Pitfalls in the use of surrogate markers for human immunodeficiency virus disease: further evidence on pathogenesis.
The administration of drugs to human immunodeficiency virus patients with a pronounced CD4+ T lymphocytopenia may cause non-specific binding of the murine antibodies used in flow cytometry. This has produced spurious reports of early thymocytes in the circulating blood of human immunodeficiency virus-infected individuals following treatment with an anti-adhesion monoclonal mouse antibody (Cytolin+). Recent clinical experience with Cytolin+ confirms the pathogenic role of leukocyte adhesion pathways in human immunodeficiency virus infection. However, this experience also illustrates how comparisons of viral burden can be misleading. For nine patients with low CD4 counts, Cytolin+ alone reduced the mean ribonucleic acid-polymerase chain reaction by 0.45 log to 39 800 particles per mL. Ten patients with more advanced disease added Cytolin+ to an established regimen of standard antiretroviral drugs. Their mean polymerase chain reaction was only reduced by 0.2 log to 91 501. Yet, 67% of the former patients experienced a major clinical event within seven months, whereas the latter patients remained stable during this time.