PubMed · 8098433
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R M Anderson. 1993-05-15. AIDS predictions.. https://pubmed.ncbi.nlm.nih.gov/8098433/
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In this study, immunoglobulin variable (Ig V) region genes, c-myc re-arrangement and sequence and p53 status were analyzed in clones derived from a Burkitt's lymphoma cell line (LAM) in which it was previously demonstrated that Epstein-Barr virus (EBV) infection occurred late during lymphomagenesis. Such evidence was based on the finding that 2 groups of cellular clones, characterized by the same c-myc re-arrangement but different EBV-fused termini, were obtained from the LAM cell line. The Ig V gene sequences were identical for the 2 groups of clones with different EBV-fused termini. The Ig variable heavy (V(H)) gene sequence displayed a substantial accumulation of point mutations (but no intra-clonal diversification), whereas the productive Ig V lambda (V(lambda)) gene sequence was virtually unmutated. Studies on the Ig V kappa (V(kappa)) locus suggested a receptor revision event (with a switch from kappa to lambda chain production) prior to EBV infection. Likewise, it was determined that the mutations observed in both p53 alleles and in the re-arranged c-myc gene occurred before EBV infection. Based on these findings, we present a model for the various steps of lymphomagenesis. It is proposed that stimulation by an antigen or a superantigen initially favored the clonal expansion and accumulation of other cytogenetic changes, including those involved in receptor editing. These events occurred prior to or during the germinal center (GC) phase of B-cell maturation. Thereafter, possibly upon exit of the cells from the GC, EBV infection occurred, further promoting lymphomagenesis.
BACKGROUND: The intriguing differences in the natural course, transmissibility, and epidemiological characteristics of human immunodeficiency virus type 1 (HIV-1) and HIV-2 are still insufficiently explained. Differences in plasma viral load are an obvious possibility, but this has been difficult to investigate because of the lack of tests for HIV-2 RNA. OBJECTIVE: To compare plasma HIV RNA load between individuals infected with HIV-1 and HIV-2 in Guinea-Bissau, a West African country with high prevalence and incidence of HIV-1 and HIV-2 infection. METHODS: A total of 102 participants were recruited from ongoing prospective cohort studies. These included 19 HIV-1 and 29 HIV-2 seroincident cases tested at a median of less than 2 years after seroconversion as well as seroprevalent cases with single (9 HIV-1 cases and 31 HIV-2 cases) or dual (n = 14) infections. Plasma HIV RNA levels were determined by a commercial HIV-1 assay and an experimental HIV-2 assay based on the same principles. RESULTS: The viral set point, ie, the semi-equilibrium reached after seronconversion, was 28-fold lower in recent HIV-2 seroconverters than in recent HIV-1 seroconverters (median, 2500 and 70,000 RNA copies per milliliter, respectively; P<. 001). This difference appeared to persist to symptomatic stages of the diseases. Dually infected individuals had lower plasma HIV-1 RNA levels than singly infected individuals. CONCLUSIONS: The differences between HIV-1 and HIV-2 infection are likely to be caused by differences in plasma viral set point and load, but the mechanisms through which HIV-2 infection is contained to a higher degree than HIV-1 remain to be identified. Arch Intern Med. 2000;160:3286-3293.