We studied an outbreak of A(H1N1) influenza in an Israeli military unit of 336 healthy young men to determine the relation of cigarette smoking to the incidence of clinically apparent influenza and to the influenza-antibody response. Of 168 smokers, 68.5 per cent had influenza, as compared with 47.2 per cent of nonsmokers (P less than 0.0001). Influenza was also more severe in the smokers; 50.6 per cent of the smokers lost work days or required bed rest, or both, as compared with 30.1 per cent of the nonsmokers. The proportion of all influenza in smokers that was attributable to smoking was 31.2 per cent (95 per cent confidence intervals, 16.5 to 43.1 per cent). For severe influenza, the attributable risk in the smokers was 40.6 per cent (95 per cent confidence intervals, 21.6 to 54.8 per cent). A quarter of all severe morbidity from influenza in the overall study population was attributable to smoking. Antibody levels to A/USSR/90/77(H1N1) antigen were higher in smokers but not markedly so. We conclude that smoking is a major determinant of morbidity in epidemic influenza and may contribute substantially to incapacitation in outbreaks in populations that smoke heavily.

Many experiments have shown convincingly that natural killer (NK) cell activity against viral infections is an important early defence mechanism in mice. Since the NK response occurs soon after infection, often long before clinical signs of disease become manifest, it has been difficult to design studies to monitor accurately NK cell kinetics following infection, without actually administering pathogens to volunteers. There is therefore little data pertaining to the role of NK cells in humans. Nevertheless, a number of studies have shown elevated NK activity in response to herpes simplex and influenza virus infections in humans. Our study was designed to show that NK activity could be provoked in humans by exposure to viral particles without actual live viral infection. The development of NK cell response in the peripheral blood of volunteers shortly after vaccination with killed influenza trivalent vaccine was studied. The results demonstrate that killed virus vaccine induces and augments NK cell activity for relatively long periods. Such data may prove valuable for designing possible modes of augmenting NK activity as a therapeutic tool.

Subacute sclerosing panencephalitis (SSPE), a disease related to measles (rubeola) infection, was more common in Arabs and Sephardi Jews than in Ashkenazi Jews in Israel. There were no familial aggregates and it is unlikely that genetic differences account for this selectivity. Among several non-genetic factors which might explain the selectivity, family size emerged as a possible risk factor. Family size has not previously been suspected as influencing the risk of SSPE. Preponderance of SSPE in rural areas and among the poor would also be compatible with this idea as family size tends to be larger in rural and lower socioeconomic groups. In large families, there may be a greater change that older siblings will transmit measles to very young siblings. In small families, measles may be acquired from peers at about school age when risk of SSPE may be lower.

An outbreak of influenza caused by the A(H1N1) subtype in military recruits in February 1978 afforded an opportunity to study the association of ABO blood groups with influenza morbidity and serological response. Fifty-eight per cent of 336 recruits became clinically ill. There was no differential distribution of clinical influenza by blood group. However, seroconversion to a titre of greater than or equal to 20 was significantly and appreciably higher in groups A and B than O and AB. Also, among those with serologically confirmed clinical influenza, the occurrence was significantly higher in groups A and B than groups O and AB.

An enzyme-linked immunosorbent assay (ELISA) was developed and used for the detection of IgG and IgM antibodies to West Nile virus in human sera. Thirteen paired sera of clinical cases and 24 control sera taken randomly from a blood bank repository were tested. The sera were reacted in microtiter plates coated with PEG-treated WNV antigen. IgG or IgM antibodies were quantitated by the use of alkaline-phosphatase-conjugated anti-human IgG or IgM antibodies. Of the 24 randomly collected serum samples, 7 were positive in the IgG-ELISA test. One positive by the IgM-ELISA was found to contain rheumatoid factor. In 12 of 13 paired sera of clinical cases, IgM as well as IgG antibodies were detected in the second serum sample taken about 3 wk after the onset of clinical signs. The IgM positive sera were screened for rheumatoid factor (RF) on IgG-coated plates. None of them contained RF. Antibody titers obtained by ELISA showed a good correlation with titers obtained by hemagglutination inhibition, complement fixation, and neutralization tests. The ELISA tests for detection of IgM and IgG antibodies to WNV therefore can replace the other serological methods for epidemiological surveillance and diagnostic purposes.