Metabolic labeling was performed as previously described [19, 45] . Briefly, 293T cells were transfected using the calciumphosphate method with plasmid DNA encoding individual Env. Twenty-four hours later, cells were starved in cysteine and methionine-free DMEM for 30 minutes, pulse-labeled with 62.5 mCi 35 S-cysteine and -methionine for 1 h at 37uC, washed with fresh media and chased for 4 h at 37uC in complete growth medium. Media were then collected and cells washed and lysed (50 mM Tris pH 8.0, 150 mM NaCl, 0.4 mM EDTA, 1% Triton X-100, 0.1% NP-40, 10 mg/ml aprotinin (Sigma), 10 mg/ml leupeptin (Sigma) and 1 mM phenylmethylsulfonyl fluoride (Sigma). The XMRV Env proteins in media and in cell lysates were immunoprecipitated using anti-FLAG beads and resolved by SDS-PAGE. Dried gels were autoradiographed and band intensities of XMRV SU in the cultured media were quantified using the Quantity One software (Bio-Rad, Hercules, CA). The Impact of Weather on Influenza and Pneumonia Mortality in New York City, 1975–2002: A Retrospective Study The substantial winter influenza peak in temperate climates has lead to the hypothesis that cold and/or dry air is a causal factor in influenza variability. We examined the relationship between cold and/or dry air and daily influenza and pneumonia mortality in the cold season in the New York metropolitan area from 1975–2002. We conducted a retrospective study relating daily pneumonia and influenza mortality for New York City and surroundings from 1975–2002 to daily air temperature, dew point temperature (a measure of atmospheric humidity), and daily air mass type. We identified high mortality days and periods and employed temporal smoothers and lags to account for the latency period and the time between infection and death. Unpaired t-tests were used to compare high mortality events to non-events and nonparametric bootstrapped regression analysis was used to examine the characteristics of longer mortality episodes. We found a statistically significant (p = 0.003) association between periods of low dew point temperature and above normal pneumonia and influenza mortality 17 days later. The duration (r = −0.61) and severity (r = −0.56) of high mortality episodes was inversely correlated with morning dew point temperature prior to and during the episodes. Weeks in which moist polar air masses were common (air masses characterized by low dew point temperatures) were likewise followed by above normal mortality 17 days later (p = 0.019). This research supports the contention that cold, dry air may be related to influenza mortality and suggests that warning systems could provide enough lead time to be effective in mitigating the effects. It is well known that intra-annual mortality exhibits a pronounced winter peak in locations with seasonal climates [1] , [2] . In the United States, mortality arising from respiratory disease is 50% higher in winter than in summer [1] . One contributor to this excess winter mortality is influenza [3] , the timing and severity of which can vary significantly from year to year. The association between the annual influenza peak and winter weather in temperate locations has lead to the hypothesis that weather variability could influence influenza mortality variations [4] , [5] .