Consistent multidecadal variability in global temperature reconstructions and simulations over the Common Era

Multidecadal surface temperature changes may be forced by natural as well as anthropogenic factors, or arise unforced from the climate system. Distinguishing these factors is essential for estimating sensitivity to multiple climatic forcings and the amplitude of the unforced variability. Here we present 2,000-year-long global mean temperature reconstructions using seven different statistical methods that draw from a global collection of temperature-sensitive palaeoclimate records. Our reconstructions display synchronous multidecadal temperature fluctuations that are coherent with one another and with fully forced millennial model simulations from the Coupled Model Intercomparison Project Phase 5 across the Common Era. A substantial portion of pre-industrial (1300–1800 CE) variability at multidecadal timescales is attributed to volcanic aerosol forcing. Reconstructions and simulations qualitatively agree on the amplitude of the unforced global mean multidecadal temperature variability, thereby increasing confidence in future projections of climate change on these timescales. The largest warming trends at timescales of 20 years and longer occur during the second half of the twentieth century, highlighting the unusual character of the warming in recent decades

Connection between weak stratospheric vortex events and the Pacific Decadal Oscillation

We investigate the possible impacts of the Pacific Decadal Oscillation (PDO) on the occurrence of weak stratospheric polar vortex (WSV) events in the Northern Hemisphere winter. WSV events, which are defined when polar-cap geopotential height anomalies at 50 hPa fall below the 10th percentile in winter, are observed more frequently during positive PDO phases than during negative PDO phases. Additionally, tropospheric wave forcings that drive WSV events are remarkably different between the two phases of the PDO. During the positive PDO phase, the vertical propagation of wavenumber-one waves plays a predominant role with a rather minor contribution of wavenumber-two waves. This contrasts with the negative PDO phase when the WSV events are primarily caused by wavenumber-two waves. This difference is partly related to the PDO-induced tropospheric circulation anomalies over the North Pacific whose zonal wavenumber-one component constructively (destructively) interferes with climatological planetary-scale waves during positive (negative) PDO winters. The predominant wavenumber-two wave forcings during the negative PDO phase are likely related to the enhanced tropospheric eddy activity over Alaska that results from the poleward shift of the Pacific jet in response to the negative PDO.N

Optimization of Multimeric Human Papillomavirus L2 Vaccines

We sought to define the protective epitopes within the amino terminus of human papillomavirus (HPV) type 16 minor capsid protein L2. Passive transfer of mice with rabbit antisera to HPV16 L2 peptides 17–36, 32–51 and 65–81 provided significant protection against vaginal HPV16 challenge, whereas antisera to 47–66, 108–120 or 373–392 did not. Vaccination with L1 virus-like particles induces a high titer, but generally type-restricted neutralizing antibody response. Conversely, vaccination with L2 11–88, especially multimers thereof, induces antibodies that neutralize a broad range of papillomavirus types, albeit at lower titers than for L1 VLP. With the intent of enhancing the immunogenicity and the breadth of protection by focusing the immune response to the key protective epitopes, we designed L2 fusion proteins consisting of residues ∼11–88 of eight divergent mucosal HPV types 6, 16, 18, 31, 39, 51, 56, 73 (11–88×8) or residues ∼13–47 of fifteen HPV types (13–47×15). The 11–88×8 was significantly more immunogenic than 13–47×15 in Balb/c mice regardless of the adjuvant used, suggesting the value of including the 65–81 protective epitope in the vaccine. Since the L2 47–66 peptide antiserum failed to elicit significant protection, we generated an 11–88×8 construct deleted for this region in each subunit (11–88×8Δ). Mice were vaccinated with 11–88×8 and 11–88×8Δ to determine if deletion of this non-protective epitope enhanced the neutralizing antibody response. However, 11–88×8Δ was significantly less immunogenic than 11–88×8, and even the addition of a known T helper epitope, PADRE, to the construct (11–88×8ΔPADRE) failed to recover the immunogenicity of 11–88×8 in C57BL/6 mice, suggesting that while L2 47–66 is not a critical protective or T helper epitope, it nevertheless contributes to the immunogenicity of the L2 11–88×8 multimer vaccine