Antigenic and Morphological Similarities of Progressive Pneumonia Virus, a Recently Isolated “Slow Virus” of Sheep, to Visna and Maedi Viruses

Progressive pneumonia virus, the causative agent of a slow, pulmonary disease of Montana sheep, was shown to be antigenically related to two other slow viruses of sheep, visna and maedi. Electron microscopic examination of infected cells revealed that the virus matures by a budding process and that the budding particles as well as the mature, extracellular virions bear striking resemblances to the oncogenic ribonucleic acid (RNA) viruses. Recent findings of an RNA-dependent deoxyribonucleic acid polymerase associated with the virions of this group of slow viruses lend further support to the notion that they may tentatively be classified with the oncogenic RNA tumor viruses.     

Soluble Antigens of Vaccinia-infected Mammalian Cells: III. Relation of “Early” and “Late” Proteins to Virus Structure

The structural proteins of vaccinia virus can be divided into two classes on the basis of their times of synthesis in the infected cell. The production of one of these classes of proteins begins prior to the onset of viral deoxyribonucleic acid (DNA) replication. These are referred to as "early" proteins. Synthesis of the second class of structural proteins follows the onset of viral DNA replication; hence, the term "late" proteins for this class. We are able, by immunological procedures, to identify three "early" virus-structural proteins. These materials, when incorporated into virions, appear to be associated with the "core" of the virion and do not elicit production of virus-neutralizing antibody. It would seem, therefore, that those virus-structural proteins synthesized early in the course of infection act as internal components of the virion. The "late" proteins may be subdivided into two groups on the basis of certain physical properties and molecular weight differences. The first of these groups, comprised of at least two proteins, corresponds to the classical LS antigens and elicits production of neutralizing antibodies. These proteins, when incorporated into virions, are found only in the outer ("coat") fraction of the virion. The second group of "late" antigens, also comprised of two proteins, termed the G antigens, do not elicit synthesis of neutralizing antibody. One of these proteins is associated with the virus "core"; the other is found in the "coat" fraction of the virion and appears to occupy an intermediary, subsurface position. Procedures suitable for the isolation of the G antigens are described, in addition to the partial characterization of these antigens.     

Why Did Bluetongue Spread the Way It Did? Environmental Factors Influencing the Velocity of Bluetongue Virus Serotype 8 Epizootic Wave in France

Understanding where and how fast an infectious disease will spread during an epidemic is critical for its control. However, the task is a challenging one as numerous factors may interact and drive the spread of a disease, specifically when vector-borne diseases are involved. We advocate the use of simultaneous autoregressive models to identify environmental features that significantly impact the velocity of disease spread. We illustrate this approach by exploring several environmental factors influencing the velocity of bluetongue (BT) spread in France during the 2007-2008 epizootic wave to determine which ones were the most important drivers. We used velocities of BT spread estimated in 4,495 municipalities and tested sixteen covariates defining five thematic groups of related variables: elevation, meteorological-related variables, landscape-related variables, host availability, and vaccination. We found that ecological factors associated with vector abundance and activity (elevation and meteorological-related variables), as well as with host availability, were important drivers of the spread of the disease. Specifically, the disease spread more slowly in areas with high elevation and when heavy rainfall associated with extreme temperature events occurred one or two months prior to the first clinical case. Moreover, the density of dairy cattle was correlated negatively with the velocity of BT spread. These findings add substantially to our understanding of BT spread in a temperate climate. Finally, the approach presented in this paper can be used with other infectious diseases, and provides a powerful tool to identify environmental features driving the velocity of disease spread.     

From Victim to Victor: “Breaking Bad” and the Dark Potential of the Terminally Empowered

As treatments for malignancies have improved incrementally over the preceding decades, patients with cancer have been encouraged to reject an attitude of hopelessness and to choose instead the role of fighters. The recasting of the cancer patient as warrior and winner, upheld through the Livestrong movement, reaches its monstrous apotheosis in the form of Walter White, the central figure in the AMC television series “Breaking Bad.” The story begins with Walt as the protagonist, but the arc of this conversion narrative transforms him into the antagonist, exploring the darkest potential of his post-diagnosis empowerment. His awareness of his own mortality enables him to take risks that his more rational, pre-cancer self would have avoided. Rather than being rendered impotent by fear of an impending death, he finds himself emboldened, liberated from behavioral norms, capable of heretofore-unthinkable violence and even murder. As Walt moves from victim to victor, the viewer realizes the perils of a survive-at-all-costs mentality and is forced to question their own, initially sympathetic perception of Walt. The series subverts the notion of the cancer patient made noble through struggle by portraying a man betrayed by his own body who then becomes willing to betray everything else in the amoral service of his pride.     

Genetic Engineering of Tobacco with Double Resistance to Both Virus and Insect

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Transformation of Murine Cells by Two “Slow Viruses,” Visna Virus and Progressive Pneumonia Virus

Visna and progressive pneumonia virus (PPV), two antigenically related, non-oncogenic "slow viruses" which have ribonucleic acid (RNA)-dependent deoxyribonucleic acid (DNA) polymerase activity, were examined for their ability to transform cells. Murine cells which had been exposed to either visna or PPV developed foci of altered, spindle-shaped cells 3 to 4 weeks after infection. Visna and PPV transformed lines were established from these cultures. There was no evidence that other oncogenic DNA or RNA viruses were involved in the observed transformation. Visna or PPV could be "rescued" from all transformed lines by co-cultivation with normal sheep testis cells. "Rescued" virus was identified as visna or PPV, and they retained the capacity to transform mouse cells. These experiments may have important implications in the understanding of both viral carcinogenesis and "slow" viral infections.     

Consequences of trisomy syndromes – 21 and beyond

The mechanisms underlying pathologies in Down syndrome remain poorly understood. In this forum article we compare the cellular phenotypes of chromosome 21 trisomy with other trisomic cells. We argue that both effects of the extra chromosome 21 and the global consequences of chromosome gain must be considered to understand complex pathologies of Down syndrome.