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Receptors1
Departments of
*
Microbiology/Immunology and
Anatomy, Division of Immunobiology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298;
Department of Microbiology, Brigham Young University, Provo, UT 84602; and
Department of Neurology, Johns Hopkins University, Baltimore, MD 21287
Large quantities of HIV are found trapped on the surface of
follicular dendritic cells (FDCs), and virus persists on these cells
until they ultimately die. We recently found that FDCs maintain HIV
infectivity for long periods in vivo and in vitro. Because FDCs trap
Ags (and virus) in the form of immune complexes and are rich in
Fc
Rs, we reasoned that Ab and FcRs may be required for
FDC-mediated maintenance of HIV infectivity. To investigate this
hypothesis, HIV immune complexes were formed in vitro and incubated for
increasing times with or without FDCs, after which the remaining
infectious virus was determined by HIV-p24 production in rescue
cultures. FDCs maintained HIV infectivity in vitro in a dose-dependent
manner but required the presence of specific Ab for this activity
regardless of whether laboratory-adapted or primary X4 and R5 isolates
were tested. In addition, Abs against either virally or host-encoded
proteins on the virion permitted FDC-mediated maintenance of HIV
infectivity. We found that the addition of FDCs to HIV immune complexes
at the onset of culture gave optimal maintenance of infectivity.
Moreover, blocking FDC-FcRs or killing the FDCs dramatically reduced
their ability to preserve virus infectivity. Finally, FDCs appeared to
decrease the spontaneous release of HIV-1 gp120, suggesting that
FDC-virus interactions stabilize the virus particle, thus contributing
to the maintenance of infectivity. Therefore, optimal maintenance of
HIV infectivity requires both Ab against particle-associated
determinants and FDC-FcRs.
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