Diagnosing eclipse-induced wind changes

Responses in surface winds to solar eclipses have an almost mystical status but are difficult to detect in observations because of their transient nature. High spatial resolution (approx. 1.5 km grid) meteorological models now provide a new technique for their investigation. Measurements from the southern UK meteorological network during the 11 August 1999 total solar eclipse are compared with a high-resolution model ignorant of the lunar shadow’s influence. Differences between the model output and measurements at the eclipse time show transient eclipse zone temperature decreases of up to 3 degrees C, which also depressed the day’s maximum temperature compared with the model prediction. Coherent responses in temperature, and wind speed and direction measurements are detected in the inland cloud-free region (from 51 to 52 degrees N and −2 to 0 degrees E). A mean regional wind speed decrease of 0.7 m s−1 during the maximum eclipse hour is apparent with a mean anticlockwise wind direction change of 17 degrees; no such changes occurred in the model output. Such regional circulation changes are consistent with Clayton’s 1901 cold-cored eclipse cyclone hypothesis, which may be related to the anecdotal ‘eclipse wind’.

An intronic G run within HIV-1 intron 2 is critical for splicing regulation of vif mRNA

Within target T lymphocytes, human immunodeficiency virus type I (HIV-1) encounters the retroviral restriction factor APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G; A3G), which is counteracted by the HIV-1 accessory protein Vif. Vif is encoded by intron-containing viral RNAs that are generated by splicing at 3' splice site (3'ss) A1 but lack splicing at 5'ss D2, which results in the retention of a large downstream intron. Hence, the extents of activation of 3'ss A1 and repression of D2, respectively, determine the levels of vif mRNA and thus the ability to evade A3G-mediated antiviral effects. The use of 3'ss A1 can be enhanced or repressed by splicing regulatory elements that control the recognition of downstream 5'ss D2. Here we show that an intronic G run (G(I2)-1) represses the use of a second 5'ss, termed D2b, that is embedded within intron 2 and, as determined by RNA deep-sequencing analysis, is normally inefficiently used. Mutations of G(I2)-1 and activation of D2b led to the generation of transcripts coding for Gp41 and Rev protein isoforms but primarily led to considerable upregulation of vif mRNA expression. We further demonstrate, however, that higher levels of Vif protein are actually detrimental to viral replication in A3G-expressing T cell lines but not in A3G-deficient cells. These observations suggest that an appropriate ratio of Vif-to-A3G protein levels is required for optimal virus replication and that part of Vif level regulation is effected by the novel G run identified here.