Post-transcriptional restriction of human adenovirus expression in monkey cells.

Infection of the continuous simian cell lines CV-1 and BSC-1 with human adenovirus type 2 (Ad2) is abortive. However, the restriction of Ad2 reproduction in these cells can be overcome by increasing the Ad2 infectious dose or by coinfection with simian virus 40. Vero, another established simian cell line free of detectable endogenous simian virus 40 DNA, is not restricted in its ability to promote Ad2 growth even at low input multiplicities of Ad2 and in the absence of SV40 helper. The amount of structural Ad2 proteins in total cell extracts of enhanced BSC-1 cells is at least two orders of magnitude higher than that of unenhanced cells. In contrast, comparable quantities of Ad2 mRNA specifying these proteins are found in both the enhanced and the unenhanced cell. Both sets of mRNA can be translated in a cell-free system with equal efficiency.     

Loss to Clinic and Five-Year Mortality among HIV-Infected Antiretroviral Therapy Initiators

Missing outcome data due to loss to follow-up occurs frequently in clinical cohort studies of HIV-infected patients. Censoring patients when they become lost can produce inaccurate results if the risk of the outcome among the censored patients differs from the risk of the outcome among patients remaining under observation. We examine whether patients who are considered lost to follow up are at increased risk of mortality compared to those who remain under observation. Patients from the US Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) who newly initiated combination antiretroviral therapy between January 1, 1998 and December 31, 2009 and survived for at least one year were included in the study. Mortality information was available for all participants regardless of continued observation in the CNICS. We compare mortality between patients retained in the cohort and those lost-to-clinic, as commonly defined by a 12-month gap in care. Patients who were considered lost-to-clinic had modestly elevated mortality compared to patients who remained under observation after 5 years (risk ratio (RR): 1.2; 95% CI: 0.9, 1.5). Results were similar after redefining loss-to-clinic as 6 months (RR: 1.0; 95% CI: 0.8, 1.3) or 18 months (RR: 1.2; 95% CI: 0.8, 1.6) without a documented clinic visit. The small increase in mortality associated with becoming lost to clinic suggests that these patients were not lost to care, rather they likely transitioned to care at a facility outside the study. The modestly higher mortality among patients who were lost-to-clinic implies that when we necessarily censor these patients in studies of time-varying exposures, we are likely to incur at most a modest selection bias.     

Changes in the gaze fixation reaction in rhesus monkeys during the initial stage of water immersion

The gaze fixation reaction was studied in three rhesus monkeys before and during thermoneutral (34.5 degrees C) water immersion to the mid-chest level. The angular vestibulo-ocular reflex gain increased and the head angular velocity decreased significantly in all monkeys in 5 h after the start of immersion. Additionally, one animal was immersed to the neck level. Two hours in the condition of more pronounced support deprivation decreased significantly angular velocity of the head but not increased the angular vestibulo-ocular reflex gain. Therefore, support deprivation act upon the head movement control first.     

HIV antigens can induce TGF-beta(1)-producing immunoregulatory CD8+ T cells

HIV-infected individuals may progressively lose both HIV-specific and unrelated CTL responses despite the high number of circulating CD8+ T cells. In this study, we report that approximately 25% of HIV+ donors produced TGF-beta(1) in response to stimulation with HIV proteins or peptides. The production of TGF-beta(1) was sufficient to significantly reduce the IFN-gamma response of CD8+ cells to both HIV and vaccinia virus proteins. Ab to TGF-beta reversed the suppression. We found the source of the TGF-beta(1) to be predominantly CD8+ cells. Different peptide pools stimulated TGF-beta(1) and IFN-gamma in the same individual. The TGF-beta(1) secreting cells have distinct peptide specificity from the IFN-gamma producing cells. This represents an important mechanism by which an HIV-specific response can nonspecifically suppress both HIV-specific and unrelated immune responses.