Abstract
Shortly after the pioneering Montagnier/Gallo discoveries of HIV as the etiologic agent of AIDS, the CD4 antigen was identified as the primary receptor for HIV entry. The focus of the present story begins with 1986 report from Richard Axel’s group that recombinant human CD4 conferred permissiveness to HIV-1 infection when expressed on diverse human cell types, but not on mouse cells. The block was at an early replication step after virion binding, perhaps virus internalization (1).
Highlights
After the pioneering Montagnier/Gallo discoveries of HIV as the etiologic agent of AIDS, the CD4 antigen was identified as the primary receptor for HIV entry
In a reductionist system using the corresponding vaccinia recombinants, we showed that cells expressing HIV-1 Env formed syncytia when mixed with cells expressing human CD4, provided the latter were of human origin [3]
They had shown that a target gene linked to the phage T7 promoter is activated by the vaccinia-encoded T7 RNA polymerase expressed in the same cell; the presence of all components in the cytoplasm leads to robust transient expression of the target gene [7]
Summary
After the pioneering Montagnier/Gallo discoveries of HIV as the etiologic agent of AIDS, the CD4 antigen was identified as the primary receptor for HIV entry. The focus of the present story begins with 1986 report from Richard Axel’s group that recombinant human CD4 conferred permissiveness to HIV-1 infection when expressed on diverse human cell types, but not on mouse cells.
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