Specific cell surface requirements for the infection of CD4-positive cells by human immunodeficiency virus types 1 and 2 and by simian immunodeficiency virus

Abstract

Human CD4 was expressed on a range of mammalian cell lines. CD4+ non-primate cells, derived from rat, hamster, mink, cat, and rabbit, bind recombinant gp120 of human immunodeficiency virus type 1 (HIV-1) but are resistant to HIV-1 infection. CD4 expression on various human, rhesus, and African green monkey cell lines confers differential susceptibilities for HIV-1, HIV-2, and simian immunodeficiency (SIV) strains. For example, CD4+ TE671 rhabdomyosarcoma cells are sensitive to HIV-1 and HIV-2 but resistant to SIV, whereas CD4+ U87 glioma cells are resistant to HIV-1 infection but sensitive to HIV-2 and SIV. HIV-1 infection was not dependent on human major histocompatibility class I expression. Studies of cell fusion and of infection by vesicular stomatitis virus pseudotypes bearing HIV-1 and HIV-2 envelopes showed that the differential cell tropisms of HIV-1, HIV-2, and SIV are determined at the cell surface.

Human immunodeficiency virus type 1 infection of human CD4-transgenic rabbits

“…To establish that these cells synthesized the antigen found in the supernatant precautions were necessary. A quantity of the inoculum might adsorb to the cell membrane but fail to penetrate, as happens with other non-primate cells transfected with huCD4 (Clapham et al, 1991;McKnight et al, 1994). Subsequently, this antigen can then be released into the culture supernatant and might be confused with antigen that has been synthesized by the cells.…”

Frequency of polymorphisms of genes coding for HIV-1 co-receptors CCR5 and CCR2 in a Brazilian population

“…Evidence suggesting additional receptors first came from the fact that HIV-1 could not efficiently replicate in other animal cells engineered to express human CD 4 [1]. The discovery of co-receptors for HIV-1 entry, such as CXCR4, CCR5, CCR2, and CCR3, which are chemokine receptors, have provided insights into this phenomenon [2].…”

“…In fact, different HIV-1 strains have distinct cell tropisms; viruses with T-cell tropism utilize the CXCR4 co-receptor, while those with selective macrophagemonocyte tropism utilize the CCR5 or CCR2 co-receptors [2,7]. The strain usually involved in the primary infection -macrophage-tropic isolates -is the strain that uses the CCR5 or CCR2 co-receptors expressed on mucosal dendritic cells.…”

Human retroviruses and AIDS 1997

“…In contrast to the laboratory adapted strains of HTV-1, both SIV and HIV-2 infection and syncytium formation can be enhanced by sub-inhibitory concentrations of the soluble receptor. Incubation of sCD4 with SIVagm viruses not only accelerates the kinetics of infection but also leads to a 100-fold increase in the titer of the virus (Allan et al, 1990;Clapham et al, 1991;Sekigawa et al, 1990;Werner et al, 1990). A similar enhancement of infectivity has recently been observed with HIV-1 when poorly neutralizable primary isolates are treated with sub-inhibitory concentrations of sCD4 (Sullivan etal., 1995).…”