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Phoney wars : New Zealand society in the Second World War
Phoney Wars: New Zealand Society in the Second World War, argues that we had no business going to war against either Germany in 1939 or Japan in 1941. Our motives for doing so were muddled and contradictory. Also we were never in danger of being bombed by any \"enemy\" air force or invaded by any \"enemy\" army. Eldred-Grigg questions the war as a story of \"good\" against \"bad\". Everyone knows the Axis powers behaved ruthlessly, but how many are aware of the brutality of the Allied powers in bombing and starving not only Axis but even Allied peoples? New Zealand colluded in and helped carry out such brutal aggressions. Were we, in going to war, really on the side of the angels? The author's previous book, The Great Wrong War: New Zealand Society in World War I (2010), polarised readers, with its author accused by some of betraying his country, while others congratulated him for setting the record straight. Ultimately there was no compelling reason for New Zealand to involve itself in the war ... All military effort by the dominion was more or less meaningless. New Zealand could have enjoyed the blessings of its safety without going onto a gruelling and wasteful war footing. Nearly eighty years on, the reasons for New Zealand going to war need to be interrogated closely. Was it in the best interests of the people of New Zealand?
Book
Nanobodies from camelid mice and llamas neutralize SARS-CoV-2 variants
Since the start of the COVID-19 pandemic, SARS-CoV-2 has caused millions of deaths worldwide. Although a number of vaccines have been deployed, the continual evolution of the receptor-binding domain (RBD) of the virus has challenged their efficacy. In particular, the emerging variants B.1.1.7, B.1.351 and P.1 (first detected in the UK, South Africa and Brazil, respectively) have compromised the efficacy of sera from patients who have recovered from COVID-19 and immunotherapies that have received emergency use authorization
1
–
3
. One potential alternative to avert viral escape is the use of camelid VHHs (variable heavy chain domains of heavy chain antibody (also known as nanobodies)), which can recognize epitopes that are often inaccessible to conventional antibodies
4
. Here, we isolate anti-RBD nanobodies from llamas and from mice that we engineered to produce VHHs cloned from alpacas, dromedaries and Bactrian camels. We identified two groups of highly neutralizing nanobodies. Group 1 circumvents antigenic drift by recognizing an RBD region that is highly conserved in coronaviruses but rarely targeted by human antibodies. Group 2 is almost exclusively focused to the RBD–ACE2 interface and does not neutralize SARS-CoV-2 variants that carry E484K or N501Y substitutions. However, nanobodies in group 2 retain full neutralization activity against these variants when expressed as homotrimers, and—to our knowledge—rival the most potent antibodies against SARS-CoV-2 that have been produced to date. These findings suggest that multivalent nanobodies overcome SARS-CoV-2 mutations through two separate mechanisms: enhanced avidity for the ACE2-binding domain and recognition of conserved epitopes that are largely inaccessible to human antibodies. Therefore, although new SARS-CoV-2 mutants will continue to emerge, nanobodies represent promising tools to prevent COVID-19 mortality when vaccines are compromised.
Multivalent nanobodies against SARS-CoV-2 from mice engineered to produce camelid nanobodies recognize conserved epitopes that are inaccessible to human antibodies and show promise as a strategy for dealing with viral escape mutations.
Journal Article
Victory City : a history of New York and New Yorkers during World War II
\"While the war launched and leveled nations, spurred economic growth, and saw the rise and fall of global fascism, New York City would eventually emerge as the new capital of the world. From the [Great Depression] to VJ-Day, an array of ... New Yorkers rose to fame, from Mayor Fiorello La Guardia to Franklin and Eleanor Roosevelt, Langston Hughes to Joe Louis, to Robert Moses and Joe DiMaggio ... [This book offers a] new look into the greatest city on earth during the most transformative--and costliest--war in human history\"--Publisher marketing.
Book
Development and characterization of a reverse genetics system for the lineage II Chicava strain of Machupo virus in a guinea pig model
Machupo virus (MACV) is a New World mammarenavirus (hereafter referred to as \"arenavirus\") and the etiologic agent of Bolivian hemorrhagic fever (BHF). No vaccine or antiviral therapy exists for BHF, which causes up to 35% mortality in humans. New World arenaviruses evolve separately in different locations. To date, up to eight lineages of MACV have been identified in Bolivia. While the prototype MACV Carvallo strain belongs to lineage I discovered in the Memore Province in the 1960s, the MACV lineage II strains have become the dominantly-circulating lineage in the same province since 1993.
