Port, we show that soluble mimics of CD4 inhibit HIV-1 infection by prematurely triggering the viral envelope glycoproteins. The unstable activated state of the virus lasts only a few minutes, after which the virus loses the ability to infect cells. This novel strategy for inhibition may be generally applicable to other viruses besides HIV-1, some of which are also activated by binding to their re

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N ( ) Homeless, self-described, n ( ) Receiving public assistance or social security disability, n ( ) Employed, n ( ) CES-D short-form scorea, median (IQR) 44 (85) 8 (15) 47 (42?2) 29 (56) 20 (39) 41 (79) 8 (15) 11 (5?6) 44 (80) 11 (20) 47 (41?1) 27 (49) 12 (23) 50 (91) 8 (15) 11 (6?5) 19 (37) 17 (33) 4 (8) 7 (13) 5 (10) 27 (52) 20 (36) 18 (33) 4 (7) 7 (13) 6 (11) 24 (44)Substance abuse relatedDu

D daily for 4 consecutive days to be 60 mg/m2. DLTs were cough, asthenia, anorexia, sensory neuropathy, serum sickness, and hypertensive encephalopathy. The spectrum of adverse effects, the most common of which were pain, fever, and tachycardia, was similar to that previously described with the parent antibody, ch14.18, in children,4,20,21 except that none of our patients had potentially life-thre

Vioral complications [66-69]. Microglia, as a major target of HIV-1 infection in the CNS, are typically a viral reservoir [70-72] and are also key in HIV-1 neuroinvasiveness-penetration into the CNS by the virus [72,73]. Most importantly, a discrepancy between the localization of HIV-infected cells and the severity of neurocognitive symptoms has been described [74-76]. Thus, other mechanisms secon

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Racteristics), the alpha level was corrected utilizing the Sidak equation toRacteristics), the alpha lev