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Many Americans are infected with HCV. Most were born between 1945 and 1964 and can be identified with current screening criteria. History of injection drug use is the strongest risk factor for infection.

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There would appear to be little argument that the large outbreaks of E. coli O157:H7 which have occurred since the early 1980s represent a distinct, new phenomenon. The number of reported cases have increased dramatically, starting from zero in 1981; however, it is also clear that this increase in reported cases is in part an artifact of improved surveillance and reporting. Available data suggest that E. coli O157:H7 infections were present prior to 1982, although numbers appear to have been small. At a molecular level, the organism shows evidence of clonal origin, but there is not the striking clonality, with virtually identical pulsed-field gel electrophoresis and ribotyping patterns, which has been seen in situations such as the emergence of Vibrio cholerae O139 Bengal in the Indian subcontinent in 1992 or the introduction of V. cholerae O1 into naïve populations in South America in 1991 (127-129). Findings are more consistent with the image of an organism which arose from a common ancestor, but which has had time to become distributed geographically and to show some evidence of genetic divergence. While this is an "emerging" infection, at least in terms of its distribution and public recognition, it is unlikely that it will be possible to identify the "first" O157:H7 case or to track the clonal spread of the organism through cattle or human populations.

Because chronic liver disease may develop many years after acute hepatitis C virus (HCV) infection, the past incidence of acute infections is a major determinant of the future burden of HCV-associated complications. We estimated past incidence of acute HCV infection using national seroprevalence data and relative age-specific incidence data from a sentinel counties surveillance system. Projections of the future prevalence of HCV-infected patients were derived from models that included an 85% drop in HCV infection incidence as observed for reported cases in the early 1990s. The models showed a large increase in the incidence of HCV infections from the late 1960s to the early 1980s. The degree of increase was dependent on the assumed rate of antibody loss; a model with 2.5% annual antibody loss showed annual incidence increasing from 45,000 infections (95% confidence interval [95% CI]: 0-110,000) in the early 1960s to 380,000 infections (95% CI: 250,000 to 500,000) in the 1980s. Projections showed that although the prevalence of HCV infection may be declining currently because of the decline in incidence in the 1990s, the number of persons infected for H20 years could increase substantially before peaking in Hepatitis C virus (HCV) infection is the most common chronic blood-borne infection in the United States and causes approximately 15% of all reported episodes of acute viral hepatitis. 1,2 Injection drug use and high-risk sexual activity are the most frequently identified risk factors associated with acute disease. Blood transfusion was a major risk factor for acquiring HCV infection before donor screening for human immunodeficiency virus infection, and surrogate marker testing for non-A, non-B hepatitis began in the mid-1980s, followed by screening for antibody to HCV (anti-HCV) in 1990. Young adults (ages 20 to 35 years) are at highest risk for acute infection, having an incidence 6 times higher than that of persons over 40 years 1 (Centers for Disease Control and Prevention [CDC], unpublished data).The most significant feature of HCV infection is the high rate of chronic infection and chronic hepatitis, which in the long term can lead to cirrhosis. 3 It is unknown how many of the nearly 4 million persons infected in the United States 2 will ultimately develop these complications.Direct determination of the incidence of new infections is impractical because most acute HCV infections are asymptomatic 4,5 and clinical disease is greatly under-reported. 6 In the past, the incidence of HCV infection has been estimated by adjusting the number of reported cases to account for under-reporting and for asymptomatic infections. An alternative method is to model incidence from prevalence data using ''catalytic modeling. '' 7,8 PATIENTS AND METHODSData Sources. The third National Health and Nutrition Examination Survey (NHANES III) was a cross-sectional national survey conducted from 1988 to 1994 that provided nationally representative prevalence estimates for a variety of health measures and conditions. 9 A total of...

As part of the 2000 Global Burden of Disease study, we quantified the death and disability from injection-associated infections with hepatitis B virus (HBV), hepatitis C virus (HCV) and human immunodeficiency virus (HIV). We modelled the fraction of incident infections attributable to health care injections in the year 2000 on the basis of the annual number of injections, the proportion of injections administered with reused equipment, the probability of transmission following percutaneous exposure, the prevalence of active infection, the prevalence of immunity and the total incidence. Infections in 2000 were converted into disability-adjusted life years (DALYs) in 2000-2030 using natural history parameters, background mortality, duration of disease, disability weights, age weights and a 3% discount rate. Four Global Burden of Disease regions where reuse of injection equipment in the absence of sterilization was negligible were excluded from the analysis. In the remaining 10 regions, in 2000, persons received an average of 3.4 injections per year, 39.3% of which were given with reused equipment. In 2000, contaminated injections caused an estimated 21 million HBV infections, two million HCV infections and 260,000 HIV infections, accounting for 32%, 40% and 5%, respectively, of new infections for a burden of 9,177,679 DALYs between 2000 and 2030. Injection overuse and unsafe practices account for a substantial burden of death and disability worldwide. There is a need for policies and plans for the safe and appropriate use of injections in countries where practices are poor.

The COVID-19 pandemic caused by the novel coronavirus SARS-CoV-2 has spread globally, with >52,000 cases in California as of May 4, 2020. Here we investigate the genomic epidemiology of SARS-CoV-2 in Northern California from late January to mid-March 2020, using samples from 36 patients spanning 9 counties and the Grand Princess cruise ship. Phylogenetic analyses revealed the cryptic introduction of at least 7 different SARS-CoV-2 lineages into California, including epidemic WA1 strains associated with Washington State, with lack of a predominant lineage and limited transmission between communities. Lineages associated with outbreak clusters in 2 counties were defined by a single base substitution in the viral genome. These findings support contact tracing, social distancing, and travel restrictions to contain SARS-CoV-2 spread in California and other states.

Zha, and for many useful conversations. All errors are mine. The views expressed here are entirely my own and not official statements of the Federal Reserve Bank of Minneapolis or the Federal Reserve. The views expressed herein are those of the author and do not necessarily reflect the views of the National Bureau of Economic Research.NBER working papers are circulated for discussion and comment purposes. They have not been peer-reviewed or been subject to the review by the NBER Board of Directors that accompanies official NBER publications.