New knowledge of the relationship between the varicella-zoster virus and its host suggests a heretofore unappreciated dynamic pattern. Molecular finger-printing has demonstrated a degree of heterogeneity between different strains of virus. It is probable that exogenous reinfection with different strains and endogenous reactivation are commonplace events, although usually asymptomatic. The lability of the endogenous interaction inversely parallels the responsiveness of the cell-mediated immune system--a major factor in viral containment by the human host. Thus, the therapeutic use of immunosuppressive or cytotoxic substances increases the morbidity and mortality associated with varicella-zoster. Promising new approaches to the prevention and treatment of the virus should alter the balance in favor of the host.

Many clinicians believe that slow-acting therapeutic agents, such as fold, penicillamine, the antimalarials, and cytotoxic drugs, can retard joint destruction in rheumatoid arthritis. We reviewed 60 published studies employing these drugs to evaluate critically the evidence that drug therapy can slow the radiographic progression of disease. Seventeen studies were found that included radiographic assessment of both treated and control groups; they were analyzed using methodologic criteria known to be important in affecting the results of drug trials. In addition to numerous qualitative methodologic deficiencies, many studies showed inadequacies in sample size and duration of treatment, and the drug dosage used varied from one study to another. We found evidence suggesting that both gold and cyclophosphamide can retard radiographic progression of joint destruction. At present, there are too few technically adequate studies to permit even provisional conclusions concerning other agents.

Guidelines for the prophylaxis or therapy of herpesvirus infections are shown in Table 1. Progress is so rapid in this area that frequent revisions of such guidelines will be necessary. Newer drugs or new formulations of older agents are constantly being developed. Combination therapies--e.g., interferon plus acyclovir--appear promising in laboratory models of herpesvirus infections and will undoubtedly receive clinical investigation in the years ahead. The problem of dealing with latent virus infections still eludes us, and major breakthroughs will be necessary before we can discuss cure of recurrent infections. Nevertheless, important strides have been made in the past few years, and further progress is predictable in the years ahead.

A rapid and exciting accumulation of data about cellular oncogenes in human tumors has resulted from convergent research on DNA-mediated gene transfer, retroviruses, and tumor cytogenetics. Such work promises to increase our understanding of the genetic events that predispose to, and result in, malignant disease. This knowledge may quickly find clinical application in tumor classification and prediction of risk. Ultimately, therapeutic benefits may be achieved as we begin to explore the mechanisms by which transforming gene products act to defeat the normal regulatory processes of cells.