The triangular relationship between trust, affect, and risk perception


Various incidents in the past, such as the bovine spongiform encephalopathy crisis in the UK, have shown that people’s perceptions of hazards influence the risk management process. In this literature review, we investigated how people’s affective evaluations and their trust in responsible agencies shape risk perception. In addition, we explored the relation between affect and trust, and the implications of these factors for risk management.

Affect and trust appear to be important determinants of risk perception. Both factors act as heuristics when people have insufficient time, cognitive capacity, or motivation to evaluate risks deliberately. Trust and affect influence each other but more research is needed to clarify the direction of this relation. Risk managers should consider people’s instantaneous responses to risks in addition to their deliberate responses. Additionally, they should focus on compatible values and other trust-enhancing factors.

SOURCE: Risk Management

Inhibition of coronavirus in epithelial lung cells by chloroquine


Chloroquine, a diprotic weak base that increases the pH of acidic vesicles, has been used for the treatment of malaria and inflammatory diseases, such as rheumatoid arthritis. Chloroquine has antimicrobial effects even against viruses, such as human immunodeficiency virus type 1 (HIV-1) and SARS-CoV.

Coronavirus, an enveloped virus, enters the cell cytoplasm by endocytosis and matures in the membrane transport system, such as the trans-Golgi network. Endoplasmic reticulum stress caused by virus infection induces the activation of p38 mitogen-activated protein kinase (MAPK) and [can trigger] host cell apoptosis [‘programmed cell death’].

Chloroquine [can] inhibit the activation of p38 MAPK and cytokine production. In this study, we examined the correlation between CQ and the activation of p38 MAPK in human coronavirus 229E (HCoV-229E) infection .

The amount of viral RNA incorporated into the cells was not significantly influenced by chloroquine (Fig. 1b). These data demonstrate that chloroquine has no influence on the process prior to the internalization of HCoV-229E into cells.

Fig. 1. Inhibitory effects of CQ on virus replication and infectivity of HCoV-229E.

HCoV-229E infection induced the phosphorylation of p38 MAPK, which was inhibited by 25 μM chloroquine, [demonstrating] that chloroquine can neutralize the effect of HCoV-229E-infection on p38 MAPK.

SOURCE: Antiviral research

Epidemiological aspects of olfactory dysfunction

URI associated with anosmia (Ciafalo et al). Upper respiratory infections (in green) as causative event for anosmia. Patients were assessed AFTER the event. DATASOURCES: Rhinology. WIDGET:


We enrolled 234 patient (113 male and 130 female), aged between 8 and 84, that had been examined for olfactory dysfunction (2002-2004). Infectious diseases of the upper airways, craniofacial traumas and rhinosinusal pathologies were the aetiopathogenetic factors that were mainly responsible for olfactory dysfunctions. In essence, viruses could be the viral agents involved. A research study carried out by Sugiura shows the likely role played by parainfluenza virus, adenovirus, herpex simplex and zoster. In this study all patients with olfactory disorders after URI had increased antibody titres in particular for parainfluenza virus type 3. Viruses attack the olfactory neuroepithelium, destroying it and favouring its metaplastic transformation into respiratory epithelium.

Olfactory dysfunction may be caused by various aetiopathogenetic factors, damaging the olfactory pathway’s neurosensory or conduction structure. Based on our experience, upper respiratory infections were the main cause for olfactory sensory deficit; cranio-facial traumas, idiopathic causes and rhinosinusal pathologies came next. We observed very few cases of neurological, toxic and congenital pathologies. Female patients and women over 60 in particular, were the most affected. Most serious olfactory dysfunction was observed in trauma and respiratory infection sufferers.

SOURCE: Rhinology

Editor’s note: anosmia, or loss of the sense of smell, has been suggested, but not yet studied, as a possible early symptom in COVID-19, and possibly a reason to trigger a self-isolation period when attempting to control an evolving pandemic.

Chloroquine is a potent inhibitor of SARS coronavirus


We report that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.

Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection.

SOURCE: Virology Journal

Pathogenesis of SARS


Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver.

Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus.

There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441-700 of the spike protein (S protein) as the major epitope.

SOURCE: Current Opinion in Immunology

Risk as feelings


Virtually all current theories of choice under risk or uncertainty are cognitive and consequentialist. They assume that people assess the desirability and likelihood of possible outcomes of choice alternatives and integrate this information through some type of expectation-based calculus to arrive at a decision. The authors propose an alternative theoretical perspective, the risk-as-feelings hypothesis, that highlights the role of affect experienced at the moment of decision making. Drawing on research from clinical, physiological, and other subfields of psychology, they show that emotional reactions to risky situations often diverge from cognitive assessments of those risks. When such divergence occurs, emotional reactions often drive behavior. The risk-as-feelings hypothesis is shown to explain a wide range of phenomena that have resisted interpretation in cognitive-consequentialist terms.

SOURCE: Psychology Bulletin

EDITOR’S NOTE: This article, published in 2001, is the origin of the idea that affect (positive or negative personal reactions or feelings, moods, and emotions) can be as important as, or even more important than cognition (higher-level functions of the brain including language, imagination, perception, and planning) when dealing with risk.