Publications

In this review, Warner Greene and colleagues discuss recent studies that have revealed an intriguing molecular interplay between two pathogenic human retroviruses, HIV-1 and HTLV-1, and certain cellular genes that normally control T-cell growth. Activation of T cells during an immune response results in the induction of select transcription factors that bind specifically to kappa B enhancer elements present in both the IL-2R alpha and IL-2 genes. Normal T-cell growth is in part regulated by the transient expression of these genes. The Tax protein of HTLV-1 induces these same kappa B-specific proteins, but in contrast to immune stimulation, HTLV-1 infection of T cells leads to constitutive IL-2R alpha gene expression and immortalization. A second human retrovirus, HIV-1, can subvert the normal action of the kappa B-binding factors induced by these immune stimuli. Rather than promoting T-cell growth, these factors may augment viral replication and promote T-cell death.

STUDY OBJECTIVE

To evaluate the usefulness of poison control center detection in occupational illness surveillance.

DESIGN

Case series of all occupationally related exposures referred for poison control center consultation over 6 months. Follow-up structured interviews were done of exposed persons and health care providers. Cases were traced under established occupational illness reporting programs.

SETTING

A regional poison control center.

PATIENTS

Consecutive sample of 461 symptomatic occupational exposure cases. After exclusions and losses to follow-up, interview of 301 patients and the treating physician, physician's assistant, or nurse practitioner for the 223 of the patients under direct medical care.

MEASUREMENTS AND MAIN RESULTS

One hundred and fifty-five persons (61%; CI, 55% to 67%) had systemic or respiratory illness; 109 (36%; CI, 31% to 41%) had eye or skin conditions. Work practices were associated with exposures more often than technical failure; 118 persons (39%; CI, 33% to 45%) reported lack of respirators or other appropriate personal protective equipment. For 223 persons who received direct medical care, only five treating health care providers (2%; CI, 0.2% to 4%) reported occupational specialization, although occupational care was a regular practice activity for 128 of the health care providers (57%; CI, 51% to 63%). Sixty-seven cases (22%; CI, 17% to 27%) were detected by the Doctor's First Report surveillance program; 97 cases (32%; CI, 27% to 37%) comprised the maximal detection estimated for Occupational Safety and Health Administration surveillance.

CONCLUSIONS

Poison control center detection provides a useful surveillance measure for occupational illness. The proportion of case detection failures by established surveillance programs suggests that the incidence of occupational illness in the United States, which is calculated from these incomplete programs, may be three to five times greater than previously estimated.

The L3T4 surface molecule defines a subset of murine lymphocytes which are homologous to CD4+ lymphocytes in humans, and are functionally characterized as "helper/inducer" cells. To determine the role of helper/inducer lymphocytes in the host defense against herpes simplex virus type 1 (HSV-1) encephalitis, we utilized a monoclonal antibody to selectively deplete L3T4+ lymphocytes from BALB/c mice prior to experimental HSV infection. Susceptibility to HSV was only minimally increased by the depletion of L3T4+ cells, although mice receiving anti-L3T4 were profoundly immunosuppressed; splenic lymphocytes did not respond to stimulation by virus antigen in vitro, and L3T4+ lymphocyte-depleted mice failed to produce antibodies to HSV-1. However, mice receiving anti-L3T4 had a prolonged increase in natural killer cell activity following HSV infection as compared to controls. These data demonstrate that L3T4+ lymphocytes contribute minimally to host resistance to acute neural HSV infection, even though elimination of these lymphocytes markedly inhibits the genesis of immune responses.