ABSTRACT
To evaluate the risk of transmission of SARS coronavirus outside of the health-care setting, close household and community contacts of laboratory-confirmed SARS cases were identified and followed up for clinical and laboratory evidence of SARS infection. Individual- and household-level risk factors for transmission were investigated. Nine persons with serological evidence of SARS infection were identified amongst 212 close contacts of 45 laboratory-confirmed SARS cases (secondary attack rate 4.2%, 95% CI 1.5-7). In this cohort, the average number of secondary infections caused by a single infectious case was 0.2. Two community contacts with laboratory evidence of SARS coronavirus infection had mild or sub-clinical infection, representing 3% (2/65) of Vietnamese SARS cases. There was no evidence of transmission of infection before symptom onset. Physically caring for a symptomatic laboratory-confirmed SARS case was the only independent risk factor for SARS transmission (OR 5.78, 95% CI 1.23-24.24).
Subject(s)
Disease Outbreaks , Severe Acute Respiratory Syndrome/transmission , Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Infant , Male , Middle Aged , Risk Factors , Severe Acute Respiratory Syndrome/epidemiology , Severe Acute Respiratory Syndrome/etiology , Vietnam/epidemiologyABSTRACT
Interferon treatment of human leukocytes before stimulation with Sendai virus enhanced interferon synthesis but did not affect their leukocyte migration inhibitory factor (LIF) production. The same interferon pretreatment markedly enhanced both LIF and interferon productions when leukocytes were stimulated with concanavalin A.
Subject(s)
Concanavalin A/pharmacology , Interferons/pharmacology , Leukocyte Migration-Inhibitory Factors/biosynthesis , Leukocytes/metabolism , Lymphokines/biosynthesis , Parainfluenza Virus 1, Human/physiology , Cells, Cultured , Humans , Interferons/biosynthesisABSTRACT
Pretreatments with relatively low (25-250 U/ml) concentrations of interferon (IFN) enhanced while 5000-10 000 U/ml concentrations of IFN inhibited leukocyte inhibitory factor (LIF) and migration inhibitory factor (MIF) production of concanavalin A (Con A) stimulated human leukocytes. The lymphokine regulatory activity of IFN correlated with the antiviral activity of IFN preparations regardless of their specific activity and it showed species specificity. Modulation of lymphokine production depended not only upon the amount of IFN used but also on the length of IFN pretreatment. Blocking of lymphokine production by high concentration of IFN could not be explained by the effect of IFN on cell viability.
