Here we provide evidence that the neutralizing antihexon monoclonal antibody 9C12 inhibits adenovirus infection by blocking microtubule-dependent translocation of the virus to the microtubule-organizing center following endosome penetration. These studies identify a previously undescribed mechanism by which neutralizing antibodies block virus infection, a situation that may be relevant for other nonenveloped viruses that use microtubule-dependent transport during cell entry.”
“OBJECTIVE: The brain-derived Nutlin3 neurotrophic factor (BDNF)
Va166Met polymorphism has been shown to be related to variability in episodic memory. We studied whether the Met allele is associated with poor learning and memory in survivors of aneurysmal subarachnoid hemorrhage (SAH).
METHODS: Ninety-six patients were examined with a neuropsychological test battery approximately I year after SAH. Their deoxyribonucleic acid samples were genotyped for the BDNF Va166Met polymorphism. The Met carriers were compared to the Val/Val homozygous patients on the test performances.
RESULTS: In the total sample, there was no GDC-0973 solubility dmso difference between the genotype groups. However, among the patients with no cerebral infarction, the Met carriers had inferior
learning and memory performance than the Val/Val homozygotes, but the groups did not differ on the nonmemory test performances. The patients with left and bilateral infarctions had deficits in verbal memory, which may have concealed the effect of the BDNF Val66Met polymorphism on memory in the total sample.
CONCLUSION: As a whole, the BDNF Va166Met polymorphism was not associated with learning and memory performance in patients recovering from SAH. However, the Met allele might predict poor memory function among patients with SAH not complicated by a cerebral infarction. These findings support earlier reports of an association between the Met allele and low memory performance. Longitudinal studies comparing
functional recovery from SAH between Met and Val/Val patients without cerebral infarctions are warranted.”
“Human herpesvirus 8 (HHV-8), which is associated with the endothelial tumor Kaposi’s sarcoma, encodes three CC/beta-chemokines. These are expressed early during productive CRT0066101 (lytic) infection and are believed to be involved in immune evasion, in addition to viral pathogenesis via induction of angiogenic cytokines. Here we report that two of the HHV-8 chemokines, CCR8 agonists vCCL-1 and vCCL-2, have direct effects on endothelial survival and virus replication. The v-chemokines stimulated virus replication when added to infected cultures exogenously, and CCR8 knockdown absent v-chemokine supplementation inhibited virus production, indicative of autocrine effects of endogenously produced vCCLs. This was verified and proreplication functions of each chemokine were demonstrated via shRNA-mediated vCCL depletion.
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