Effect of inflammation on handgrip strength in the non-critically ill is independent from age, gender and body composition.

BACKGROUND/OBJECTIVES: We investigated whether C-reactive protein (CRP) as indicator of acute inflammation is associated with maximal isometric handgrip strength in non-critically ill patients. SUBJECTS/METHODS: Handgrip strength was measured with Jamar dynamometer in 620 hospitalized patients (56.4±15.9 years old, 52.3% men). CRP was measured with immunoturbidimetric assay. Fat free mass (FFM) was assessed by bioelectrical impedance analysis. A general linear model regression analysis corrected for confounding variables such as age, sex, FFM, body mass index, comorbidity count and diagnosis category (malignant/benign disease) was performed to test the association between elevated levels of CRP and handgrip strength. RESULTS: CRP was an independent predictor of grip strength (CRP: ß-coefficient: -0.169, P=0.018) even after adjustment for relevant confounders. All groups with inflammation showed significant reduction in handgrip strength, corresponding to a loss of ∼1.6 kg in mild inflammation, 3.2 kg in moderate inflammation and 2.9 kg in severe inflammation compared with patients without inflammation. DISCUSSION: Our data demonstrate the independent association between inflammation and handgrip strength in non-critically ill patients. If not corrected, reduced strength may have implications for the patients' functional status and prognosis. Increasing physical activity and resistance training during convalescence are recommended.

Human immunodeficiency virus type 1 shedding pattern in semen correlates with the compartmentalization of viral Quasi species between blood and semen.

High levels of human immunodeficiency virus (HIV) type 1 have been detected in semen at all stages of disease. However, it is not clear whether HIV-1 is shed in semen continuously or intermittently. In a prospective longitudinal study, viral RNA was measured weekly for 10 weeks in semen and blood of HIV-seropositive subjects. Results showed three different patterns of HIV-1 shedding in semen: none (28%), continuous (28%), and intermittent (44%). In contrast, there was no change in blood plasma virus load during the study period. Phylogenetic analysis of the envelope sequences of HIV-1 RNA in semen and blood revealed distinct virus populations in semen and blood of intermittent shedders but similar virus populations in the semen and blood of continuous shedder. These results indicate for the first time that HIV-1 is shed primarily in an intermittent manner and that shedding patterns of HIV-1 in semen are related to compartmentalization of HIV-1 between semen and blood.

Dependence of CD8+ T-cell-mediated suppression of HIV type 1 on viral phenotypes and mediation of phenotype-dependent suppression by viral envelope gene and not by beta-chemokines.

CD8+ T-cell-mediated HIV-1 suppressive activity has been shown against a number of strains of HIV-1 and HIV-2. In this study using a semiquantitative assay, we showed that CD8+ T cells from seropositive subjects and herpes virus saimiri transformed CD8+ T-cell clones from HIV-1-infected subjects exhibited 5 to 100-fold higher suppressive activity against slow replicating nonsyncytia-inducing strains (Slow/NSI) as compared to fast replicating syncytia-inducing strains (Fast/SI) of HIV-1. Such differential suppressive activity was not due to beta-chemokines as evidenced by the lack of blocking activity of antibodies to RANTES, MIP-1beta, and MIP-1alpha on the antiviral activities of CD8+ T cells. Moreover, there was no correlation between the level of CD8+ T-cell suppression and the level of these beta-chemokines in culture supernatant. Results from the CD8+ T-cell-mediated suppressive activity against two molecular cloned virus ME1 (Slow/NSI), ME46 (Fast/SI), and their interstrain recombinants indicate that the envelope gene carries a major genetic determinant responsible for this phenotypic-dependent differential suppressive activity.