Time course of natural killer cell activity and lymphocyte proliferation in response to two acute stressors in healthy men.

To clarify the time course of immune system activity during and after acute stressor exposure, this study collected immune measures from 31 men at 6 times (before, during, and after 2 common laboratory stressors; mental arithmetic with harassment or a cold pressor task). The 6-min stressor period was associated with increased self-report of pain and distress in both stressor groups and with increased systolic and diastolic blood pressure and heart rate in the mental arithmetic group. Increased natural killer cell activity in this group was observed during the task (2 and 5 min into the task) and 5 min after the task ended. A significant Group x Time effect was observed for lymphocyte proliferation to pokeweed mitogen, and a significant Group x Time x Dilution effect was observed for proliferation to concanavalin A. Inspection of the data suggested that this interaction was due to a reduction in proliferation in both stressor groups during the task period.

The UL37 protein of herpes simplex virus type 1 is associated with the tegument of purified virions.

The herpes simplex virus type 1 (HSV-1) UL37 open reading frame encodes a 120-kDa late (gamma 1) phosphoprotein in infected cells. Analysis of isolated mature HSV virions and light particles revealed that the UL37 protein is a component of the virion. Detergent solubilization and protease digestion experiments suggest that the UL37 protein is part of the tegument structure. Indirect immunofluorescence experiments using HSV-1-infected cells and cells infected with a vaccinia recombinant virus that expresses the UL37 gene demonstrated that the UL37 protein is present in both the nucleus and cytoplasm of infected cells and that localization to the nucleus does not require additional HSV proteins.

Neutrophil dysfunctions in sickle cell disease.

The abnormal susceptibility towards certain infections in SCD patients has a partial explanation in the well described functional defects of the spleen and of the alternative complement pathway; such defects probably account for the etiology of fulminant, often fatal, childhood infections with encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae). On the other hand, the frequent systemic infections with enteric organisms in SCD patients, particularly of the salmonella species, and also with Staphylococcus aureus, are more difficult to explain. We therefore reviewed the potential contribution of neutrophil (PMN) dysfunctions to the increased infective tendency of SCD patients and included some previously unpublished data from our laboratory. While notable discrepancies still exist--and need further clarification--a tentative working hypothesis can be extracted from the available data: dysfunctions of neutrophils affect their locomotion (as reflected by decreased chemotaxis and in vivo migration), their phagocytic processes and their bactericidal performance. The latter concerns the ineffective killing of Staphylococcus aureus, Candida albicans, and Streptococcus pneumoniae. Dysfunctional bactericidal activity, in turn, apparently relates to a poor or at times non-existent PMN oxidative activity, which prevents the prompt disposal of microorganisms. Under certain circumstances salmonella species seem to further paralyze the oxidative machinery of PMNs in SCD. Serum from some patients contains a poorly defined inhibitor, or lacks an enhancing factor, and such serum abnormalities aggravate the existing defects just described. Interestingly recent findings suggest that dysfunctional PMNs may originate from the mandatory demargination of leukocytes secondary to the functional asplenia of SCD; a predominance of non-rosetting (EA-) PMNs among such leukocytes could produce the operational explanation for an exaggerated representation of dysfunctional PMNs in SCD patients with leukocytis.