We report the development of a reverse genetics system for the MACV lineage II Chicava strain, using a pRF42 plasmid encoding the L and S segment genomic RNA under the transcriptional control of a murine DNA-dependent RNA polymerase I promoter sequence. Rescue of the recombinant MACV Chicava strain (rMACV-Chicava) was accomplished by expression of the L protein and nucleoprotein genes of the MACV Carvallo strain in trans in transfected baby hamster kidney (BHK-21) cells. We characterized the multiplication kinetics of rMACV-Chicava in African green monkey kidney epithelial Vero cells, followed by determining the virulence phenotype in outbred Hartley guinea pigs.
We demonstrated that the multiplication kinetics in Vero cells, virulence phenotype in guinea pigs, and neutralizing antibody titers are indistinguishable between rMACV-Chicava and the wild-type parental virus.
We conclude that rMACV-Chicava provides a useful model system to investigate the emergence of MACV lineage II strains and the guinea pig model has utility for the development of candidate vaccines and therapeutic antibodies for BHF.
Journal Article
Cryo-EM structure of the human ferritin–transferrin receptor 1 complex
Human transferrin receptor 1 (CD71) guarantees iron supply by endocytosis upon binding of iron-loaded transferrin and ferritin. Arenaviruses and the malaria parasite exploit CD71 for cell invasion and epitopes on CD71 for interaction with transferrin and pathogenic hosts were identified. Here, we provide the molecular basis of the CD71 ectodomain-human ferritin interaction by determining the 3.9 Å resolution single-particle cryo-electron microscopy structure of their complex and by validating our structural findings in a cellular context. The contact surfaces between the heavy-chain ferritin and CD71 largely overlap with arenaviruses and
Plasmodium vivax
binding regions in the apical part of the receptor ectodomain. Our data account for transferrin-independent binding of ferritin to CD71 and suggest that select pathogens may have adapted to enter cells by mimicking the ferritin access gate.
The human transferrin receptor 1 (CD71) is a transmembrane protein responsible for iron uptake. Here the authors present the 3.9 Å resolution cryo-EM structure of the CD71 ectodomain-human ferritin (H-Ft) complex and find that H-Ft binds a CD71 region different from the transferrin one that overlaps with the surface recognized by select pathogens.
Journal Article
Structure of Machupo virus polymerase in complex with matrix protein Z
The
Arenaviridae
family includes several viruses that cause severe human hemorrhagic fevers with high mortality, with no effective countermeasures currently available. The arenavirus multi-domain L protein is involved in viral transcription and replication and represents a promising target for antiviral drugs. The arenavirus matrix protein Z is a small multi-functional protein that inhibits the activities of the L protein. Here we report the structure of Machupo virus L protein in complex with Z determined by cryo-electron microscopy. The Z protein acts as a staple and binds the L protein with 1:1 stoichiometry at the intersection between the PA-C-like region, RNA-dependent RNA polymerase and PB2-N-like region. Binding of the Z protein may lock the multiple domains of L into a fixed arrangement leading to loss of catalytic activity. These results further our understanding of the inhibitory mechanism of arenavirus replication machinery and provide a novel perspective to develop antiviral drugs.
The RNA polymerase L of arenaviruses is of interest for drug design and its activity is inhibited by the matrix protein Z. Here, the authors present the cryo-EM structure of the Machupo virus polymerase L in complex with matrix protein Z and discuss the inhibitory mechanism.
Journal Article
Sport, war and society in Australia and New Zealand
\"Sport and war have been closely linked in Australian and New Zealand society since the nineteenth century. Sport has, variously, been advocated as appropriate training for war, lambasted as a distraction from the war effort, and resorted to as an escape from wartime trials and tribulations. War has limited the fortunes of some sporting codes - and some individuals - while others have blossomed in the changed circumstances. The chapters in this book range widely over the broad subject of Australian and New Zealand sport and their relation to the cataclysmic world wars of the first half of the twentieth century. They examine the mythology of the links between sport and war, sporting codes, groups of sporting individuals, and individual sportspeople. Revealing complex and often unpredictable effects of total wars upon individuals and social groups which as always, created chaos, and the sporting field offered no exception. This book was originally published as a special issue of the International Journal of the History of Sport\"--Page [i].
Book
Structure and stabilization of the antigenic glycoprotein building blocks of the New World mammarenavirus spike complex
Although the emergence of New World (NW) hemorrhagic fever mammarenaviruses poses an unceasing threat to human health, there is a paucity of reagents capable of protecting against the transmission of these pathogens from their natural rodent reservoirs. This is, in part, attributed to our limited understanding of the structure and function of the NW glycoprotein spike complex presented on the NW arenavirus surface. Here, we provide a detailed molecular-level description of how the two major components of this key therapeutic target assemble to form a key building block of the NW arenaviral spike complex. The insights gleaned from this work provide a framework for guiding the structure-based development of NW arenaviral vaccines.
Journal Article