectins, such as snowdrop lectin and Griffithsin,
and to T-20 and maraviroc, two anti-HIV drugs currently in clinical use. Based
on these results, BanLec is a potential component for an anti-viral microbicide
that could be used to prevent the sexual transmission of HIV-1.
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