30.2% of patients with the acquired immunodeficiency syndrome (AIDS) were homozygous for Gc 1 fast (Gc 1f) compared with 0.8% of controls (p less than 0.0001); patients with other clinical manifestations of HIV infection were also more likely than controls to have Gc 1f.
No significant differences in GC phenotype distribution were seen between controls and any of the at risk groups or patients, neither between HIV-Ab-positive/Ag-negative and HIV-Ab-positive/Ag-positive homosexual men nor between HIV-Ab-positive/Ag-positive homosexual men and AIDS patients, suggesting that the GC system is not involved in the infective susceptibility or progression of HIV infection to AIDS-related complex and AIDS.
Genetic subtypes of group-specific component (Gc), a protein possibly influencing susceptibility to human immunodeficiency virus infection, were assessed by isoelectric focusing of plasma from 88 patients with multiple sclerosis (MS) and related to frequencies among 3394 control individuals subjected to paternity studies.
A previous report suggested a relationship between particular phenotypes of group specific component (Gc), and susceptibility or resistance to HIV infection, whereas other recent investigations failed to corroborate this finding.
Because prolonged treatment of HIV infection with 3'-azido-3'-deoxythymidine (AZT) is associated with in vitro resistance to AZT, we examined whether HIV could induce/amplify the expression of p-glycoprotein in infected cells resulting in reduced drug accumulation leading to reduced sensitivity to AZT.
In a second experiment, HIV infection was studied: (1) sequentially by RT assay and P24 immunocapture on several clones; (2) by cocultivation of infected clones with umbilical cord lymphocytes.
In a second experiment, HIV infection was studied: (1) sequentially by RT assay and P24 immunocapture on several clones; (2) by cocultivation of infected clones with umbilical cord lymphocytes.
In a second experiment, HIV infection was studied: (1) sequentially by RT assay and P24 immunocapture on several clones; (2) by cocultivation of infected clones with umbilical cord lymphocytes.
In a second experiment, HIV infection was studied: (1) sequentially by RT assay and P24 immunocapture on several clones; (2) by cocultivation of infected clones with umbilical cord lymphocytes.
In a second experiment, HIV infection was studied: (1) sequentially by RT assay and P24 immunocapture on several clones; (2) by cocultivation of infected clones with umbilical cord lymphocytes.
These results demonstrate that elevated levels of IL-6 are associated with HIV-infection, and suggest that IL-6 over-production may contribute to the polyclonal B cell activation seen in AIDS and HIV infection.
In a second experiment, HIV infection was studied: (1) sequentially by RT assay and P24 immunocapture on several clones; (2) by cocultivation of infected clones with umbilical cord lymphocytes.
Surface CD4 protein was detected on these cells, and recombinant soluble CD4 (sCD4) blocked infection, indicating that HIV infection was mediated by the cell surface CD4 protein.
Infection of multiple stages and multiple subsets of the T-cell lineage in man, mediated via the CD4 molecule, may explain the inability of the T-cell pool to regenerate in the setting of progressive HIV infection.
Surface CD4 protein was detected on these cells, and recombinant soluble CD4 (sCD4) blocked infection, indicating that HIV infection was mediated by the cell surface CD4 protein.
The sCD4 produced by the viral vectors is immunoprecipitated by monoclonal antibodies against CD4, which specifically block human immunodeficiency virus (HIV) infection of helper/inducer T cells.
Although knowledge has accumulated about GP110-CD4 interaction, viral penetration into human CD4+ lymphocytes remains unclear, in spite of the fact that all studies on HIV infection were performed on cell-transformed lineages, or on human polyclonal CD4+ cells.