Forthal D, Landucci G, Little S, Daar E; Conference on Retroviruses and Opportunistic Infections.

7th Conf Retrovir Oppor Infect Jan 30 Feb 2 2000 Conf Retrovir Oppor Infect 7th 2000 San Franc Calif. 2000 Jan 30-Feb 2; 7: 183 (abstract no. 571).

Univ. of California, Irvine.

Neutralizing Ab is generally undetectable until months after AcHIV. However, it is not known if Ab can inhibit virus by mechanisms other than neutralization during AcHIV. We determined the ability of 14 plasma samples from 10 untreated patients, obtained 6-28 days (median=19.5) after onset of AcHIV symptoms, to inhibit HIV in the presence of natural killer effector cells. A primary heterologous R5 strain (HIV657) or primary autologous isolates from 4 of the 10 patients were used to infect PHA-stimulated CD4 cells. After 48 hours, infected cells were washed, and 10% patient plasma (or HIV-negative plasma) with or without effector cells (effector:target=10:1) was added; viral yield was determined by measuring supernatant p24 at 7 or 10 days. Since plasma was not washed off, Ab could bind to infected cells and to cell-free virus produced by infected cells. In the presence of HIV-negative plasma, NK effector cells had no effect on viral yield. Without effector cells, patient plasma also did not reduce viral yield, indicating a lack of neutralizing activity and inability to inhibit cell-to-cell spread. However, with effector cells, plasma from 5 patients inhibited viral yield from cells infected with the heterologous HIV657 strain by 90-99%, and 3 inhibited by 70-90%. The % inhibition correlated inversely with plasma viral load obtained the same day (R= -0.5; p=0.05). 5 plasma tested with both autologous virus and HIV657 had almost identical anti-viral activity against both strains; 2 of these plasma also had similar activity when tested with other primary heterologous strains. Finally, one plasma with no activity against HIV657 reduced viral yield by 70% after centrifugation to remove immune complexes. Thus, 1) a potent anti-viral Ab response occurs during AcHIV and may play a role in controlling viremia; 2) The Ab is directed at infected cells and requires effector cells; 3) similar activity against different strains suggests that antigenic determinants are conserved or the Ab is directed against a number of different epitopes; 4) immune complexes may mask or down-regulate Ab activity during AcHIV.

Publication Types:

• Meeting Abstracts

Keywords:

• Acquired Immunodeficiency Syndrome
• Antibodies, Viral
• Antigen-Antibody Complex
• CD4-Positive T-Lymphocytes
• HIV Infections
• HIV Seropositivity
• Humans
• Viral Load
• Viremia
• Virus Diseases
• immunology

Other ID:

• GWAIDS0005950

UI: 102243447

From Meeting Abstracts