As SARS-CoV-2 infections and death counts continue to rise, it remains unclear why some individuals recover from infection, whereas others rapidly progress and die. Although the immunological mechanisms that underlie different clinical trajectories remain poorly defined, pathogen-specific antibodies often point to immunological mechanisms of protection. Here, we profiled SARS-CoV-2-specific humoral responses in a cohort of 22 hospitalized individuals. Despite inter-individual heterogeneity, distinct antibody signatures resolved individuals with different outcomes. Although no differences in SARS-CoV-2-specific IgG levels were observed, spike-specific humoral responses were enriched among convalescent individuals, whereas functional antibody responses to the nucleocapsid were elevated in deceased individuals. Furthermore, this enriched immunodominant spike-specific antibody profile in convalescents was confirmed in a larger validation cohort. These results demonstrate that early antigen-specific and qualitative features of SARS-CoV-2-specific antibodies point to differences in disease trajectory, highlighting the potential importance of functional antigen-specific humoral immunity to guide patient care and vaccine development.

Following its emergence in Wuhan, China, in late November or early December 2019, the SARS-CoV-2 virus has rapidly spread globally. Genome sequencing of SARS-CoV-2 allows reconstruction of its transmission history, although this is contingent on sampling. We have analyzed 453 SARS-CoV-2 genomes collected between 20 February and 15 March 2020 from infected patients in Washington State, USA. We find that most SARS-CoV-2 infections sampled during this time derive from a single introduction in late January or early February 2020 which subsequently spread locally before active community surveillance was implemented.

Purpose of review Sarcoidosis, the multiorgan, granulomatous disease of unknown etiology, remains mysterious. Several important investigations in the past two years add to accumulating evidence for both occupational and environmental causes of granulomatous inflammation. Recent findings This review considers the most recent studies that contribute to the hypothesis that sarcoidosis occurs when individuals are exposed to foreign antigens and to inorganic particulates that promote inflammation. Major recent findings, such as those emerging from the study of World Trade Center responders, the study of nanoparticles, and cases of work-associated sarcoidosis support the probability that occupational, as well as environmental, exposures to inflammatory stimuli trigger sarcoidosis-like illness. Major recent studies of microbially-rich indoor environments, including moldy indoor workplaces and mycobacterially-contaminated settings, contribute to the evidence that a variety of microbial antigens serve as targets for the hypersensitivity immune response in an inflammatory milieu. Summary There is increasing evidence that sarcoidosis can occur in workplace settings in which there is exposure to both foreign antigens and inorganic triggers of inflammation that promote an exuberant granulomatous immune response. It is likely that sarcoidosis has more than one cause.

Congregate living situations, such as homeless shelters, are high-risk settings for transmission of SARS-CoV-2 among residents and staff. This article describes findings from a study using active surveillance for SARS-CoV-2 that took place in 14 homeless shelters in King County, Washington, between 1 January and 24 April 2020.

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The outbreak of bubonic plague that struck London and Westminster in 1636 provoked the usual frenzied response to epidemics, including popular flight and government-mandated quarantine. The government asserted that plague control measures were acts of public health for the benefit of all. However, contrary to this government narrative of disease prevention there was a popular account that portrayed quarantine and isolation as personal punishment rather than prudent policy. In examining the 1636 outbreak on the parish as well as the individual level, reasons for this inconsistency between official and unofficial perspectives emerge. Quarantine and its effects were not classless, and its implementation was not always strictly in the name of public health. Government application of quarantine was remarkably effective, but it could never be uncontroversial both because of circumstances and because of misuse. The flight of the wealthiest from London and Westminster left only the more socially vulnerable to be quarantined. Though plague policy was financially sensitive to the poorest, it was costly to the middling sort. Another cause of controversy was the government's use of quarantine as a punishment to control individuals found breaking other laws. Though not widely publicized, popular narratives continually included grievances about the cruelty and inequity of quarantine and the militaristic nature of its implementation. Despite these objections, quarantine remained a staple of the government response to plague outbreaks throughout the seventeenth century.

Summary Noroviruses (NoV) are the most common cause of epidemic gastroenteritis world-wide. NoV infections are often asymptomatic, although individuals still shed large amounts of NoV in their stool. Understanding the differences between asymptomatic and symptomatic individuals would help in elucidating mechanisms of NoV pathogenesis. Our goal was to compare the serum cytokine responses and faecal viral RNA titres of asymptomatic and symptomatic NoV-infected individuals. We tested serum samples from infected subjects (n = 26; 19 symptomatic, seven asymptomatic) from two human challenge studies of GI.1 NoV for 16 cytokines. Samples from prechallenge and days 1-4 post-challenge were tested for these cytokines. Cytokine levels were compared to stool NoV RNA titres quantified previously by reverse transcription–polymerase chain reaction (RT–qPCR). While both symptomatic and asymptomatic groups had similar patterns of cytokine responses, the symptomatic group generally exhibited a greater elevation of T helper type 1 (Th1) and Th2 cytokines and IL-8 post-challenge compared to the asymptomatic group (all P < 0·01). Daily viral RNA titre was associated positively with daily IL-6 concentration and negatively with daily IL-12p40 concentration (all P < 0·05). Symptoms were not associated significantly with daily viral RNA titre, duration of viral shedding or cumulative shedding. Symptomatic individuals, compared to asymptomatic, have greater immune system activation, as measured by serum cytokines, but they do not have greater viral burden, as measured by titre and shedding, suggesting that symptoms may be immune-mediated in NoV infection.

SUMMARY Foodborne illness is a major cause of morbidity and loss of productivity in developed nations. Though low socioeconomic status (SES) is generally associated with negative health outcomes, its impact on foodborne illness is poorly understood. We conducted a systematic review to examine the association between SES and laboratory-confirmed illness caused by eight important foodborne pathogens. We completed this systematic review using PubMed for all papers published between 1 January 1980 and 1 January 2013 that measured the association between foodborne illness and SES in highly developed countries and identified 16 studies covering 4 pathogens. The effect of SES varied across pathogens: the majority of identified studies for Campylobacter, salmonellosis, and E. coli infection showed an association between high SES and illness. The single study of listeriosis showed illness was associated with low SES. A reporting bias by SES could not be excluded. SES should be considered when targeting consumer level public health interventions for foodborne pathogens.