Immunoglobulin V(H) usage during primary infection of rhesus monkeys with chimeric simian-human immunodeficiency viruses

Abstract

It has been suggested that naive immunoglobulins encoded by the V H 3 gene family interact aberrantly with human immunodeficiency virus type 1 (HIV-1) gp120 via a superantigenic epitope, causing initial expansion and eventual depletion of V H 3-expressing B cells. However, this possibility has not been prospectively assessed during an AIDS virus infection. We determined V H family usage in rhesus monkeys during primary infection with chimeric viruses expressing HIV-1 envelopes on a simian immunodeficiency virus (SIV mac) backbone (SHIVs). Four SHIVs with different envelopes and pathogenicities were studied. V H family usage was prospectively assessed in peripheral blood mononuclear cells and lymph node cells of these monkeys by a semiquantitative PCR technique. In the first months following SHIV infection, a period of intense viral antigenemia, representation of various V H families increased or decreased for individual monkeys, but no single V H family was consistently altered. In particular, the average representation of V H 3-bearing B lymphocytes did not change. This observation suggests that the envelope glycoprotein of HIV-1 does not selectively expand or deplete the V H 3 repertoire of primate B cells during acute AIDS virus infection, contrary to predictions of the gp120 superantigen hypothesis.

Isolation of Anti-Ricin Protective Antibodies Exhibiting High Affinity from Immunized Non-Human Primates

“…The seven λ light chains were coded by four IGLV genes and three IGLJ genes, while the three κ light chain clones were coded by three IGKV genes combined with the same IGKJ gene ( Table 2 ). In accordance with previous reports [ 28 , 29 , 30 , 31 ], the IGHV genes originated mostly from two subgroups (IGHV3 and 4), while the IGHD and the IGHJ genes were more diverse. Interestingly, two of the antibodies isolated from the holotoxin-based vaccine library share the same VDJ-germline genes of the VH, with different VL genes, probably due to the combinatorial assembly of the same VH chain with two different VL chains during library generation.…”

HIV-1 Antigen–specific and –nonspecific B Cell Responses Are Sensitive to Combination Antiretroviral Therapy

“…HIV-1 antigen load could obviously be an influence on antigen-specific IgG-ASCs, but the majority of circulating IgG-ASCs are not specific for HIV-1 antigens yet are sensitive to a lowering in their concentration. Although HIV-1 has been reported to contain a superantigen(s) ( 29 , 30 ), this is controversial and the balance of the evidence is not compelling ( 31 , 32 ). HIV-1 has also been reported to directly activate B cells in vitro ( 33 , 34 ), and in one study this effect was reported to be mediated by the COOH terminus of gp41 ( 35 ).…”