We found that inoculation of irradiated HTLV-2-infected T cells into Indian rhesus macaques elicited humoral and T-cell

responses to HTLV-2 antigens at both systemic and mucosal sites. Low levels of HTLV-2 provirus DNA were detected in the blood, lymphoid tissues, and gastrointestinal tracts of infected animals. Exposure of HTLV-2-infected or naive macaques to SIVmac251 demonstrated comparable levels of SIVmac251 viral replication, similar rates of mucosal and peripheral CD4(+) T-cell loss, and increased T-cell proliferation. Additionally, neither the magnitude nor the functional capacity of the SIV-specific T-cell-mediated immune response was different in HTLV-2/SIVmac251 coinfected animals versus SIVmac251 singly infected controls. Thus, HTLV-2 targets mucosal sites, persists, and importantly does buy Galunisertib not exacerbate SIVmac251 infection. These data provide the impetus for the development of an attenuated HTLV-2-based vectored vaccine for HIV-1; this approach could elicit persistent mucosal immunity that may prevent HIV-1/SIVmac251 infection.”
“BACKGROUND: Pulmonary complications are frequently observed after severe traumatic brain injury (TBI), but little is known about the consequences of lung injury on brain tissue oxygenation and metabolism.

OBJECTIVE: We examined the association between lung Selleck CX-6258 function and brain tissue oxygen tension (PbtO(2)) in patients with severe

TBI.

METHODS: We analyzed data from 78 patients with severe, nonpenetrating TBI who underwent continuous PbtO(2) and intracranial pressure monitoring. Acute lung injury was defined by the presence of pulmonary infiltrates with a PaO(2)/FiO(2) (PF) ratio less than 300 and the absence of left ventricular failure. A total of 587 simultaneous measurements of PbtO(2) and PF ratio were examined using longitudinal data analysis.

RESULTS: PbtO(2) correlated strongly with PaO(2) and PF ratio (P < .05) independent

of PaCO(2), brain temperature, cerebral perfusion pressure, and hemoglobin. Acute lung injury was associated with lower PbtO(2) (34.6 +/- 13.8 mm Hg at PF ratio > 300 vs 30.2 +/- 10.8 mm Hg [ PF ratio 200-300], 28.9 +/- 9.8 mm Hg [ PF ratio 100-199], and 21.1 +/- 7.4 mm Hg [ PF ratio < 100], all P values <. 3-deazaneplanocin A 01). After adjusting for intracranial pressure, Marshall computed tomography score, and APACHE II (Acute Physiology and Chronic Health Evaluation) score, acute lung injury was an independent risk factor for compromised PbtO(2) (PbtO(2) < 20 mm Hg; adjusted odds ratio: 2.13, 95% confidence interval: 1.21-3.77; P < .01).

CONCLUSION: After severe TBI, PbtO(2) correlates with PF ratio. Acute lung injury is associated with an increased risk of compromised PbtO(2), independent from intracerebral and systemic injuries. Our findings support the use of lung-protective strategies to prevent brain hypoxia in TBI patients.