Immunoglobulin V&lt;sub&gt;H&lt;/sub&gt;3-Positive AIDS-Related Burkitt’s Lymphoma: A Possible Role for the HIV gp120 Superantigen

Amariglio, N.; Vonsover, Ami; Hakim, I.; Neumann, Yoram; Mark, Z.; Brok‐Simoni, Frida; Ben‐Bassat, Isaac; Rechavi, Gideon

doi:10.1159/000204265

Cited by 8 publications

(1 citation statement)

References 12 publications

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“…Impaired B-cell responses to mitogens (38) are not corrected when B cells of HIV-1-infected donors are provided with helper T cells from uninfected donors (23). HIV-1-infected individuals are at increased risk for monoclonal gammopathy and for B-cell lymphoma, which sometimes produce antibodies reactive with HIV-1 viral proteins (1). The mechanisms accounting for these immunopathogenic features of HIV-1 infection remain uncertain.…”

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confidence: 99%

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

Margolin

Reimann

Sodroski

et al. 1997

J Virol

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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.

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confidence: 99%