The interactions of people using public transportation in large metropolitan areas may help spread an influenza epidemic. An agent-based model computer simulation of New York City's (NYC's) five boroughs was developed that incorporated subway ridership into a Susceptible-Exposed-Infected-Recovered disease model framework. The model contains a total of 7,847,465 virtual people. Each person resides in one of the five boroughs of NYC and has a set of socio-demographic characteristics and daily behaviors that include age, sex, employment status, income, occupation, and household location and membership. The model simulates the interactions of subway riders with their workplaces, schools, households, and community activities. It was calibrated using historical data from the 1957-1958 influenza pandemics and from NYC travel surveys. The surveys were necessary to enable inclusion of subway riders into the model. The model results estimate that if influenza did occur in NYC with the characteristics of the 1957-1958 pandemic, 4% of transmissions would occur on the subway. This suggests that interventions targeted at subway riders would be relatively ineffective in containing the epidemic. A number of hypothetical examples demonstrate this feature. This information could prove useful to public health officials planning responses to epidemics.

Transfusion-transmitted HTLV-I and -II are similar. The data suggest that a donor's lymphocytes become noninfectious when they lose the ability to be activated or to proliferate.

No abstract

Serologic screening of donors for antibodies to HIV-1 and HTLV-I coupled with exclusion of donors from groups having a relatively high risk for infection has led to a low incidence of transfusion-transmitted HIV-1 and HTLV-I/II infection in the United States. A small risk remains, however, despite these measures. We estimate the residual risk for HIV-1 and HTLV-II infection from transfusion of screened blood during the time of this study to be about 1 in 60,000 units.

Cryptococcal meningoencephalitis (CM) is the major cause of infection-related neurological death, typically seen in immunocompromised patients. However, T cell–driven inflammatory response has been increasingly implicated in lethal central nervous system (CNS) immunopathology in human patients and murine models. Here, we report marked up-regulation of the chemokine receptor CXCR3 axis in human patients and mice with CM. CXCR3 deletion in mice improves survival, diminishes neurological deficits, and limits neuronal damage without suppressing fungal clearance. CD4+ T cell accumulation and TH1 skewing are reduced in the CNS but not spleens of infected CXCR3−/− mice. Adoptive transfer of WT, but not CXCR3−/− CD4+ T cells, into CXCR3−/− mice phenocopies the pathology of infected WT mice. Collectively, we found that CXCR3+CD4+ T cells drive lethal CNS pathology but are not required for fungal clearance during CM. The CXCR3 pathway shows potential as a therapeutic target or for biomarker discovery to limit CNS inflammatory damages.